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Mol. Cells 2013; 36(2): 112-118

Published online August 31, 2013

https://doi.org/10.1007/s10059-013-0012-2

© The Korean Society for Molecular and Cellular Biology

CCN4 Regulates Vascular Smooth Muscle Cell Migration and Proliferation

Hao Liu, Wenpeng Dong, Zhiqi Lin, Jingbo Lu, Heng Wan, Zhongxin Zhou, Zhengjun Liu

1Department of Vascular Surgery, Nanfang Hospital, Southern Medical University, Guangzhou 510515, Guangdong, China, 2Department of Cardiovascular Surgery, Guangzhou General Hospital of Guangzhou Military Command, Guangzhou 510010, Guangdong, China, 3These authors contributed equally to this work.

Received: January 11, 2013; Revised: May 15, 2013; Accepted: May 21, 2013

Abstract

The migration and proliferation of vascular smooth muscle cells (VSMCs) are essential elements during the development of atherosclerosis and restenosis. An increasing number of studies have reported that extracellular matrix (ECM) proteins, including the CCN protein family, play a significant role in VSMC migration and proliferation. CCN4 is a member of the CCN protein family, which controls cell development and survival in multiple systems of the body. Here, we sought to determine whether CCN4 is involved in VSMC migration and proliferation. We examined the effect of CCN4 using rat cultured VSMCs. In cultured VSMCs, CCN4 stimulated the adhesion and migration of VSMCs in
a dose-dependent manner, and this effect was blocked by an antibody for integrin α5β1. CCN4 expression was enhanced by the pro-inflammatory cytokine tumor necrosis factor α (TNF-α). Furthermore, knockdown of CCN4 by siRNA significantly inhibited the VSMC proliferation. CCN4 also could up-regulate the expression level of marker proteins of the VSMCs phenotype. Taken together, these results suggest that CCN4 is involved in the migration and proliferation of VSMCs. Inhibition of CCN4 may provide a promising strategy for the prevention of restenosis after vascular interventions.

Keywords CCN4, marker protein, small interfering RNA, vascular smooth muscle cell

Article

Research Article

Mol. Cells 2013; 36(2): 112-118

Published online August 31, 2013 https://doi.org/10.1007/s10059-013-0012-2

Copyright © The Korean Society for Molecular and Cellular Biology.

CCN4 Regulates Vascular Smooth Muscle Cell Migration and Proliferation

Hao Liu, Wenpeng Dong, Zhiqi Lin, Jingbo Lu, Heng Wan, Zhongxin Zhou, Zhengjun Liu

1Department of Vascular Surgery, Nanfang Hospital, Southern Medical University, Guangzhou 510515, Guangdong, China, 2Department of Cardiovascular Surgery, Guangzhou General Hospital of Guangzhou Military Command, Guangzhou 510010, Guangdong, China, 3These authors contributed equally to this work.

Received: January 11, 2013; Revised: May 15, 2013; Accepted: May 21, 2013

Abstract

The migration and proliferation of vascular smooth muscle cells (VSMCs) are essential elements during the development of atherosclerosis and restenosis. An increasing number of studies have reported that extracellular matrix (ECM) proteins, including the CCN protein family, play a significant role in VSMC migration and proliferation. CCN4 is a member of the CCN protein family, which controls cell development and survival in multiple systems of the body. Here, we sought to determine whether CCN4 is involved in VSMC migration and proliferation. We examined the effect of CCN4 using rat cultured VSMCs. In cultured VSMCs, CCN4 stimulated the adhesion and migration of VSMCs in
a dose-dependent manner, and this effect was blocked by an antibody for integrin α5β1. CCN4 expression was enhanced by the pro-inflammatory cytokine tumor necrosis factor α (TNF-α). Furthermore, knockdown of CCN4 by siRNA significantly inhibited the VSMC proliferation. CCN4 also could up-regulate the expression level of marker proteins of the VSMCs phenotype. Taken together, these results suggest that CCN4 is involved in the migration and proliferation of VSMCs. Inhibition of CCN4 may provide a promising strategy for the prevention of restenosis after vascular interventions.

Keywords: CCN4, marker protein, small interfering RNA, vascular smooth muscle cell

Mol. Cells
Sep 30, 2022 Vol.45 No.9, pp. 603~672
COVER PICTURE
The Target of Rapamycin Complex (TORC) is a central regulatory hub in eukaryotes, which is well conserved in diverse plant species, including tomato (Solanum lycopersicum). Inhibition of TORC genes (SlTOR, SlLST8, and SlRAPTOR) by VIGS (virus-induced gene silencing) results in early fruit ripening in tomato. The red/ orange tomatoes are early-ripened TORC-silenced fruits, while the green tomato is a control fruit. Top, left, control fruit (TRV2-myc); top, right, TRV2-SlLST8; bottom, left, TRV2-SlTOR; bottom, right, TRV2-SlRAPTOR(Choi et al., pp. 660-672).

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