Modulation of Vascular Smooth Muscle Cell Phenotype by High Mobility Group AT-Hook 1

정유진; 이해선; 하정민; 진서연; 금혜진; Vafaeinik Farzaneh; 하홍구; 송상헌; 김치대; 배순식

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자료유형: 학술저널

저자정보: 정유진 (부산대학교) 이해선 (Gene and Cell Therapy Center for Vessel-Associated Disease Medical Research Institute and Departmen) 하정민 (Gene and Cell Therapy Center for Vessel-Associated Disease Medical Research Institute and Departmen) 진서연 (Gene and Cell Therapy Center for Vessel-Associated Disease Medical Research Institute and Departmen) 금혜진 (Gene and Cell Therapy Center for Vessel-Associated Disease Medical Research Institute and Departmen) Vafaeinik Farzaneh (Gene and Cell Therapy Center for Vessel-Associated Disease Medical Research Institute and Departmen) 하홍구 (Department of Urology Pusan National University Hospital Busan Republic of Korea.) 송상헌 (Department of Internal Medicine Pusan National University Hospital Busan Korea.) 김치대 (부산대학교) 배순식 (부산대학교)

저널정보: 한국지질동맥경화학회(구 한국지질학회) 지질·동맥경화학회지 지질·동맥경화학회지 제10권 제1호

발행연도: 2021.1

수록면: 99 - 110 (12page)

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Objective The purpose of this study is to examine the effect of high mobility group AT-hook 1 (HMGA1) on the phenotyptic change of vascular smooth muscle cells (VSMCs). Methods Gene silencing and overexpression of HMGA1 were introduced to evaluate the effect of HMGA1 expression on the phenotypic change of VSMCs. Marker gene expression of VSMCs was measured by promoter assay, quantitative polymerase chain reaction, and western blot analysis. Common left carotid artery ligation model was used to establish in vivo neointima formation. Results HMGA1 was expressed strongly in the synthetic type of VSMCs and significantly downregulated during the differentiation of VSMCs. Silencing of HMGA1 in the synthetic type of VSMCs enhanced the expression of contractile marker genes thereby enhanced angiotensin II (Ang II)-dependent contraction, however, significantly suppressed proliferation and migration. Stimulation of contractile VSMCs with platelet-derived growth factor (PDGF) enhanced HMGA1 expression concomitant with the downregulation of marker gene expression which was blocked significantly by the silencing of HMGA1. Silencing of HMGA1 retained the Ang II-dependent contractile function, which was curtailed by PDGF stimulation, however, overexpression of HMGA1 in the contractile type of VSMCs suppressed marker gene expression. Proliferation and migration were enhanced significantly by the overexpression of HMGA1. Furthermore, the Ang II-dependent contraction was reduced significantly by the overexpression of HMGA1. Finally, the expression of HMGA1 was enhanced significantly in the ligated artery, especially in the neointima area. Conclusion HMGA1 plays an essential role in the phenotypic modulation of VSMCs. Therefore, paracrine factors such as PDGF may affect vascular remodeling through the regulation of HMGA1.

#HMGA #Smooth muscle #Phenotype #Cell proliferation #Platelet-derived growth factor

참고문헌 (31)

참고문헌 신청

Steucke KE / 2015 / Vascular smooth muscle cell functional contractility depends on extracellular mechanical properties / J Biomech 48:3044~3051

Rovner AS / 1986 / Expression of smooth muscle and nonmuscle myosin heavy chains in cultured vascular smooth muscle cells / J Biol Chem 261:14740~14745

Owens GK / 1998 / Molecular control of vascular smooth muscle cell differentiation / Acta Physiol Scand 164:623~635

Gomez D / 2012 / Smooth muscle cell phenotypic switching in atherosclerosis / Cardiovasc Res 95:156~164

Zhang MJ / 2016 / An overview of potential molecular mechanisms involved in VSMC phenotypic modulation / Histochem Cell Biol 145:119~130

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정유진

소속기관 부산대학교

주요연구분야 의약학 > 임상의학 > 내과학

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