Skip Navigation



Journal of Biochemistry Advance Access published online on May 28, 2008
Journal of Biochemistry, doi:10.1093/jb/mvn068
This Article
Right arrow Advance Access manuscript (PDF)
Right arrow All Versions of this Article:
144/3/313    most recent
mvn068v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Request Permissions
Google Scholar
Right arrow Articles by Wang, C.
Right arrow Articles by Wen, J.-K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Wang, C.
Right arrow Articles by Wen, J.-K.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© 2008 The Japanese Biochemical Society

Krüppel-like factor 4 is required for the expression of vascular smooth muscle cell differentiation marker genes induced by all-trans retinoic acid

Chao Wang, Mei Han, Xin-Ming Zhao and Jin-Kun Wen*

Department of Biochemistry and Molecular Biology, Hebei Medical University, Shijiazhuang 050017, China

* Corresponding author: Dr. Jin-Kun Wen, E-mail address: wjk{at}hebmu.edu.cn, Tel: +86 311 86266180, Fax: +86 311 86696826

Received February 16, 2008; Accepted May 2, 2008


  Abstract

SUMMARY

Krüppel-like factor 4 (KLF4) is involved in phenotypic modulation of vascular smooth muscle cells (VSMCs). All-trans retinoic acid (ATRA) inhibits VSMC proliferation and induces VSMC differentiation. However, the role of KLF4 in ATRA-elicited VSMC phenotypic modulation remains unclear. Here, we show that treatment of VSMCs with ATRA resulted in significant inhibition of proliferation and migration of VSMCs, as well as up-regulation of KLF4 and the VSMC differentiation marker genes SM22{alpha} and SM {alpha}-actin ({alpha}-SMA). At the same time, the KLF4 target gene p53 was up-regulated, while the VSMC dedifferentiation marker gene nonmuscle myosin heavy chain-B (SMemb) was down-regulated. We also show that overexpression of KLF4 in VSMCs increased the expression of p53, SM22{alpha} and {alpha}-SMA, but decreased the expression of SMemb and VSMC proliferation and migration. Silencing of KLF4 expression by KLF4-specific small interfering RNA (siRNA) abrogated the inducing effects of ATRA on p53, SM22{alpha} and {alpha}-SMA expression, and neutralized the inhibitory effects of ATRA on SMemb expression and VSMC proliferation and migration. Thus, our data suggest that KLF4 is required for the expression of VSMC differentiation marker genes induced by ATRA and that this transcription factor is one of the key mediators of retinoid actions in VSMCs.

Key Words: all-trans retinoic acid, expression, KLF4, marker gene, VSMC


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Genes Dev.Home page
M. Xin, E. M. Small, L. B. Sutherland, X. Qi, J. McAnally, C. F. Plato, J. A. Richardson, R. Bassel-Duby, and E. N. Olson
MicroRNAs miR-143 and miR-145 modulate cytoskeletal dynamics and responsiveness of smooth muscle cells to injury
Genes & Dev., September 15, 2009; 23(18): 2166 - 2178.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
B. Zheng, M. Han, M. Bernier, X.-h. Zhang, F. Meng, S.-b. Miao, M. He, X.-m. Zhao, and J.-k. Wen
Kruppel-like Factor 4 Inhibits Proliferation by Platelet-derived Growth Factor Receptor {beta}-mediated, Not by Retinoic Acid Receptor {alpha}-mediated, Phosphatidylinositol 3-Kinase and ERK Signaling in Vascular Smooth Muscle Cells
J. Biol. Chem., August 21, 2009; 284(34): 22773 - 22785.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.