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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2007;27:448.)
© 2007 American Heart Association, Inc.

Editorials

RhoA-Dependent Vascular Smooth Muscle Cell–Specific Transcription

Adding Diaphanous Formins to the Puzzle

Erik Larsson; Xianghua Zhou; Levent M. Akyürek

From the Sahlgrenska Center for Cardiovascular and Metabolic Research, The Wallenberg Laboratory and Institute of Biomedicine, Department of Medical Chemistry and Cell Biology, Göteborg University, Sweden.

Correspondence to Dr Levent M. Akyürek, The Wallenberg Laboratory, Göteborg University, Bruna Stråket 16, SE-413 45 Göteborg, Sweden. E-mail levent.akyurek@wlab.gu.se

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

Phenotypic modulation of vascular smooth muscle cells (SMCs) plays an integral role in both vascular development and vasculoproliferative disorders. SMC-specific marker genes include caldesmon, smooth muscle myosin heavy chain, -smooth muscle actin, calponin, SM22, and - and ß-tropomyosins. Studies aimed at understanding the role of coactivators and corepressors of phenotypic modulation of SMC have been stimulated by the cloning and characterization of these SMC-specific genes and the discovery that the widely expressed serum response factor (SRF) is central to the expression of SMC-specific genes. SRF directly regulates the coordinated expression of several contractile and cytoskeletal genes through one or more CArG-box elements in the regulatory sequences of SMC-specific genes. This CArG-dependent program of SMC differentiation is modulated during both vascular development and arterial remodeling.¹ Myocardin and myocardin-related transcription factors (MRTFs) bind to SRF, potently stimulate SRF-dependent transcription, and are necessary and sufficient for SMC differentiation.² The RhoA pathway appears to activate myocardins by altering their binding to G-actins and causing translocation of myocardins from the cytoplasm to the nucleus.³ The regulation of the myocardins is key to understanding how SRF target genes are activated during SMC differentiation or growth factor-induced proliferation.

See page 478

The role of RhoA effectors in SMC-specific transcription and actin polymerization has not been extensively explored. In this issue of Arteriosclerosis, Thrombosis, and Vascular Biology, Staus et al studied two RhoA effectors, diaphanous formins 1 and 2 (Dia1 and Dia2), which activate SMC-specific transcription regulated by the myocardin family of SRF cofactors.⁴ These effectors . . . [Full Text of this Article]

Related Article:

Diaphanous 1 and 2 Regulate Smooth Muscle Cell Differentiation by Activating the Myocardin-Related Transcription Factors

Dean P. Staus, Alicia L. Blaker, Joan M. Taylor, and Christopher P. Mack
Arterioscler Thromb Vasc Biol 2007 27: 478-486. [Abstract] [Full Text] [PDF]

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