Literature DB >> 11971673

Vascular smooth muscle cells derived from atherosclerotic human arteries exhibit greater adhesion, migration, and proliferation than venous cells.

Peter L Faries1, Darren I Rohan, Mark C Wyers, Michael L Marin, Larry H Hollier, William C Quist, Frank W LoGerfo.   

Abstract

BACKGROUND: Phenotypic variation of vascular smooth muscle cells (VSMC) may result in altered biological behavior and responses. Within the vessel wall, arterial VSMC have a greater propensity to form atherosclerotic lesions as compared to venous VSMC. In this study the rates of proliferation, adhesion, and migration were compared between VSMC of atherosclerotic arterial and venous origin.
MATERIALS AND METHODS: Human VSMC cultures were isolated from 18 infragenicular arteries at the time of below knee amputation and from 20 saphenous veins during lower extremity revascularization surgery. Cell cultures were isolated from the media of each specimen and maintained in distinct cell lines for all assays. Cells from passages 2 and 3 were assayed for their proliferative capacity using total DNA fluorescence photometry and for adhesion and migration using a modified Boyden chamber.
RESULTS: Patient age and the incidence of atherosclerotic risk factors did not vary significantly between the arterial and the venous patient groups. VSMC of atherosclerotic arterial origin demonstrated greater proliferation (arterial, 162 +/- 59 absorption units, vs. venous, 106 +/- 56 absorption units, P < 0.001), adhesion (arterial, 74.1 +/- 22.6 cells/microscopic field, vs. venous, 41.3 +/- 12.8 cells/microscopic field, P < 0.001) and migration (arterial, 427 +/- 185 cells/microscopic field, vs venous, 119 +/- 101 cells/microscopic field, P < 0.001) than VSMC of venous origin.
CONCLUSION: Human atherosclerotic arterial VSMC exhibit significantly increased rates of proliferation, adhesion, and migration as compared to human venous VSMC. These observations of VSMC in culture are consistent with the clinical predilection for the hyperplasic responses that result in the development of atherosclerosis in the arterial wall. Possible intrinsic differences in VSMC phenotype should be considered in designing methods to limit atherosclerosis.

Entities:  

Mesh:

Year:  2002        PMID: 11971673     DOI: 10.1006/jsre.2002.6399

Source DB:  PubMed          Journal:  J Surg Res        ISSN: 0022-4804            Impact factor:   2.192


  6 in total

1.  Rab1 GTPase regulates phenotypic modulation of pulmonary artery smooth muscle cells by mediating the transport of angiotensin II type 1 receptor under hypoxia.

Authors:  Hongjin Yin; Qi Li; Guisheng Qian; Yaoli Wang; Yuncheng Li; Guangyu Wu; Guansong Wang
Journal:  Int J Biochem Cell Biol       Date:  2010-11-21       Impact factor: 5.085

2.  miR181a protects against angiotensin II-induced osteopontin expression in vascular smooth muscle cells.

Authors:  Ebony Washington Remus; Alicia N Lyle; Daiana Weiss; Natalia Landàzuri; Martina Weber; Charles Searles; W Robert Taylor
Journal:  Atherosclerosis       Date:  2013-02-05       Impact factor: 5.162

3.  Retinol binding protein 4 promotes hyperinsulinism‑induced proliferation of rat aortic smooth muscle cells.

Authors:  Fei Li; Ke Xia; Md Sayed Ali Sheikh; Jinfang Cheng; Chuanchang Li; Tianlun Yang
Journal:  Mol Med Rep       Date:  2014-03-07       Impact factor: 2.952

Review 4.  RNAi therapy to the wall of arteries and veins: anatomical, physiologic, and pharmacological considerations.

Authors:  Christoph S Nabzdyk; Leena Pradhan-Nabzdyk; Frank W LoGerfo
Journal:  J Transl Med       Date:  2017-07-28       Impact factor: 5.531

5.  Ginseng extracts restore high-glucose induced vascular dysfunctions by altering triglyceride metabolism and downregulation of atherosclerosis-related genes.

Authors:  Gabriel Hoi-Huen Chan; Betty Yuen-Kwan Law; John Man-Tak Chu; Kevin Kin-Man Yue; Zhi-Hong Jiang; Chi-Wai Lau; Yu Huang; Shun-Wan Chan; Patrick Ying-Kit Yue; Ricky Ngok-Shun Wong
Journal:  Evid Based Complement Alternat Med       Date:  2013-09-30       Impact factor: 2.629

6.  Inhibition of Aortic Intimal Hyperplasia and Vascular Smooth Muscle Proliferation and Extracellular Matrix Protein Expressions by Astragalus-Angelica Combination.

Authors:  Huifang Yan; Xiwei Peng; Hao Xu; Jiahuan Zhu; Changqing Deng
Journal:  Evid Based Complement Alternat Med       Date:  2018-08-13       Impact factor: 2.629

  6 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.