Role of transcription factors in mediating post-ischemic cerebral inflammation and brain damage
Inflammation is a known precipitator of neuronal death after cerebral ischemia. The mechanisms that promote or curtail the start and spread of inflammation in brain are still being debated. By virtue of their capability to modulate gene expression, several transcription factors induced in the ischem...
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| Published in | Neurochemistry international Vol. 50; no. 7; pp. 1014 - 1027 |
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| Main Authors | , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
Elsevier Ltd
01.06.2007
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| Subjects | |
| Online Access | Get full text |
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| Abstract | Inflammation is a known precipitator of neuronal death after cerebral ischemia. The mechanisms that promote or curtail the start and spread of inflammation in brain are still being debated. By virtue of their capability to modulate gene expression, several transcription factors induced in the ischemic brain can modulate the post-ischemic inflammation. While the induction of transcription factors such as IRF1, NF-κB, ATF-2, STAT3, Egr1 and C/EBPβ is thought to promote post-ischemic inflammation, activation of transcription factors such as HIF-1, CREB, c-fos, PPARα, PPARγ and p53 is thought to prevent post-ischemic inflammation and neuronal damage. Of these, PPARγ which is a ligand-activated transcription factor was recently shown to prevent inflammatory gene expression in several animal models CNS disorders. This review article discusses some of the molecular mechanisms of PPARγ induction by its agonists following focal cerebral ischemia. |
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| AbstractList | Inflammation is a known precipitator of neuronal death after cerebral ischemia. The mechanisms that promote or curtail the start and spread of inflammation in brain are still being debated. By virtue of their capability to modulate gene expression, several transcription factors induced in the ischemic brain can modulate the post-ischemic inflammation. While the induction of transcription factors such as IRF1, NF-kappaB, ATF-2, STAT3, Egr1 and C/EBPbeta is thought to promote post-ischemic inflammation, activation of transcription factors such as HIF-1, CREB, c-fos, PPARalpha, PPARgamma and p53 is thought to prevent post-ischemic inflammation and neuronal damage. Of these, PPARgamma which is a ligand-activated transcription factor was recently shown to prevent inflammatory gene expression in several animal models CNS disorders. This review article discusses some of the molecular mechanisms of PPARgamma induction by its agonists following focal cerebral ischemia. Inflammation is a known precipitator of neuronal death after cerebral ischemia. The mechanisms that promote or curtail the start and spread of inflammation in brain are still being debated. By virtue of their capability to modulate gene expression, several transcription factors induced in the ischemic brain can modulate the post-ischemic inflammation. While the induction of transcription factors such as IRF1, NF-κB, ATF-2, STAT3, Egr1 and C/EBPβ is thought to promote post-ischemic inflammation, activation of transcription factors such as HIF-1, CREB, c-fos, PPARα, PPARγ and p53 is thought to prevent post-ischemic inflammation and neuronal damage. Of these, PPARγ which is a ligand-activated transcription factor was recently shown to prevent inflammatory gene expression in several animal models CNS disorders. This review article discusses some of the molecular mechanisms of PPARγ induction by its agonists following focal cerebral ischemia. |
| Author | Park, Seung-Won Vemuganti, Raghu Yi, Jae-Hyuk Kapadia, Ramya |
| AuthorAffiliation | 5 Department of Neurological Surgery (SP), Chung-Ang University, Seoul, Korea 4 Regenerative Medicine Program, University of Wisconsin, Madison, WI, USA 1 Department of Neurological Surgery, University of Wisconsin, Madison, WI, USA 3 Cardiovascular Research Center, University of Wisconsin, Madison, WI, USA 2 Neuroscience Training Program, University of Wisconsin, Madison, WI, USA |
| AuthorAffiliation_xml | – name: 3 Cardiovascular Research Center, University of Wisconsin, Madison, WI, USA – name: 2 Neuroscience Training Program, University of Wisconsin, Madison, WI, USA – name: 5 Department of Neurological Surgery (SP), Chung-Ang University, Seoul, Korea – name: 1 Department of Neurological Surgery, University of Wisconsin, Madison, WI, USA – name: 4 Regenerative Medicine Program, University of Wisconsin, Madison, WI, USA |
| Author_xml | – sequence: 1 givenname: Jae-Hyuk surname: Yi fullname: Yi, Jae-Hyuk organization: Department of Neurological Surgery, University of Wisconsin, Madison, WI, USA – sequence: 2 givenname: Seung-Won surname: Park fullname: Park, Seung-Won organization: Department of Neurological Surgery, University of Wisconsin, Madison, WI, USA – sequence: 3 givenname: Ramya surname: Kapadia fullname: Kapadia, Ramya organization: Department of Neurological Surgery, University of Wisconsin, Madison, WI, USA – sequence: 4 givenname: Raghu surname: Vemuganti fullname: Vemuganti, Raghu email: Vemugant@neurosurg.wisc.edu organization: Department of Neurological Surgery, University of Wisconsin, Madison, WI, USA |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/17532542$$D View this record in MEDLINE/PubMed |
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| Snippet | Inflammation is a known precipitator of neuronal death after cerebral ischemia. The mechanisms that promote or curtail the start and spread of inflammation in... |
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| SubjectTerms | Animals Brain - physiopathology Brain Damage, Chronic - physiopathology Brain Ischemia - physiopathology CCAAT-Enhancer-Binding Protein-beta - physiology Cell Adhesion Molecules - physiology Cerebral ischemia Humans Inflammation Inflammation - etiology Inflammation - physiopathology NF-kappa B - physiology Peroxisome Proliferator-Activated Receptors - physiology PPAR gamma Signal Transduction Transcription factors Transcription Factors - physiology |
| Title | Role of transcription factors in mediating post-ischemic cerebral inflammation and brain damage |
| URI | https://dx.doi.org/10.1016/j.neuint.2007.04.019 https://www.ncbi.nlm.nih.gov/pubmed/17532542 https://search.proquest.com/docview/70669211 https://pubmed.ncbi.nlm.nih.gov/PMC2040388 |
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