Aberrant astrocytes impair vascular reactivity in Huntington disease
Objective Huntington disease (HD) is an inherited neurodegenerative disease caused by the mutant huntingtin gene (mHTT), which harbors expanded CAG repeats. We previously reported that the brain vessel density is higher in mice and patients with HD than in controls. The present study determines whet...
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| Published in | Annals of neurology Vol. 78; no. 2; pp. 178 - 192 |
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| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Blackwell Publishing Ltd
01.08.2015
Wiley Subscription Services, Inc |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Objective
Huntington disease (HD) is an inherited neurodegenerative disease caused by the mutant huntingtin gene (mHTT), which harbors expanded CAG repeats. We previously reported that the brain vessel density is higher in mice and patients with HD than in controls. The present study determines whether vascular function is altered in HD and characterizes the underlying mechanism.
Methods
The brain vessel density and vascular reactivity (VR) to carbogen challenge of HD mice were monitored by 3D ΔR2‐mMRA and blood oxygenation level–dependent (BOLD)/flow‐sensitive alternating inversion recovery (FAIR) magnetic resonance imaging (MRI), respectively. The amount of vascular endothelial growth factor (VEGF)‐A and the pericyte coverage were determined by immunohistochemistry and enzyme‐linked immunosorbent assay in human and mouse brain sections, primary mouse astrocytes and pericytes, and human astrocytes derived from induced pluripotent stem cells.
Results
Expression of mHTT in astrocytes and neurons is sufficient to increase the brain vessel density in HD mice. BOLD and FAIR MRI revealed gradually impaired VR to carbogen in HD mice. Astrocytes from HD mice and patients contained more VEGF‐A, which triggers proliferation of endothelial cells and may be responsible for the augmented neurovascular changes. Moreover, an astrocytic inflammatory response, which reduces the survival of pericytes through an IκB kinase–dependent pathway, mediates the low pericyte coverage of blood vessels in HD brains.
Interpretation
Our findings suggest that the inflammation‐prone HD astrocytes provide less pericyte coverage by promoting angiogenesis and reducing the number of pericytes and that these changes can explain the inferior VR in HD mice. The resultant impaired VR might hinder cerebral hemodynamics and increase brain atrophy during HD progression. Ann Neurol 2015;78:178–192 |
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| AbstractList | OBJECTIVEHuntington disease (HD) is an inherited neurodegenerative disease caused by the mutant huntingtin gene (mHTT), which harbors expanded CAG repeats. We previously reported that the brain vessel density is higher in mice and patients with HD than in controls. The present study determines whether vascular function is altered in HD and characterizes the underlying mechanism.METHODSThe brain vessel density and vascular reactivity (VR) to carbogen challenge of HD mice were monitored by 3D ΔR2 -mMRA and blood oxygenation level-dependent (BOLD)/flow-sensitive alternating inversion recovery (FAIR) magnetic resonance imaging (MRI), respectively. The amount of vascular endothelial growth factor (VEGF)-A and the pericyte coverage were determined by immunohistochemistry and enzyme-linked immunosorbent assay in human and mouse brain sections, primary mouse astrocytes and pericytes, and human astrocytes derived from induced pluripotent stem cells.RESULTSExpression of mHTT in astrocytes and neurons is sufficient to increase the brain vessel density in HD mice. BOLD and FAIR MRI revealed gradually impaired VR to carbogen in HD mice. Astrocytes from HD mice and patients contained more VEGF-A, which triggers proliferation of endothelial cells and may be responsible for the augmented neurovascular changes. Moreover, an astrocytic inflammatory response, which reduces the survival of pericytes through an IκB kinase-dependent pathway, mediates the low pericyte coverage of blood vessels in HD brains.INTERPRETATIONOur findings suggest that the inflammation-prone HD astrocytes provide less pericyte coverage by promoting angiogenesis and reducing the number of pericytes and that these changes can explain the inferior VR in HD mice. The resultant impaired VR might hinder cerebral hemodynamics and increase brain atrophy during HD progression. Objective Huntington disease (HD) is an inherited neurodegenerative disease caused by the mutant huntingtin gene (mHTT), which harbors expanded CAG repeats. We previously reported that the brain vessel density is higher in mice and patients with HD than in controls. The present study determines whether vascular function is altered in HD and characterizes the underlying mechanism. Methods The brain vessel density and vascular reactivity (VR) to carbogen challenge of HD mice were monitored by 3D Delta R sub(2)-mMRA and blood oxygenation level-dependent (BOLD)/flow-sensitive alternating inversion recovery (FAIR) magnetic resonance imaging (MRI), respectively. The amount of vascular endothelial growth factor (VEGF)-A and the pericyte coverage were determined by immunohistochemistry and enzyme-linked immunosorbent assay in human and mouse brain sections, primary mouse astrocytes and pericytes, and human astrocytes derived from induced pluripotent stem cells. Results Expression of mHTT in astrocytes and neurons is sufficient to increase the brain vessel density in HD mice. BOLD and FAIR MRI revealed gradually impaired VR to carbogen in HD mice. Astrocytes from HD mice and patients contained more VEGF-A, which triggers proliferation of endothelial cells and may be responsible for the augmented neurovascular changes. Moreover, an astrocytic inflammatory response, which reduces the survival of pericytes through an I Kappa B kinase-dependent pathway, mediates the low pericyte coverage of blood vessels in HD brains. Interpretation Our findings suggest that the inflammation-prone HD astrocytes provide less pericyte coverage by promoting angiogenesis and reducing the number of pericytes and that these changes can explain the inferior VR in HD mice. The resultant impaired VR might hinder cerebral hemodynamics and increase brain atrophy during HD progression. Ann Neurol 2015; 78:178-192 Objective Huntington disease (HD) is an inherited neurodegenerative disease caused by the mutant huntingtin gene (mHTT), which harbors expanded CAG repeats. We previously reported that the brain vessel density is higher in mice and patients with HD than in controls. The present study determines whether vascular function is altered in HD and characterizes the underlying mechanism. Methods The brain vessel density and vascular reactivity (VR) to carbogen challenge of HD mice were monitored by 3D [Delta]R2-mMRA and blood oxygenation level-dependent (BOLD)/flow-sensitive alternating inversion recovery (FAIR) magnetic resonance imaging (MRI), respectively. The amount of vascular endothelial growth factor (VEGF)-A and the pericyte coverage were determined by immunohistochemistry and enzyme-linked immunosorbent assay in human and mouse brain sections, primary mouse astrocytes and pericytes, and human astrocytes derived from induced pluripotent stem cells. Results Expression of mHTT in astrocytes and neurons is sufficient to increase the brain vessel density in HD mice. BOLD and FAIR MRI revealed gradually impaired VR to carbogen in HD mice. Astrocytes from HD mice and patients contained more VEGF-A, which triggers proliferation of endothelial cells and may be responsible for the augmented neurovascular changes. Moreover, an astrocytic inflammatory response, which reduces the survival of pericytes through an I[kappa]B kinase-dependent pathway, mediates the low pericyte coverage of blood vessels in HD brains. Interpretation Our findings suggest that the inflammation-prone HD astrocytes provide less pericyte coverage by promoting angiogenesis and reducing the number of pericytes and that these changes can explain the inferior VR in HD mice. The resultant impaired VR might hinder cerebral hemodynamics and increase brain atrophy during HD progression. Ann Neurol 2015;78:178-192 Objective Huntington disease (HD) is an inherited neurodegenerative disease caused by the mutant huntingtin gene (mHTT), which harbors expanded CAG repeats. We previously reported that the brain vessel density is higher in mice and patients with HD than in controls. The present study determines whether vascular function is altered in HD and characterizes the underlying mechanism. Methods The brain vessel density and vascular reactivity (VR) to carbogen challenge of HD mice were monitored by 3D ΔR2‐mMRA and blood oxygenation level–dependent (BOLD)/flow‐sensitive alternating inversion recovery (FAIR) magnetic resonance imaging (MRI), respectively. The amount of vascular endothelial growth factor (VEGF)‐A and the pericyte coverage were determined by immunohistochemistry and enzyme‐linked immunosorbent assay in human and mouse brain sections, primary mouse astrocytes and pericytes, and human astrocytes derived from induced pluripotent stem cells. Results Expression of mHTT in astrocytes and neurons is sufficient to increase the brain vessel density in HD mice. BOLD and FAIR MRI revealed gradually impaired VR to carbogen in HD mice. Astrocytes from HD mice and patients contained more VEGF‐A, which triggers proliferation of endothelial cells and may be responsible for the augmented neurovascular changes. Moreover, an astrocytic inflammatory response, which reduces the survival of pericytes through an IκB kinase–dependent pathway, mediates the low pericyte coverage of blood vessels in HD brains. Interpretation Our findings suggest that the inflammation‐prone HD astrocytes provide less pericyte coverage by promoting angiogenesis and reducing the number of pericytes and that these changes can explain the inferior VR in HD mice. The resultant impaired VR might hinder cerebral hemodynamics and increase brain atrophy during HD progression. Ann Neurol 2015;78:178–192 Huntington disease (HD) is an inherited neurodegenerative disease caused by the mutant huntingtin gene (mHTT), which harbors expanded CAG repeats. We previously reported that the brain vessel density is higher in mice and patients with HD than in controls. The present study determines whether vascular function is altered in HD and characterizes the underlying mechanism. The brain vessel density and vascular reactivity (VR) to carbogen challenge of HD mice were monitored by 3D ΔR2 -mMRA and blood oxygenation level-dependent (BOLD)/flow-sensitive alternating inversion recovery (FAIR) magnetic resonance imaging (MRI), respectively. The amount of vascular endothelial growth factor (VEGF)-A and the pericyte coverage were determined by immunohistochemistry and enzyme-linked immunosorbent assay in human and mouse brain sections, primary mouse astrocytes and pericytes, and human astrocytes derived from induced pluripotent stem cells. Expression of mHTT in astrocytes and neurons is sufficient to increase the brain vessel density in HD mice. BOLD and FAIR MRI revealed gradually impaired VR to carbogen in HD mice. Astrocytes from HD mice and patients contained more VEGF-A, which triggers proliferation of endothelial cells and may be responsible for the augmented neurovascular changes. Moreover, an astrocytic inflammatory response, which reduces the survival of pericytes through an IκB kinase-dependent pathway, mediates the low pericyte coverage of blood vessels in HD brains. Our findings suggest that the inflammation-prone HD astrocytes provide less pericyte coverage by promoting angiogenesis and reducing the number of pericytes and that these changes can explain the inferior VR in HD mice. The resultant impaired VR might hinder cerebral hemodynamics and increase brain atrophy during HD progression. |
| Author | Chern, Yijuang Kuo, Hung-Chih Chen, Hui-Mei Chen, Chiao-Chi Hsiao, Han-Yun Huang, Chien-Hsiang Hsu, Yi-Hua Chiu, Feng-Lan Chang, Chen Chen, Yu-Chen |
| Author_xml | – sequence: 1 givenname: Han-Yun surname: Hsiao fullname: Hsiao, Han-Yun organization: Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan – sequence: 2 givenname: Yu-Chen surname: Chen fullname: Chen, Yu-Chen organization: Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan – sequence: 3 givenname: Chien-Hsiang surname: Huang fullname: Huang, Chien-Hsiang organization: Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan – sequence: 4 givenname: Chiao-Chi surname: Chen fullname: Chen, Chiao-Chi organization: Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan – sequence: 5 givenname: Yi-Hua surname: Hsu fullname: Hsu, Yi-Hua organization: Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan – sequence: 6 givenname: Hui-Mei surname: Chen fullname: Chen, Hui-Mei organization: Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan – sequence: 7 givenname: Feng-Lan surname: Chiu fullname: Chiu, Feng-Lan organization: Institute of Cellular and Organismic Biology, Academia Sinica, Taipei, Taiwan – sequence: 8 givenname: Hung-Chih surname: Kuo fullname: Kuo, Hung-Chih organization: Institute of Cellular and Organismic Biology, Academia Sinica, Taipei, Taiwan – sequence: 9 givenname: Chen surname: Chang fullname: Chang, Chen email: bmychern@ibms.sinica.edu.tw organization: Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan – sequence: 10 givenname: Yijuang surname: Chern fullname: Chern, Yijuang email: bmychern@ibms.sinica.edu.tw organization: Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan |
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| References | Lythgoe DJ, Williams SCR, Cullinane M, Markus HS. Mapping of cerebrovascular reactivity using bold magnetic resonance imaging. Magn Reson Imaging 1999;17:495-502. Nitta T, Hata M, Gotoh S, et al. Size-selective loosening of the blood-brain barrier in claudin-5-deficient mice. J Cell Biol 2003;161:653-660. Sedlacik J, Kutschbach C, Rauscher A, et al. Investigation of the influence of carbon dioxide concentrations on cerebral physiology by susceptibility-weighted magnetic resonance imaging (SWI). Neuroimage 2008;43:36-43. Khoshnan A, Ko J, Watkin EE, et al. Activation of the IkappaB kinase complex and nuclear factor-kappaB contributes to mutant huntingtin neurotoxicity. J Neurosci 2004;24:7999-8008. Schilling G, Becher MW, Sharp AH, et al. Intranuclear inclusions and neuritic aggregates in transgenic mice expressing a mutant N-terminal fragment of huntingtin. Hum Mol Genet 1999;8:397-407. Winkler EA, Sengillo JD, Bell RD, et al. Blood-spinal cord barrier pericyte reductions contribute to increased capillary permeability. J Cereb Blood Flow Metab 2012;32:1841-1852. Chen JJ, Salat DH, Rosas HD. Complex relationships between cerebral blood flow and brain atrophy in early Huntington's disease. Neuroimage 2012;59:1043-1051. Bradford J, Shin JY, Roberts M, et al. Expression of mutant huntingtin in mouse brain astrocytes causes age-dependent neurological symptoms. Proc Natl Acad Sci U S A 2009;106:22480-22485. Lin CY, Hsu YH, Lin MH, et al. Neurovascular abnormalities in humans and mice with Huntington's disease. Exp Neurol 2013;250C:20-30. Silvestrini M, Pasqualetti P, Baruffaldi R, et al. Cerebrovascular reactivity and cognitive decline in patients with Alzheimer disease. Stroke 2006;37:1010-1015. Franciosi S, Ryu JK, Shim Y, et al. Age-dependent neurovascular abnormalities and altered microglial morphology in the YAC128 mouse model of Huntington disease. Neurobiol Dis 2012;45:438-449. Brown WR, Thore CR. Review: cerebral microvascular pathology in ageing and neurodegeneration. Neuropathol Appl Neurobiol 2011;37:56-74. Peppiatt CM, Howarth C, Mobbs P, Attwell D. Bidirectional control of CNS capillary diameter by pericytes. Nature 2006;443:700-704. Kalaria RN. Vascular basis for brain degeneration: faltering controls and risk factors for dementia. Nutr Rev 2010;68(suppl 2):S74-S87. Cantin S, Villien M, Moreaud O, et al. Impaired cerebral vasoreactivity to CO2 in Alzheimer's disease using BOLD fMRI. Neuroimage 2011;58:579-587. Siow TY, Chen CC, Wan N, et al. In vivo evidence of increased nNOS activity in acute MPTP neurotoxicity: a functional pharmacological MRI study. Biomed Res Int 2013;2013:964034. Wolf RC, Gron G, Sambataro F, et al. Magnetic resonance perfusion imaging of resting-state cerebral blood flow in preclinical Huntington's disease. J Cereb Blood Flow Metab 2011;31:1908-1918. Neufeld G, Cohen T, Gengrinovitch S, Poltorak Z. Vascular endothelial growth factor (VEGF) and its receptors. FASEB J 1999;13:9-22. Tigges U, Welser-Alves JV, Boroujerdi A, Milner R. A novel and simple method for culturing pericytes from mouse brain. Microvasc Res 2012;84:74-80. Bonkowski D, Katyshev V, Balabanov RD, et al. The CNS microvascular pericyte: pericyte-astrocyte crosstalk in the regulation of tissue survival. Fluids Barriers CNS 2011;8:8. Walker FO. Huntington's disease. Lancet 2007;369:218-228. Rauscher A, Sedlacik J, Barth M, et al. Noninvasive assessment of vascular architecture and function during modulated blood oxygenation using susceptibility weighted magnetic resonance imaging. Magn Reson Med 2005;54:87-95. Allaman I, Belanger M, Magistretti PJ. Astrocyte-neuron metabolic relationships: for better and for worse. Trends Neurosci 2011;34:76-87. Chen CC, Chen YC, Hsiao HY, et al. Neurovascular abnormalities in brain disorders: highlights with angiogenesis and magnetic resonance imaging studies. J Biomed Sci 2013;20:47. Harris GJ, Codori AM, Lewis RF, et al. Reduced basal ganglia blood flow and volume in pre-symptomatic, gene-tested persons at-risk for Huntington's disease. Brain 1999;122(pt 9):1667-1678. Ross CA, Tabrizi SJ. Huntington's disease: from molecular pathogenesis to clinical treatment. Lancet Neurol 2011;10:83-98. Armulik A, Abramsson A, Betsholtz C. Endothelial/pericyte interactions. Circ Res 2005;97:512-523. Huang YC, Wu YR, Tseng MY, et al. Increased prothrombin, apolipoprotein A-IV, and haptoglobin in the cerebrospinal fluid of patients with Huntington's disease. PLoS One 2011;6:e15809. Chiarini A, Whitfield J, Bonafini C, et al. Amyloid-beta(25-35), an amyloid-beta(1-42) surrogate, and proinflammatory cytokines stimulate VEGF-A secretion by cultured, early passage, normoxic adult human cerebral astrocytes. J Alzheimers Dis 2010;21:915-926. Bell RD, Winkler EA, Sagare AP, et al. Pericytes control key neurovascular functions and neuronal phenotype in the adult brain and during brain aging. Neuron 2010;68:409-427. Oberheim NA, Takano T, Han X, et al. Uniquely hominid features of adult human astrocytes. J Neurosci 2009;29:3276-3287. Mangiarini L, Sathasivam K, Seller M, et al. Exon 1 of the HD gene with an expanded CAG repeat is sufficient to cause a progressive neurological phenotype in transgenic mice. Cell 1996;87:493-506. Lin HH, Lai SC, Chau LY. Heme oxygenase-1/carbon monoxide induces vascular endothelial growth factor expression via p38 kinase-dependent activation of Sp1. J Biol Chem 2011;286:3829-3838. Vis JC, Nicholson LF, Faull RL, et al. Connexin expression in Huntington's diseased human brain. Cell Biol Int 1998;22:837-847. Markus H, Cullinane M. Severely impaired cerebrovascular reactivity predicts stroke and TIA risk in patients with carotid artery stenosis and occlusion. Brain 2001;124:457-467. Hsiao HY, Chiu FL, Chen CM, et al. Inhibition of soluble tumor necrosis factor is therapeutic in Huntington's disease. Hum Mol Genet 2014;23:4328-4344. Neng L, Zhang W, Hassan A, et al. Isolation and culture of endothelial cells, pericytes and perivascular resident macrophage-like melanocytes from the young mouse ear. Nat Protoc 2013;8:709-720. Lin CY, Lin MH, Cheung WM, et al. In vivo cerebromicrovasculatural visualization using 3D DeltaR2-based microscopy of magnetic resonance angiography (3DDeltaR2-mMRA). Neuroimage 2009;45:824-831. Ringelstein EB, Van Eyck S, Mertens I. Evaluation of cerebral vasomotor reactivity by various vasodilating stimuli: comparison of CO2 to acetazolamide. J Cereb Blood Flow Metab 1992;12:162-168. Winkler EA, Bell RD, Zlokovic BV. Central nervous system pericytes in health and disease. Nat Neurosci 2011;14:1398-1405. Chou SY, Weng JY, Lai HL, et al. Expanded-polyglutamine huntingtin protein suppresses the secretion and production of a chemokine (CCL5/RANTES) by astrocytes. J Neurosci 2008;28:3277-3290. Gusella JF, Wexler NS, Conneally PM, et al. A polymorphic DNA marker genetically linked to Huntington's disease. Nature 1983;306:234-238. Cepeda-Prado E, Popp S, Khan U, et al. R6/2 Huntington's disease mice develop early and progressive abnormal brain metabolism and seizures. J Neurosci 2012;32:6456-6467. Hsiao HY, Chen YC, Chen HM, et al. A critical role of astrocyte-mediated nuclear factor-kappaB-dependent inflammation in Huntington's disease. Hum Mol Genet 2013;22:1826-1842. Hua J, Unschuld PG, Margolis RL, et al. Elevated arteriolar cerebral blood volume in prodromal Huntington's disease. Mov Disord 2014;29:396-401. 2009; 45 2001; 124 2007; 369 2013; 22 2013; 20 2004; 24 2006; 37 2011; 31 2011; 10 2011; 34 1999; 122 2014; 29 2011; 37 2013; 250C 2011; 14 2012; 59 2011; 58 1999; 8 2013; 8 2011; 6 1992; 12 2011; 8 2012; 32 2014; 23 1998; 22 2009; 29 2010; 21 2010; 68 2013; 2013 1999; 17 2008; 28 1999; 13 2003; 161 2005; 97 2005; 54 2008; 43 2012; 45 1996; 87 1983; 306 2011; 286 2006; 443 2009; 106 2012; 84 26018216 - Ann Neurol. 2015 Aug;78(2):158-9 |
| References_xml | – reference: Schilling G, Becher MW, Sharp AH, et al. Intranuclear inclusions and neuritic aggregates in transgenic mice expressing a mutant N-terminal fragment of huntingtin. Hum Mol Genet 1999;8:397-407. – reference: Tigges U, Welser-Alves JV, Boroujerdi A, Milner R. A novel and simple method for culturing pericytes from mouse brain. Microvasc Res 2012;84:74-80. – reference: Chiarini A, Whitfield J, Bonafini C, et al. Amyloid-beta(25-35), an amyloid-beta(1-42) surrogate, and proinflammatory cytokines stimulate VEGF-A secretion by cultured, early passage, normoxic adult human cerebral astrocytes. J Alzheimers Dis 2010;21:915-926. – reference: Silvestrini M, Pasqualetti P, Baruffaldi R, et al. Cerebrovascular reactivity and cognitive decline in patients with Alzheimer disease. Stroke 2006;37:1010-1015. – reference: Walker FO. Huntington's disease. Lancet 2007;369:218-228. – reference: Rauscher A, Sedlacik J, Barth M, et al. Noninvasive assessment of vascular architecture and function during modulated blood oxygenation using susceptibility weighted magnetic resonance imaging. Magn Reson Med 2005;54:87-95. – reference: Chen JJ, Salat DH, Rosas HD. Complex relationships between cerebral blood flow and brain atrophy in early Huntington's disease. Neuroimage 2012;59:1043-1051. – reference: Huang YC, Wu YR, Tseng MY, et al. Increased prothrombin, apolipoprotein A-IV, and haptoglobin in the cerebrospinal fluid of patients with Huntington's disease. PLoS One 2011;6:e15809. – reference: Winkler EA, Sengillo JD, Bell RD, et al. Blood-spinal cord barrier pericyte reductions contribute to increased capillary permeability. J Cereb Blood Flow Metab 2012;32:1841-1852. – reference: Gusella JF, Wexler NS, Conneally PM, et al. A polymorphic DNA marker genetically linked to Huntington's disease. Nature 1983;306:234-238. – reference: Sedlacik J, Kutschbach C, Rauscher A, et al. Investigation of the influence of carbon dioxide concentrations on cerebral physiology by susceptibility-weighted magnetic resonance imaging (SWI). Neuroimage 2008;43:36-43. – reference: Siow TY, Chen CC, Wan N, et al. In vivo evidence of increased nNOS activity in acute MPTP neurotoxicity: a functional pharmacological MRI study. Biomed Res Int 2013;2013:964034. – reference: Chen CC, Chen YC, Hsiao HY, et al. Neurovascular abnormalities in brain disorders: highlights with angiogenesis and magnetic resonance imaging studies. J Biomed Sci 2013;20:47. – reference: Kalaria RN. Vascular basis for brain degeneration: faltering controls and risk factors for dementia. Nutr Rev 2010;68(suppl 2):S74-S87. – reference: Oberheim NA, Takano T, Han X, et al. Uniquely hominid features of adult human astrocytes. J Neurosci 2009;29:3276-3287. – reference: Chou SY, Weng JY, Lai HL, et al. Expanded-polyglutamine huntingtin protein suppresses the secretion and production of a chemokine (CCL5/RANTES) by astrocytes. J Neurosci 2008;28:3277-3290. – reference: Vis JC, Nicholson LF, Faull RL, et al. Connexin expression in Huntington's diseased human brain. Cell Biol Int 1998;22:837-847. – reference: Hsiao HY, Chen YC, Chen HM, et al. A critical role of astrocyte-mediated nuclear factor-kappaB-dependent inflammation in Huntington's disease. Hum Mol Genet 2013;22:1826-1842. – reference: Neng L, Zhang W, Hassan A, et al. Isolation and culture of endothelial cells, pericytes and perivascular resident macrophage-like melanocytes from the young mouse ear. Nat Protoc 2013;8:709-720. – reference: Armulik A, Abramsson A, Betsholtz C. Endothelial/pericyte interactions. Circ Res 2005;97:512-523. – reference: Harris GJ, Codori AM, Lewis RF, et al. Reduced basal ganglia blood flow and volume in pre-symptomatic, gene-tested persons at-risk for Huntington's disease. Brain 1999;122(pt 9):1667-1678. – reference: Markus H, Cullinane M. Severely impaired cerebrovascular reactivity predicts stroke and TIA risk in patients with carotid artery stenosis and occlusion. Brain 2001;124:457-467. – reference: Ross CA, Tabrizi SJ. Huntington's disease: from molecular pathogenesis to clinical treatment. Lancet Neurol 2011;10:83-98. – reference: Cantin S, Villien M, Moreaud O, et al. Impaired cerebral vasoreactivity to CO2 in Alzheimer's disease using BOLD fMRI. Neuroimage 2011;58:579-587. – reference: Bell RD, Winkler EA, Sagare AP, et al. Pericytes control key neurovascular functions and neuronal phenotype in the adult brain and during brain aging. Neuron 2010;68:409-427. – reference: Brown WR, Thore CR. Review: cerebral microvascular pathology in ageing and neurodegeneration. Neuropathol Appl Neurobiol 2011;37:56-74. – reference: Lin CY, Hsu YH, Lin MH, et al. Neurovascular abnormalities in humans and mice with Huntington's disease. Exp Neurol 2013;250C:20-30. – reference: Bradford J, Shin JY, Roberts M, et al. Expression of mutant huntingtin in mouse brain astrocytes causes age-dependent neurological symptoms. Proc Natl Acad Sci U S A 2009;106:22480-22485. – reference: Franciosi S, Ryu JK, Shim Y, et al. Age-dependent neurovascular abnormalities and altered microglial morphology in the YAC128 mouse model of Huntington disease. Neurobiol Dis 2012;45:438-449. – reference: Hsiao HY, Chiu FL, Chen CM, et al. Inhibition of soluble tumor necrosis factor is therapeutic in Huntington's disease. Hum Mol Genet 2014;23:4328-4344. – reference: Hua J, Unschuld PG, Margolis RL, et al. Elevated arteriolar cerebral blood volume in prodromal Huntington's disease. Mov Disord 2014;29:396-401. – reference: Ringelstein EB, Van Eyck S, Mertens I. Evaluation of cerebral vasomotor reactivity by various vasodilating stimuli: comparison of CO2 to acetazolamide. J Cereb Blood Flow Metab 1992;12:162-168. – reference: Winkler EA, Bell RD, Zlokovic BV. Central nervous system pericytes in health and disease. Nat Neurosci 2011;14:1398-1405. – reference: Peppiatt CM, Howarth C, Mobbs P, Attwell D. Bidirectional control of CNS capillary diameter by pericytes. Nature 2006;443:700-704. – reference: Nitta T, Hata M, Gotoh S, et al. Size-selective loosening of the blood-brain barrier in claudin-5-deficient mice. J Cell Biol 2003;161:653-660. – reference: Bonkowski D, Katyshev V, Balabanov RD, et al. The CNS microvascular pericyte: pericyte-astrocyte crosstalk in the regulation of tissue survival. Fluids Barriers CNS 2011;8:8. – reference: Neufeld G, Cohen T, Gengrinovitch S, Poltorak Z. Vascular endothelial growth factor (VEGF) and its receptors. FASEB J 1999;13:9-22. – reference: Mangiarini L, Sathasivam K, Seller M, et al. Exon 1 of the HD gene with an expanded CAG repeat is sufficient to cause a progressive neurological phenotype in transgenic mice. Cell 1996;87:493-506. – reference: Khoshnan A, Ko J, Watkin EE, et al. Activation of the IkappaB kinase complex and nuclear factor-kappaB contributes to mutant huntingtin neurotoxicity. J Neurosci 2004;24:7999-8008. – reference: Lin HH, Lai SC, Chau LY. Heme oxygenase-1/carbon monoxide induces vascular endothelial growth factor expression via p38 kinase-dependent activation of Sp1. J Biol Chem 2011;286:3829-3838. – reference: Lythgoe DJ, Williams SCR, Cullinane M, Markus HS. Mapping of cerebrovascular reactivity using bold magnetic resonance imaging. Magn Reson Imaging 1999;17:495-502. – reference: Lin CY, Lin MH, Cheung WM, et al. In vivo cerebromicrovasculatural visualization using 3D DeltaR2-based microscopy of magnetic resonance angiography (3DDeltaR2-mMRA). Neuroimage 2009;45:824-831. – reference: Allaman I, Belanger M, Magistretti PJ. Astrocyte-neuron metabolic relationships: for better and for worse. Trends Neurosci 2011;34:76-87. – reference: Wolf RC, Gron G, Sambataro F, et al. Magnetic resonance perfusion imaging of resting-state cerebral blood flow in preclinical Huntington's disease. J Cereb Blood Flow Metab 2011;31:1908-1918. – reference: Cepeda-Prado E, Popp S, Khan U, et al. R6/2 Huntington's disease mice develop early and progressive abnormal brain metabolism and seizures. J Neurosci 2012;32:6456-6467. – volume: 37 start-page: 1010 year: 2006 end-page: 1015 article-title: Cerebrovascular reactivity and cognitive decline in patients with Alzheimer disease publication-title: Stroke – volume: 54 start-page: 87 year: 2005 end-page: 95 article-title: assessment of vascular architecture and function during modulated blood oxygenation using susceptibility weighted magnetic resonance imaging publication-title: Magn Reson Med – volume: 17 start-page: 495 year: 1999 end-page: 502 article-title: Mapping of cerebrovascular reactivity using bold magnetic resonance imaging publication-title: Magn Reson Imaging – volume: 286 start-page: 3829 year: 2011 end-page: 3838 article-title: Heme oxygenase‐1/carbon monoxide induces vascular endothelial growth factor expression via p38 kinase‐dependent activation of Sp1 publication-title: J Biol Chem – volume: 124 start-page: 457 year: 2001 end-page: 467 article-title: Severely impaired cerebrovascular reactivity predicts stroke and TIA risk in patients with carotid artery stenosis and occlusion publication-title: Brain – volume: 43 start-page: 36 year: 2008 end-page: 43 article-title: Investigation of the influence of carbon dioxide concentrations on cerebral physiology by susceptibility‐weighted magnetic resonance imaging (SWI) publication-title: Neuroimage – volume: 443 start-page: 700 year: 2006 end-page: 704 article-title: Bidirectional control of CNS capillary diameter by pericytes publication-title: Nature – volume: 106 start-page: 22480 year: 2009 end-page: 22485 article-title: Expression of mutant huntingtin in mouse brain astrocytes causes age‐dependent neurological symptoms publication-title: Proc Natl Acad Sci U S A – volume: 32 start-page: 6456 year: 2012 end-page: 6467 article-title: R6/2 Huntington's disease mice develop early and progressive abnormal brain metabolism and seizures publication-title: J Neurosci – volume: 28 start-page: 3277 year: 2008 end-page: 3290 article-title: Expanded‐polyglutamine huntingtin protein suppresses the secretion and production of a chemokine (CCL5/RANTES) by astrocytes publication-title: J Neurosci – volume: 59 start-page: 1043 year: 2012 end-page: 1051 article-title: Complex relationships between cerebral blood flow and brain atrophy in early Huntington's disease publication-title: Neuroimage – volume: 58 start-page: 579 year: 2011 end-page: 587 article-title: Impaired cerebral vasoreactivity to CO2 in Alzheimer's disease using BOLD fMRI publication-title: Neuroimage – volume: 2013 start-page: 964034 year: 2013 article-title: In vivo evidence of increased nNOS activity in acute MPTP neurotoxicity: a functional pharmacological MRI study publication-title: Biomed Res Int – volume: 21 start-page: 915 year: 2010 end-page: 926 article-title: Amyloid‐beta(25‐35), an amyloid‐beta(1‐42) surrogate, and proinflammatory cytokines stimulate VEGF‐A secretion by cultured, early passage, normoxic adult human cerebral astrocytes publication-title: J Alzheimers Dis – volume: 20 start-page: 47 year: 2013 article-title: Neurovascular abnormalities in brain disorders: highlights with angiogenesis and magnetic resonance imaging studies publication-title: J Biomed Sci – volume: 14 start-page: 1398 year: 2011 end-page: 1405 article-title: Central nervous system pericytes in health and disease publication-title: Nat Neurosci – volume: 37 start-page: 56 year: 2011 end-page: 74 article-title: Review: cerebral microvascular pathology in ageing and neurodegeneration publication-title: Neuropathol Appl Neurobiol – volume: 122 start-page: 1667 issue: pt 9 year: 1999 end-page: 1678 article-title: Reduced basal ganglia blood flow and volume in pre‐symptomatic, gene‐tested persons at‐risk for Huntington's disease publication-title: Brain – volume: 84 start-page: 74 year: 2012 end-page: 80 article-title: A novel and simple method for culturing pericytes from mouse brain publication-title: Microvasc Res – volume: 306 start-page: 234 year: 1983 end-page: 238 article-title: A polymorphic DNA marker genetically linked to Huntington's disease publication-title: Nature – volume: 161 start-page: 653 year: 2003 end-page: 660 article-title: Size‐selective loosening of the blood‐brain barrier in claudin‐5‐deficient mice publication-title: J Cell Biol – volume: 68 start-page: S74 issue: suppl 2 year: 2010 end-page: S87 article-title: Vascular basis for brain degeneration: faltering controls and risk factors for dementia publication-title: Nutr Rev – volume: 8 start-page: 709 year: 2013 end-page: 720 article-title: Isolation and culture of endothelial cells, pericytes and perivascular resident macrophage‐like melanocytes from the young mouse ear publication-title: Nat Protoc – volume: 97 start-page: 512 year: 2005 end-page: 523 article-title: Endothelial/pericyte interactions publication-title: Circ Res – volume: 8 start-page: 397 year: 1999 end-page: 407 article-title: Intranuclear inclusions and neuritic aggregates in transgenic mice expressing a mutant N‐terminal fragment of huntingtin publication-title: Hum Mol Genet – volume: 22 start-page: 837 year: 1998 end-page: 847 article-title: Connexin expression in Huntington's diseased human brain publication-title: Cell Biol Int – volume: 23 start-page: 4328 year: 2014 end-page: 4344 article-title: Inhibition of soluble tumor necrosis factor is therapeutic in Huntington's disease publication-title: Hum Mol Genet – volume: 10 start-page: 83 year: 2011 end-page: 98 article-title: Huntington's disease: from molecular pathogenesis to clinical treatment publication-title: Lancet Neurol – volume: 13 start-page: 9 year: 1999 end-page: 22 article-title: Vascular endothelial growth factor (VEGF) and its receptors publication-title: FASEB J – volume: 31 start-page: 1908 year: 2011 end-page: 1918 article-title: Magnetic resonance perfusion imaging of resting‐state cerebral blood flow in preclinical Huntington's disease publication-title: J Cereb Blood Flow Metab – volume: 29 start-page: 396 year: 2014 end-page: 401 article-title: Elevated arteriolar cerebral blood volume in prodromal Huntington's disease publication-title: Mov Disord – volume: 45 start-page: 438 year: 2012 end-page: 449 article-title: Age‐dependent neurovascular abnormalities and altered microglial morphology in the YAC128 mouse model of Huntington disease publication-title: Neurobiol Dis – volume: 87 start-page: 493 year: 1996 end-page: 506 article-title: Exon 1 of the HD gene with an expanded CAG repeat is sufficient to cause a progressive neurological phenotype in transgenic mice publication-title: Cell – volume: 250C start-page: 20 year: 2013 end-page: 30 article-title: Neurovascular abnormalities in humans and mice with Huntington's disease publication-title: Exp Neurol – volume: 24 start-page: 7999 year: 2004 end-page: 8008 article-title: Activation of the IkappaB kinase complex and nuclear factor‐kappaB contributes to mutant huntingtin neurotoxicity publication-title: J Neurosci – volume: 12 start-page: 162 year: 1992 end-page: 168 article-title: Evaluation of cerebral vasomotor reactivity by various vasodilating stimuli: comparison of CO2 to acetazolamide publication-title: J Cereb Blood Flow Metab – volume: 32 start-page: 1841 year: 2012 end-page: 1852 article-title: Blood‐spinal cord barrier pericyte reductions contribute to increased capillary permeability publication-title: J Cereb Blood Flow Metab – volume: 34 start-page: 76 year: 2011 end-page: 87 article-title: Astrocyte‐neuron metabolic relationships: for better and for worse publication-title: Trends Neurosci – volume: 45 start-page: 824 year: 2009 end-page: 831 article-title: In vivo cerebromicrovasculatural visualization using 3D DeltaR2‐based microscopy of magnetic resonance angiography (3DDeltaR2‐mMRA) publication-title: Neuroimage – volume: 68 start-page: 409 year: 2010 end-page: 427 article-title: Pericytes control key neurovascular functions and neuronal phenotype in the adult brain and during brain aging publication-title: Neuron – volume: 6 start-page: e15809 year: 2011 article-title: Increased prothrombin, apolipoprotein A‐IV, and haptoglobin in the cerebrospinal fluid of patients with Huntington's disease publication-title: PLoS One – volume: 369 start-page: 218 year: 2007 end-page: 228 article-title: Huntington's disease publication-title: Lancet – volume: 29 start-page: 3276 year: 2009 end-page: 3287 article-title: Uniquely hominid features of adult human astrocytes publication-title: J Neurosci – volume: 22 start-page: 1826 year: 2013 end-page: 1842 article-title: A critical role of astrocyte‐mediated nuclear factor‐kappaB‐dependent inflammation in Huntington's disease publication-title: Hum Mol Genet – volume: 8 start-page: 8 year: 2011 article-title: The CNS microvascular pericyte: pericyte‐astrocyte crosstalk in the regulation of tissue survival publication-title: Fluids Barriers CNS – reference: 26018216 - Ann Neurol. 2015 Aug;78(2):158-9 |
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Huntington disease (HD) is an inherited neurodegenerative disease caused by the mutant huntingtin gene (mHTT), which harbors expanded CAG repeats. We... Huntington disease (HD) is an inherited neurodegenerative disease caused by the mutant huntingtin gene (mHTT), which harbors expanded CAG repeats. We... Objective Huntington disease (HD) is an inherited neurodegenerative disease caused by the mutant huntingtin gene (mHTT), which harbors expanded CAG repeats. We... OBJECTIVEHuntington disease (HD) is an inherited neurodegenerative disease caused by the mutant huntingtin gene (mHTT), which harbors expanded CAG repeats. We... |
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| SubjectTerms | Adult Aged Animals Astrocytes - metabolism Astrocytes - pathology Blood Vessels - metabolism Blood Vessels - pathology Blood Vessels - physiopathology Brain Brain - blood supply Brain - metabolism Brain - pathology Cells, Cultured Female Humans Huntingtin Protein Huntington Disease - metabolism Huntington Disease - pathology Huntington Disease - physiopathology Induced Pluripotent Stem Cells - metabolism Magnetic Resonance Angiography Magnetic Resonance Imaging Male Mice Mice, Transgenic Middle Aged Nerve Tissue Proteins - metabolism Neurons - metabolism NMR Nuclear magnetic resonance Nuclear Proteins - metabolism Pericytes - pathology Rodents Vascular endothelial growth factor Vascular Endothelial Growth Factor A - metabolism |
| Title | Aberrant astrocytes impair vascular reactivity in Huntington disease |
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