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Muscle‐specific VEGF knockout disrupts thermoregulation without altering mitochondrial morphometry or activity
Author(s) -
Mandler William Kyle,
Audet Gerald N,
Olfert I Mark
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.lb773
Subject(s) - skeletal muscle , mitochondrial biogenesis , thermoregulation , medicine , endocrinology , mitochondrion , biology , angiogenesis , thermogenesis , chemistry , adipose tissue , microbiology and biotechnology
VEGF is believed to enhance thermogenesis in response to cold exposure through promoting angiogenesis, enhancing metabolism, and upregulating mitochondrial biogenesis. Using muscle‐specific VEGF gene deleted mice, we tested the hypothesis that loss of VEGF in skeletal muscle will affect thermoregulation. VEGF knockout (KO) and wild‐type (WT) mice were exposed to 4°C for 6 hours. Core temperature was measured in 15 minute increments. Flow cytometry analysis was performed on isolated subsarcolemmal (SSM) and interfibrillar (IFM) mitochondrial subpopulations taken from cardiac and triceps surae muscle tissue of KO or WT to determine mitochondrial size and complexity. Initial temperature was lower in the KO. During cold exposure, temperatures dropped more quickly in the KO group. The average time to reach a core temperature decrease of 8°C was shorter in the KO group. There were no differences in skeletal muscle SSM or IFM in size or complexity. In the cardiac tissue, both SSM and IFM exhibited greater size in the KO group. There were no significant differences in mitochondrial density for any tissue or subpopulation. Muscle‐specific VEGF KO mice are unable to maintain core temperature to the same degree as WT in the face of a 4°C challenge and have a lower core temperature at room temperature. Skeletal muscle mitochondrial density and morphology does not appear to play a role in this effect.