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p38 mitogen-activated protein kinase regulates type-I vs type-II phenotyping of human vascular endothelial cells
p38 mitogen-activated protein kinase regulates type-I vs type-II phenotyping of human vascular endothelial cells
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AIM:To identify kinases involved in phenotype regulation of vascular endothelial cells(VECs):Proproliferative G-protein signaling 5(RGS5)high(type-I)vs anti-proliferative RGS5low(type-II)VECs.METHODS:Proteomic kinase assays were performed to identify the crucial kinase involved in the phenotype regulation of human VECs using type-I VECs,which promotes the proliferation of human vascular smooth muscle cells(VSMCs),and type-II VECs,which suppress the proliferation of human VSMCs.The assays were performed using multiple pairs of type-I and type-II VECs to obtain the least number of candidates.The involvement of the candidate kinases was verified by evaluating the effects of their specific inhibitors on the phenotype regulation of human VECs as well as the expression levels of regulator of RGS5,which is the causative gene for the“type-II to type-I”phenotype conversion of human VECs.RESULTS:p38αmitogen-activated protein kinase(p38αMAPK)was the only kinase that showed distinctive activities between type-I and type-II VECs:p38αMAPK activities were low and high in type-I and type-II VECs,respectively.We found that an enforced expression of RGS5 indeed lowered p38αMAPK activities in type-II VECs.Furthermore,treatments with a p38αMAPK inhibitor nullified the anti-proliferative potential in type-II VECs.Interestingly,MAPK inhibitor treatments enhanced the induction of RGS5 gene.Thus,there is a vicious cycle between“RGS5 induction”and“p38αMAPK inhibition”,which can explain the unidirectional process in the stress-induced“type-II to type-I”conversions of human VECs.To understand the upstream signaling of RGS5,which is known as an inhibitory molecule against the G protein-coupled receptor(GPCR)-mediated signaling,we examined the effects of RGS5 overexpression on the signaling events from sphingosine-1-phosphate(S1P)to N-cadherin,because S1P receptors belong to the GPCR family gene and N-cadherin,one of their downstream effectors,is reportedly involved in the regulation of VEC-VSMC interactions.We found th
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| 篇名 | p38 mitogen-activated protein kinase regulates type-I vs type-II phenotyping of human vascular endothelial cells | ||
| 来源期刊 | 世界转化医学杂志 | 学科 | 医学 |
| 关键词 | VASCULAR endothelial CELLS VASCULAR smooth muscle CELLS proteomic KINASE assay p38αmitogenactivated protein KINASE regulator of G-PROTEIN signaling 5 sphingosine-1-phosphate N-cadherin | ||
| 年，卷（期） | 2015,（3） | 所属期刊栏目 | |
| 研究方向 | 页码范围 | 101-112 | |
| 页数 | 12页 | 分类号 | R |
| 字数 | 语种 | ||
| DOI | |||
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VASCULAR
endothelial
CELLS
VASCULAR
smooth
muscle
CELLS
proteomic
KINASE
assay
p38αmitogenactivated
protein
KINASE
regulator
of
G-PROTEIN
signaling
5
sphingosine-1-phosphate
N-cadherin
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世界转化医学杂志
主办单位：
百世登出版集团有限公司
出版周期：
其它
ISSN：
2220-6132
CN：
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出版地：
北京市朝阳区东四环中路62号楼远洋国际中
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48
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