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VEGF-A splice varia...
VEGF-A splice variants and related receptor expression in human skeletal muscle following submaximal exercise
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- Gustafsson, T (författare)
- Karolinska Institutet
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- Ameln, H (författare)
- Karolinska Institutet
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- Fischer, H (författare)
- Karolinska Institutet
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- Sundberg, CJ (författare)
- Karolinska Institutet
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Timmons, JA (författare)
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- Jansson, E (författare)
- Karolinska Institutet
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(creator_code:org_t)
- American Physiological Society, 2005
- 2005
- Engelska.
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Ingår i: Journal of applied physiology (Bethesda, Md. : 1985). - : American Physiological Society. - 8750-7587 .- 1522-1601. ; 98:6, s. 2137-2146
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http://kipublication...
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https://doi.org/10.1...
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Abstract
Ämnesord
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- VEGF-A contributes to muscle tissue angiogenesis following aerobic exercise training. The temporal response of the VEGF-A isoforms and their target receptors has not been comprehensively profiled in human skeletal muscle. We combined submaximal exercise with and without reduced leg blood flow to establish whether ischemia-induced metabolic stress was an important physiological stimuli responsible for regulating the VEGF-A system in humans. Nine healthy men performed two 45-min bouts of one-leg knee-extension exercise, with and without blood flow restriction. Muscle biopsies were obtained at rest and 2 and 6 h after exercise. Expression (mRNA) of the VEGF-A splice variants and related receptors [VEGF receptor (VEGFR)-1, VEGFR-2, and neuropilin-1] was determined by using qPCR. VEGF-Atotal expression increased more robustly after exercise with reduced blood flow, and initially this principally reflected an increase in VEGF-A165. Six hours after exercise, there was a relatively greater increase in VEGF-A189, and this response was not influenced by blood flow conditions. VEGFR-1 mRNA expression increased 2 h after exercise, and neuropilin-1 expression was transiently reduced, while all three receptors increased by 6 h. There was no evidence for the expression of the inhibitory VEGF-A165B variant in human skeletal muscle. Our study, reflecting both VEGF-A ligand and receptors, implicates metabolic perturbation as a regulator of human muscle angiogenesis and demonstrates that VEGF-A splice variants are distinctly regulated. Our findings also indicate that all three receptor genes exhibit different pretranslational regulation, in response to exercise in humans.
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