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-actin null mouse
* Department of Molecular and Cellular Biology,
Department of Medicine, Section of Cardiovascular Sciences,
Department of Molecular Physiology and Biophysics and
§ Howard Hughes Medical Institute, Department of Genetics, Baylor College of Medicine, Houston, Texas 77030, USA
1Correspondence: Department of Cell Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA. E-mail: schwartz{at}bcm.tmc.edu
The smooth muscle (SM) 
-actin gene activated during the early stages
of embryonic cardiovascular development is switched off in late stage
heart tissue and replaced by cardiac and skeletal -actins. SM
-actin also appears during vascular development, but becomes the
single most abundant protein in adult vascular smooth muscle cells.
Tissue-specific expression of SM -actin is thought to be required
for the principal force-generating capacity of the vascular smooth
muscle cell. We wanted to determine whether SM -actin gene
expression actually relates to an actin isoform’s function. Analysis
of SM -actin null mice indicated that SM -actin is not required
for the formation of the cardiovascular system. Also, SM -actin null
mice appeared to have no difficulty feeding or reproducing. Survival in
the absence of SM -actin may result from other actin isoforms
partially substituting for this isoform. In fact, skeletal -actin
gene, an actin isoform not usually expressed in vascular smooth muscle,
was activated in the aortas of these SM -actin null mice. However,
even with a modest increase in skeletal -actin activity, highly
compromised vascular contractility, tone, and blood flow were detected
in SM -actin-defective mice. This study supports the concept that SM
-actin has a central role in regulating vascular contractility and
blood pressure homeostasis, but is not required for the formation
of the cardiovascular system.—Schildmeyer, L. A., Braun, R.,
Taffet, G., DeBiasi, M., Burns, A. E., Bradley, A., and Schwartz,
R. J. Impaired vascular contractility and blood pressure
homeostasis in the smooth muscle -actin null mouse.
Key Words: SM -actin gene • homologous recombination • vascular tone
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