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(Circulation Research. 2005;97:409.)
© 2005 American Heart Association, Inc.

Editorials

SRF Function in Vascular Smooth Muscle

When Less is More?

Blanca Camoretti-Mercado, Nickolai O. Dulin, Julian Solway

From the Section of Pulmonary and Critical Care Medicine, Department of Medicine, University of Chicago, Ill.

Correspondence to Blanca Camoretti-Mercado, PhD, The University of Chicago, 5841 S Maryland Ave, MC6026, Chicago, IL 60637. E-mail bcamoret@medicine.bsd.uchicago.edu

See related article, pages 427–433

Key Words: proliferation • migration • serum response factor • vascular smooth muscle

An extract of the first 250 words of the full text is provided, because this article has no abstract.

The transcription factor serum response factor (SRF) controls the expression of genes involved in promoting the proliferation and differentiation of muscle and nonmuscle cells.^1,2 In this issue, Kaplan-Albuquerque et al³ report that depletion of SRF from cultured vascular smooth muscle cells (VSMC) through RNA interference blocks expression of SM-specific proteins as expected, but surprisingly also promotes cell migration and proliferation. If confirmed, these unforeseen effects of SRF could have important mechanistic implications for pathological conditions involving abnormal VSMC proliferation and migration.

SRF binds to the 10-bp CArG motif found in the regulatory regions of several muscle-specific genes and also located in the serum response elements of mitogen-inducible gene promoters. In smooth muscle cells, 2 families of SRF-interacting coactivators, myocardin/MKL and p62^TCF, bind to the same region of SRF in a mutually exclusive manner and so induce either smooth muscle–specific gene expression or early response gene expression, respectively⁴. Growth signals negatively affect SM gene expression by inducing the displacement of myocardin from SRF by Elk-1, a ternary complex factor (TCF).⁵ Because VSMC cells are not terminally differentiated, they undergo phenotypic shift in response to mitogenic stimulation (such as platelet-derived growth factor [PDGF] treatment), resulting in both increased proliferation and suppression of smooth muscle contractile markers. On the other hand, exposure to constrictor agents promotes a phenotype characterized by augmented accumulation of contractile proteins and mRNA transcripts.⁶ Thus, current understanding is that SRF can promote either differentiation or proliferation of VSMC, depending on the physiological environment.

New findings presented by . . . [Full Text of this Article]

Related Article:

Depletion of Serum Response Factor by RNA Interference Mimics the Mitogenic Effects of Platelet Derived Growth Factor-BB in Vascular Smooth Muscle Cells

Nihal Kaplan-Albuquerque, Vicki Van Putten, Mary C. Weiser-Evans, and Raphael A. Nemenoff
Circ. Res. 2005 97: 427-433. [Abstract] [Full Text] [PDF]