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(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

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