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JCI online early table of contents: Jan. 10 2008
Date:1/10/2008

m infants PDA frequently has a genetic basis, and Michael Parmacek and colleagues at the University of Pennsylvania School of Medicine, Philadelphia, have now identified the gene that makes myocardin and myocardin-regulated genes as candidate genes that might have a role in PDA.

In this study, mice in which the gene that makes myocardin was selectively inactivated in smooth muscle cells (SMCs) died of PDA before day 3 of life. The SMCs in the DA of these mice lacked expression of myocardin-regulated genes, which make proteins that manifest the contractile phenotype of SMCs. As elimination of myocardin in SMCs isolated from the main blood vessel of mice markedly reduced the expression of proteins responsible for the SMC contractile phenotype, the authors suggested that myocardin has a central role in maintaining the SMC contractile phenotype and that this probably explains, in part, the development of PDA in the mice lacking myocardin in SMCs.

TITLE: Myocardin regulates expression of contractile genes in smooth muscle cells and is required for closure of the ductus arteriosus in mice

AUTHOR CONTACT:
Michael S. Parmacek
University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA.
Phone: (215) 662-3140; Fax: (215) 349-8017; E-mail: michael.parmacek@uphs.upenn.edu.

View the PDF of this article at: https://www.the-jci.org/article.php?id=33304


HEPATOLOGY: Keeping PPAR-alpha on the go leads to hepatitis C virusinduced liver cancer

Individuals who are chronically infected with hepatitis C virus (HCV) are at increased risk of developing a type of liver cancer known as hepatocellular carcinoma (HCC). However, the mechanisms underlying this increased risk have not been determined. But now, Naoki Tanaka and colleagues at Shinshu University Graduate School of Medicine,
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Contact: Karen Honey
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Journal of Clinical Investigation
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