Time- and cell type-specific induction of platelet-derived growth factor receptor-β during cerebral ischemia

During cerebral ischemia, angiogenesis occurs inside and around the infarcted area. The growth of new blood vessels may contribute to a better outcome after stroke due to accelerated and increased delivery of nutrients and oxygen to the ischemic tissue. The platelet-derived growth factor (PDGF)-B/PD...

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Published inBrain research. Molecular brain research. Vol. 113; no. 1; pp. 44 - 51
Main Authors Renner, Oliver, Tsimpas, Asterios, Kostin, Sawa, Valable, Samuel, Petit, Edwige, Schaper, Wolfgang, Marti, Hugo H.
Format Journal Article
LanguageEnglish
Published Amsterdam Elsevier B.V 12.05.2003
Elsevier
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Online AccessGet full text
ISSN0169-328X
1872-6941
DOI10.1016/S0169-328X(03)00085-8

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Abstract During cerebral ischemia, angiogenesis occurs inside and around the infarcted area. The growth of new blood vessels may contribute to a better outcome after stroke due to accelerated and increased delivery of nutrients and oxygen to the ischemic tissue. The platelet-derived growth factor (PDGF)-B/PDGF receptor (PDGFR)-β system, hitherto thought to contribute mainly to neuroprotection, may also support angiogenesis and vascular remodeling by mediating interactions of endothelial cells with pericytes after cerebral ischemia. While platelet-derived growth factor (PDGF)-B and its receptor PDGFR-β are essential factors for the recruitment of pericytes to brain capillaries during embryonic development, their role in blood vessel maturation during cerebral ischemia is not clear. The aim of the present study was to investigate the time course and location of PDGF-B and PDGFR-β expression in a mouse model of focal cerebral ischemia. In contrast to the early and continuous induction of PDGF-B, PDGFR-β mRNA was specifically upregulated in vascular structures in the infarcted area 48 h after occlusion of the middle cerebral artery. Immunohistology and confocal microscopy analysis revealed the specific upregulation of PDGFR-β on blood vessels and suggested expression mainly on pericytes. Our results imply PDGFR-β as a key factor in vascular remodeling during stroke and suggest that the pleiotropic functions of PDGF-B may be regulated via the expression of its receptor. Influencing the PDGF system therapeutically might improve angiogenesis, cellular protection, and edema inhibition.
AbstractList During cerebral ischemia, angiogenesis occurs inside and around the infarcted area. The growth of new blood vessels may contribute to a better outcome after stroke due to accelerated and increased delivery of nutrients and oxygen to the ischemic tissue. The platelet-derived growth factor (PDGF)-B/PDGF receptor (PDGFR)-beta system, hitherto thought to contribute mainly to neuroprotection, may also support angiogenesis and vascular remodeling by mediating interactions of endothelial cells with pericytes after cerebral ischemia. While platelet-derived growth factor (PDGF)-B and its receptor PDGFR-beta are essential factors for the recruitment of pericytes to brain capillaries during embryonic development, their role in blood vessel maturation during cerebral ischemia is not clear. The aim of the present study was to investigate the time course and location of PDGF-B and PDGFR-beta expression in a mouse model of focal cerebral ischemia. In contrast to the early and continuous induction of PDGF-B, PDGFR-beta mRNA was specifically upregulated in vascular structures in the infarcted area 48 h after occlusion of the middle cerebral artery. Immunohistology and confocal microscopy analysis revealed the specific upregulation of PDGFR-beta on blood vessels and suggested expression mainly on pericytes. Our results imply PDGFR-beta as a key factor in vascular remodeling during stroke and suggest that the pleiotropic functions of PDGF-B may be regulated via the expression of its receptor. Influencing the PDGF system therapeutically might improve angiogenesis, cellular protection, and edema inhibition.
During cerebral ischemia, angiogenesis occurs inside and around the infarcted area. The growth of new blood vessels may contribute to a better outcome after stroke due to accelerated and increased delivery of nutrients and oxygen to the ischemic tissue. The platelet-derived growth factor (PDGF)-B/PDGF receptor (PDGFR)-β system, hitherto thought to contribute mainly to neuroprotection, may also support angiogenesis and vascular remodeling by mediating interactions of endothelial cells with pericytes after cerebral ischemia. While platelet-derived growth factor (PDGF)-B and its receptor PDGFR-β are essential factors for the recruitment of pericytes to brain capillaries during embryonic development, their role in blood vessel maturation during cerebral ischemia is not clear. The aim of the present study was to investigate the time course and location of PDGF-B and PDGFR-β expression in a mouse model of focal cerebral ischemia. In contrast to the early and continuous induction of PDGF-B, PDGFR-β mRNA was specifically upregulated in vascular structures in the infarcted area 48 h after occlusion of the middle cerebral artery. Immunohistology and confocal microscopy analysis revealed the specific upregulation of PDGFR-β on blood vessels and suggested expression mainly on pericytes. Our results imply PDGFR-β as a key factor in vascular remodeling during stroke and suggest that the pleiotropic functions of PDGF-B may be regulated via the expression of its receptor. Influencing the PDGF system therapeutically might improve angiogenesis, cellular protection, and edema inhibition.
During cerebral ischemia, angiogenesis occurs inside and around the infarcted area. The growth of new blood vessels may contribute to a better outcome after stroke due to accelerated and increased delivery of nutrients and oxygen to the ischemic tissue. The platelet-derived growth factor (PDGF)-B/PDGF receptor (PDGFR)-beta system, hitherto thought to contribute mainly to neuroprotection, may also support angiogenesis and vascular remodeling by mediating interactions of endothelial cells with pericytes after cerebral ischemia. While platelet-derived growth factor (PDGF)-B and its receptor PDGFR-beta are essential factors for the recruitment of pericytes to brain capillaries during embryonic development, their role in blood vessel maturation during cerebral ischemia is not clear. The aim of the present study was to investigate the time course and location of PDGF-B and PDGFR-beta expression in a mouse model of focal cerebral ischemia. In contrast to the early and continuous induction of PDGF-B, PDGFR-beta mRNA was specifically upregulated in vascular structures in the infarcted area 48 h after occlusion of the middle cerebral artery. Immunohistology and confocal microscopy analysis revealed the specific upregulation of PDGFR-beta on blood vessels and suggested expression mainly on pericytes. Our results imply PDGFR-beta as a key factor in vascular remodeling during stroke and suggest that the pleiotropic functions of PDGF-B may be regulated via the expression of its receptor. Influencing the PDGF system therapeutically might improve angiogenesis, cellular protection, and edema inhibition.During cerebral ischemia, angiogenesis occurs inside and around the infarcted area. The growth of new blood vessels may contribute to a better outcome after stroke due to accelerated and increased delivery of nutrients and oxygen to the ischemic tissue. The platelet-derived growth factor (PDGF)-B/PDGF receptor (PDGFR)-beta system, hitherto thought to contribute mainly to neuroprotection, may also support angiogenesis and vascular remodeling by mediating interactions of endothelial cells with pericytes after cerebral ischemia. While platelet-derived growth factor (PDGF)-B and its receptor PDGFR-beta are essential factors for the recruitment of pericytes to brain capillaries during embryonic development, their role in blood vessel maturation during cerebral ischemia is not clear. The aim of the present study was to investigate the time course and location of PDGF-B and PDGFR-beta expression in a mouse model of focal cerebral ischemia. In contrast to the early and continuous induction of PDGF-B, PDGFR-beta mRNA was specifically upregulated in vascular structures in the infarcted area 48 h after occlusion of the middle cerebral artery. Immunohistology and confocal microscopy analysis revealed the specific upregulation of PDGFR-beta on blood vessels and suggested expression mainly on pericytes. Our results imply PDGFR-beta as a key factor in vascular remodeling during stroke and suggest that the pleiotropic functions of PDGF-B may be regulated via the expression of its receptor. Influencing the PDGF system therapeutically might improve angiogenesis, cellular protection, and edema inhibition.
Author Petit, Edwige
Schaper, Wolfgang
Valable, Samuel
Kostin, Sawa
Renner, Oliver
Tsimpas, Asterios
Marti, Hugo H.
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  surname: Marti
  fullname: Marti, Hugo H.
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Issue 1
Keywords Disorders of the nervous systems
Angiogenesis
Pericyte
Edema
Stroke
Receptor tyrosine kinase
Vascular permeability
Nervous system diseases
Rodentia
Cardiovascular disease
Cerebral disorder
Vascular disease
Vertebrata
Experimental disease
Growth factor receptor
Mammalia
Ischemia
Mouse
Animal
Central nervous system disease
Cerebrovascular disease
Platelet derived growth factor
Brain (vertebrata)
Language English
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Snippet During cerebral ischemia, angiogenesis occurs inside and around the infarcted area. The growth of new blood vessels may contribute to a better outcome after...
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StartPage 44
SubjectTerms Angiogenesis
Animals
Biological and medical sciences
Brain - blood supply
Brain - metabolism
Brain - physiopathology
Brain Ischemia - genetics
Brain Ischemia - metabolism
Cell Differentiation - genetics
Cerebral Infarction - genetics
Cerebral Infarction - metabolism
Edema
Endothelium, Vascular - metabolism
Fluorescent Antibody Technique
Medical sciences
Mice
Mice, Inbred Strains
Neovascularization, Physiologic - physiology
Neurology
Pericyte
Pericytes - metabolism
Platelet Endothelial Cell Adhesion Molecule-1 - metabolism
Platelet-Derived Growth Factor - metabolism
Reaction Time - genetics
Receptor tyrosine kinase
Receptor, Platelet-Derived Growth Factor beta - genetics
Receptor, Platelet-Derived Growth Factor beta - metabolism
Recovery of Function - physiology
RNA, Messenger - metabolism
Stroke
Up-Regulation - genetics
Vascular diseases and vascular malformations of the nervous system
Vascular permeability
Title Time- and cell type-specific induction of platelet-derived growth factor receptor-β during cerebral ischemia
URI https://www.clinicalkey.com/#!/content/1-s2.0-S0169328X03000858
https://dx.doi.org/10.1016/S0169-328X(03)00085-8
https://www.ncbi.nlm.nih.gov/pubmed/12750005
https://www.proquest.com/docview/18918477
https://www.proquest.com/docview/73288968
Volume 113
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