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May 18, 2004AJP Cell Physiology

Permanent replacement of SM-B myosin by SM-A myosin in mice led to decreased velocity of shortening and increased isometric force generation in mesenteric vessels and aorta.

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Population

Isoform-specific gene knockout mouse in which SM-B myosin is permanently replaced by SM-A myosin

Comparison

Genetic knockout of SM-B myosin vs Wild-type animals

Design

Preclinical

Key result

Permanent replacement of SM-B myosin by SM-A myosin in mice led to decreased velocity of shortening and increased isometric force generation in mesenteric vessels and aorta.

Authors

GBGopal J. BabuGPGail J. PyneYZYingbi Zhou

Discussion

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Overview

Hypothesis-generating for myosin isoform effects on vascular tone; requires confirmation in human tissues before clinical relevance.

Structured PICO

P
Population
Isoform-specific gene knockout mouse in which SM-B myosin is permanently replaced by SM-A myosin
I
Intervention
Genetic knockout of SM-B myosin (replaced by SM-A myosin)
C
Comparator
Wild-type animals
O
Outcome
Contractile properties of vascular smooth muscle (specifically peripheral mesenteric vessels and aorta)surrogate

Loss of SM-B myosin in vascular smooth muscle decreases shortening velocity, increases isometric force, and alters thin filament regulatory protein expression.

Cite This Study

Babu et al. (2004) studied Vascular smooth muscle contractile properties. SM-B myosin knockout (replacement by SM-A myosin) vs. Wild-type animals was evaluated on Contractile properties of vascular smooth muscle (velocity of shortening and isometric force generation). Permanent replacement of SM-B myosin by SM-A myosin in mice led to decreased velocity of shortening and increased isometric force generation in mesenteric vessels and aorta.

synapsesocial.com/papers/6a8c25f4f71fc1553cbeb4b0https://doi.org/10.1152/ajpcell.00029.2004
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