Loss of Bmx nonreceptor tyrosine kinase prevents pressure overload-induced cardiac hypertrophy.

Abstract

Bmx nonreceptor tyrosine kinase has an established role in endothelial and lymphocyte signaling; however, its role in the heart is unknown. To determine whether Bmx participates in cardiac growth, we subjected mice deficient in the molecule (Bmx knockout mice) to transverse aortic constriction (TAC). In comparison with wild-type mice, which progressively developed massive hypertrophy following TAC, Bmx knockout mice were resistant to TAC-induced cardiac growth at the organ and cell level. Loss of Bmx preserved cardiac ejection fraction and decreased mortality following TAC. These findings are the first to demonstrate a necessary role for the Tec family of tyrosine kinases in the heart and reveal a novel regulator (Bmx) of pressure overload-induced hypertrophic growth.

• Authors: Scherise A Mitchell-Jordan, Tanja Holopainen, Shuxun Ren, Sujing Wang, Sarah Warburton, Michael J Zhang, Kari Alitalo, Yibin Wang, Thomas M Vondriska
• Journal: Circulation research (Circ Res) Vol. 103 Issue 12 Pg. 1359-62 (Dec 05 2008) ISSN: 1524-4571 [Electronic] United States
• PMID: 18988895 (Publication Type: Comparative Study, Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't)

Chemical References

• Bmx protein, mouse
• Protein-Tyrosine Kinases

Topics

• Animals
• Blood Pressure (genetics, physiology)
• Cardiomegaly (genetics, metabolism, prevention & control)
• Male
• Mice
• Mice, Inbred BALB C
• Mice, Knockout
• Protein-Tyrosine Kinases (deficiency, genetics, physiology)