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XBP1 Deficiency in vsmc Contributes to Abdominal Aortic Aneurysm via Regulating vsmc phenotypic Switching

XBP1 Deficiency in VSMC Contributes to Abdominal Aortic Aneu...

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中国生理学会基质生物学专业委员会成立大会暨第一次全国基质生物学学术会议

作者： Guizhen Zhao Yi Fu Qingbo Xu Xian Wang Wei Kong Department of Physiology and Pathophysiology School of Basic Medical SciencesPeking University

Abdominal aortic aneurysm(AAA) is a life-threatening cardiovascular disease,characterized by chronic vascular wall inflammation,extracellular matrix degradation and apoptosis of vascular smooth muscle *** studies showed that vsmc phenotypic switching may also play an important role in the pathogenesis of AAA.X-box binding protein 1(XBP1),a basic-region leucine zipper(bZIP) transcription factor,involves spliced(XBP1s) and unspliced(XBP1u) isoforms translated from XBP1 pre-mRNA with or without inositol requiring enzyme 1 alpha(BRE1)-mediated splicing *** functions of XBP1s in cardiovascular diseases has been recently ***,little is known about the role of XBP1u,especially in vascular smooth muscle cells(vsmcs).Firstly,SMC contractile proteins and XBP1u were decreased in aneurysmal aorta compared with normal aortic ***,SMC-specific XBP 1 knockout mice were more susceptible to CaP04 and angiotensin Ⅱ(Ang Ⅱ)-induced AAA than littermate wildtype *** vitro experiments revealed that XBP1u silencing reduced vsmc contractile proteins expression,but enhanced Ang Ⅱ-induced MCP-1 and IL-6 expression,indicating that vsmcs displayed a proinflammatory phenotype following XBP1u *** XBP1u deficiency in vsmcs has no significant effect on the expression of SRF,myocardin,MRTF(myocardin-related protein factor),KLF4 and FOXOs,the transcriptional factors related to vsmc phenotypic *** XBP1u overexpression inhibited the interaction between FOXO4 and myocardin,thus promoting the transcriptional activity of *** study indicated that XBP1 deficiency in vsmcs promotes the formation of abdominal aortic aneurysm through regulating the phenotypic switching of vsmcs.

关键词： aortic aneurysm XBP1u FOXO4 vsmc phenotypic modulation

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Mitochondrial Resident Cartilage Oligomeric Matrix Protein Inhibits vsmcCalcification Via Interacting With PHB2

Mitochondrial Resident Cartilage Oligomeric Matrix Protein I...

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中国生理学会基质生物学专业委员会第二次全国基质生物学学术会议

作者：贾一挺 Meili Wang Fu Yi Wei Kong 北京大学医学部 Department of Physiology and Pathophysiology School of Basic Medical SciencesPeking University

Background:vsmc calcificationis highly related to cardiovascular morbidity and mortality among aging individuals and patients with chronic renal failure and diabetes *** dedifferentiation of vsmc exerting as chondrocyte/osteoblast phenotype mainly contributes to vsmc *** oligomeric matrix protein(COMP) inhibits vsmc calcification,but the underlie mechanism of COMP-inhibited vsmc calcification is still not fully *** and Results:Microarray profiling and bioinformatic analysis of WT and COMP-/-vsmcs revealed that COMP-deficient vsmcs exerted impaired oxidative *** in vitro studies confirmed that COMP deficiency caused mitochondrial oxidative phosphorylation dysfunction,morphological abnormality,impaired ATP synthesis,and mitochondrial fission rather *** using immunofluorescence assay,we found COMP localized inmitochondria,further confirmed by western blot analysis showing that COMP was present in purified mitochondrial *** interactome of COMP identified that COMP interacted with mitochondrial resident protein prohibitin 2(PHB2).COMP directly bound to prohibitin 2 C-terminal via its *** to COMP deficiency,PHB2-deficient vsmc exhibited loss of contractile phenotype and aggravated high phosphate-induced ***,adenovirus-mediated COMP overexpression promoted mitochondrial oxidative phosphorylation,which was partly abolished upon PHB2 ***:Our study indicated that COMP inhibited vsmc calcification through its interaction with PHB2 to maintainmitochondrialhomeostasis and the contractile phenotypic of vsmcs.

关键词： vsmc calcification COMP PHB2 mitochondrial vsmc phenotypic modulation

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