Loss of Bmx nonreceptor tyrosine kinase prevents pressure overload-induced cardiac hypertrophy.
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.
Mitchell-Jordan
Scherise A
SA
Department of Anesthesiology, David Geffen School of Medicine at University of California, Los Angeles, CA 90095, USA.
Holopainen
Tanja
T
Ren
Shuxun
S
Wang
Sujing
S
Warburton
Sarah
S
Zhang
Michael J
MJ
Alitalo
Kari
K
Wang
Yibin
Y
Vondriska
Thomas M
TM
D000818:Animals; D001794:Blood Pressure / Q000235:genetics / Q000502:physiology*; D006332:Cardiomegaly / Q000235:genetics / Q000378:metabolism* / Q000517:prevention & control*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D018345:Mice, Knockout; D011505:Protein-Tyrosine Kinases / Q000172:deficiency* / Q000235:genetics / Q000502:physiology
C492366:Bmx protein, mouse; D011505:Protein-Tyrosine Kinases