Characterization of transcriptional and posttranscriptional properties of native and cultured phenotypically modulated vascular smooth muscle cells

被引:5
|
作者
Huggins, Christopher L. [1 ]
Povstyan, Oleksandr V. [1 ]
Harhun, Maksym I. [1 ]
机构
[1] Univ London, Pharmacol & Cell Physiol Res Grp, Div Biomed Sci, London SW17 0RE, England
关键词
Vascular interstitial cell; Vascular smooth muscle cell; Aorta; Cell culture; Phenotypic modulation; Rat; (Wistar; male); RABBIT PORTAL-VEIN; PORCINE CORONARY-ARTERY; MYOSIN LIGHT-CHAIN; INTERSTITIAL-CELLS; DIFFERENTIATION MARKER; IN-VITRO; CONTRACTILE PHENOTYPE; CYTOSKELETAL PROTEINS; MOLECULAR-MECHANISMS; EXPRESSION;
D O I
10.1007/s00441-012-1541-2
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Various in vitro models are used for studying phenotypic modulation of vascular smooth muscle cells (VSMCs) and the established culture of vascular smooth muscle cells (cVSMCs) is most often used for this purpose. On the other hand, vascular interstitial cells (VICs) are native phenotypically modulated VSMCs present in blood vessels under normal physiological conditions. The aim of this work has been to compare the difference in expression of a number of VSMC-specific markers, which are commonly used for the characterisation of phenotypic modulation of VSMCs, between freshly dispersed VSMCs, VICs and cVSMCs from rat abdominal aorta. Our experiments show that VICs are present in the rat aorta and express markers of VSMCs. Both VICs and cVSMCs display the presence of sparse individual stress fibres enriched in alpha smooth muscle actin (alpha SM-actin), whereas in VSMCs, this protein is more densely packed. Compared with contractile VSMCs, both VICs and cVSMCs display decreased expression of VSMC-specific markers such as smoothelin, myosin light chain kinase and SM22 alpha; however, the expression of two major cytoskeletal and contractile proteins (smooth muscle myosin heavy chain and alpha SM-actin) was downregulated in cVSMCs but not in VICs compared with contractile VSMCs. These results suggest different mechanisms for the phenotypic modulation of cVSMCs and VICs. VICs might therefore represent a novel convenient model for studying molecular mechanisms that govern the phenotypic modulation of VSMCs.
引用
收藏
页码:265 / 275
页数:11
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