This Article Full Text Full Text (PDF) All Versions of this Article: 23/1/64    most recent 01.ATV.0000042218.13101.50v1 Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by de Waard, V. Articles by de Vries, C. J.M. Search for Related Content PubMed PubMed Citation Articles by de Waard, V. Articles by de Vries, C. J.M. Related Collections Other Ethics and Policy Coumarins Glucose intolerance Catheter-based coronary and valvular interventions: other CV surgery: other

(Arteriosclerosis, Thrombosis, and Vascular Biology. 2003;23:64.)
© 2003 American Heart Association, Inc.

Vascular Biology

Cardiac Ankyrin Repeat Protein (CARP) Expression in Human and Murine Atherosclerotic Lesions

Activin Induces Carp in Smooth Muscle Cells

Vivian de Waard; Tanja A.E. van Achterberg; Nicholas J. Beauchamp; Hans Pannekoek; Carlie J.M. de Vries

From the Department of Biochemistry, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.

Correspondence to Dr. C.J.M. de Vries, Department of Biochemistry, K1-163, Academic Medical Center, Meibergdreef 15, 1105 AZ Amsterdam, the Netherlands. E-mail c.j.devries{at}amc.uva.nl

Objective— Cardiac ankyrin repeat protein (CARP) is a transcription factor-related protein that has been studied most extensively in the heart. In the present study, we investigated the expression and the potential function of CARP in human and murine atherosclerosis.

Methods and Results— CARP expression was observed by in situ hybridization in endothelial cells lining human atherosclerotic plaques, whereas lesion macrophages were devoid of CARP. Furthermore, we established that CARP mRNA and smooth muscle (SM) -actin antigen both colocalized in a subset of intimal smooth muscle cells (SMCs), whereas no CARP mRNA was encountered in quiescent SMCs in the media. The CARP mRNA-expressing intimal SMCs were distinct from intimal SMCs that synthesized the activation marker osteopontin or proliferating cell nuclear antigen. In addition, we showed that activin A, a member of the TGFß superfamily that prevents SMC-rich lesion formation, induced CARP mRNA expression in cultured SMCs.

Conclusions— Based on our data and the knowledge that CARP reduces the proliferation of cultured SMCs, we propose that CARP is involved in inhibition of vascular lesion formation.

Key Words: cardiac ankyrin repeat protein • endothelial cells • smooth muscle cells • activin A • atherogenesis

This article has been cited by other articles:

				J. M. Spin, S. Nallamshetty, R. Tabibiazar, E. A. Ashley, J. Y. King, M. Chen, P. S. Tsao, and T. Quertermous Transcriptional profiling of in vitro smooth muscle cell differentiation identifies specific patterns of gene and pathway activation Physiol Genomics, November 17, 2004; 19(3): 292 - 302. [Abstract] [Full Text] [PDF]