求文献paper 一篇，谢了。# Biology - 生物学
j*g
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thanks a lot!
Current Neurovascular Research
ISSN (Print): 1567-2026
ISSN (Online): 1875-5739
VOLUME: 9
ISSUE: 1
DOI: 10.2174/156720212799297100
PDGF Receptor β Signaling in Pericytes Following Ischemic Brain Injury
Author(s): Koichi Arimura, Tetsuro Ago, Masahiro Kamouchi, Kuniyuki Nakamura
, Koji Ishitsuka, Junya Kuroda, Hiroshi Sugimori, Hiroaki Ooboshi, Tomio
Sasaki and Takanari Kitazono
Pages 1-9 (9)
Abstract:
Platelet derived growth factor (PDGF)-B plays a neuroprotective role in
brain damages, including ischemic stroke. It has been suggested recently
that PDGF receptor β (PDGFRβ) expressed in brain pericytes as well as in
neurons and astrocytes may mediate the neuroprotective role of PDGF-B. The
aims of this study were to elucidate the roles of PDGFRβ signaling in brain
pericytes after ischemic stroke. In a rat middle cerebral artery occlusion
(MCAO) model, PDGFRβ expression was induced specifically in the pericytes
in peri-infarct areas and its level was gradually increased. PDGF-B induced
marked phosphorylation of Akt in cultured brain pericytes. Consistently,
PDGF-B was upregulated in endothelial cells in per-infarct areas and Akt was
strongly phosphorylated in the PDGFRβ-expressing pericytes in periinfarct
areas after MCAO. In the cultured pericytes, PDGF-B induced cell growth and
anti-apoptotic responses through Akt. Furthermore, PDGF-B significantly
increased the expression of nerve growth factor (NGF) and neurotrophin-3 (NT
- 3) through Akt in the pericytes. Thus, the PDGFRβ-Akt signaling in brain
pericytes may play various important roles leading to neuroprotection after
ischemic stroke.
Keywords:
angiogenesis, blood brain barrier, endothelial cells, microvascular, PI3K,
Cell Signaling Technology, qPCR RT kit, LightCycler, SYBR, neurotrophic
factor, Apoptosis, cell growth, ischemic stroke, neuroprotection,
neurotrophins, pericyte, PDGF-B, PDGF receptor β
Affiliation:
Department of Medicine and Clinical Science, Graduate School of Medical
Sciences, Kyushu University, Fukuoka 812-8582, Japan.
Current Neurovascular Research
ISSN (Print): 1567-2026
ISSN (Online): 1875-5739
VOLUME: 9
ISSUE: 1
DOI: 10.2174/156720212799297100
PDGF Receptor β Signaling in Pericytes Following Ischemic Brain Injury
Author(s): Koichi Arimura, Tetsuro Ago, Masahiro Kamouchi, Kuniyuki Nakamura
, Koji Ishitsuka, Junya Kuroda, Hiroshi Sugimori, Hiroaki Ooboshi, Tomio
Sasaki and Takanari Kitazono
Pages 1-9 (9)
Abstract:
Platelet derived growth factor (PDGF)-B plays a neuroprotective role in
brain damages, including ischemic stroke. It has been suggested recently
that PDGF receptor β (PDGFRβ) expressed in brain pericytes as well as in
neurons and astrocytes may mediate the neuroprotective role of PDGF-B. The
aims of this study were to elucidate the roles of PDGFRβ signaling in brain
pericytes after ischemic stroke. In a rat middle cerebral artery occlusion
(MCAO) model, PDGFRβ expression was induced specifically in the pericytes
in peri-infarct areas and its level was gradually increased. PDGF-B induced
marked phosphorylation of Akt in cultured brain pericytes. Consistently,
PDGF-B was upregulated in endothelial cells in per-infarct areas and Akt was
strongly phosphorylated in the PDGFRβ-expressing pericytes in periinfarct
areas after MCAO. In the cultured pericytes, PDGF-B induced cell growth and
anti-apoptotic responses through Akt. Furthermore, PDGF-B significantly
increased the expression of nerve growth factor (NGF) and neurotrophin-3 (NT
- 3) through Akt in the pericytes. Thus, the PDGFRβ-Akt signaling in brain
pericytes may play various important roles leading to neuroprotection after
ischemic stroke.
Keywords:
angiogenesis, blood brain barrier, endothelial cells, microvascular, PI3K,
Cell Signaling Technology, qPCR RT kit, LightCycler, SYBR, neurotrophic
factor, Apoptosis, cell growth, ischemic stroke, neuroprotection,
neurotrophins, pericyte, PDGF-B, PDGF receptor β
Affiliation:
Department of Medicine and Clinical Science, Graduate School of Medical
Sciences, Kyushu University, Fukuoka 812-8582, Japan.