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J. Biol. Chem., Vol. 282, Issue 14, 10133-10137, April 6, 2007
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Response Gene to Complement 32, a Novel Regulator for Transforming Growth Factor-
-induced Smooth Muscle Differentiation of Neural Crest Cells*
1
From the
Departments of Pediatrics, and Medicine, Georgetown University Medical Center, Washington, D. C. 20057
We previously developed a robust in vitro model system for vascular smooth muscle cell (VSMC) differentiation from neural crest cell line Monc-1 upon transforming growth factor-
(TGF-) induction. Further studies demonstrated that both Smad and RhoA signaling are critical for TGF--induced VSMC development. To identify downstream targets, we performed Affymetrix cDNA array analysis of Monc-1 cells and identified a gene named response gene to complement 32 (RGC-32) to be important for the VSMC differentiation. RGC-32 expression was increased 5-fold after 2 h and 50-fold after 24 h of TGF- induction. Knockdown of RGC-32 expression in Monc-1 cells by small interfering RNA significantly inhibited the expression of multiple smooth muscle marker genes, including SM 
-actin (-SMA), SM22, and calponin. Of importance, the inhibition of RGC-32 expression correlated with the reduction of -SMA while not inhibiting smooth muscle-unrelated c-fos gene expression, suggesting that RGC-32 is an important protein factor for VSMC differentiation from neural crest cells. Moreover, RGC-32 overexpression significantly enhanced TGF--induced -SMA, SM22, and SM myosin heavy chain promoter activities in both Monc-1 and C3H10T1/2 cells. The induction of VSMC gene promoters by RGC-32 appears to be CArG-dependent. These data suggest that RGC-32 controls VSMC differentiation by regulating marker gene transcription in a CArG-dependent manner. Further studies revealed that both Smad and RhoA signaling are important for RGC-32 activation.
Received for publication, August 23, 2006 , and in revised form, February 26, 2007.
* This work was supported by an American Heart Association Scientist Development Grant (to S. C.) and National Institutes of Health Grants HL68686 (to C. S. W.) and DK52612 (to P. A. J.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
The on-line version of this article (available at http://www.jbc.org) contains two supplemental figures.
1 To whom correspondence should be addressed: Dept. of Pediatrics, Bldg. D, Rm. 363, Georgetown University Medical Center, 4000 Reservoir Rd., N. W., Washington, DC 20057. Tel.: 202-687-3401; Fax: 202-687-1503; E-mail: sc229{at}georgetown.edu
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