PMID- 26542520
OWN - NLM
STAT- MEDLINE
DCOM- 20161011
LR  - 20181113
IS  - 1522-1601 (Electronic)
IS  - 8750-7587 (Print)
IS  - 0161-7567 (Linking)
VI  - 120
IP  - 2
DP  - 2016 Jan 15
TI  - Skeletal myofiber VEGF is necessary for myogenic and contractile adaptations to 
      functional overload of the plantaris in adult mice.
PG  - 188-95
LID - 10.1152/japplphysiol.00638.2015 [doi]
AB  - The ability to enhance muscle size and function is important for overall health. 
      In this study, skeletal myofiber vascular endothelial growth factor (VEGF) was 
      hypothesized to regulate hypertrophy, capillarity, and contractile function in 
      response to functional overload (FO). Adult myofiber-specific VEGF gene-ablated 
      mice (skmVEGF(-/-)) and wild-type (WT) littermates underwent plantaris FO or sham 
      surgery (SHAM). Mass, morphology, in vivo function, IGF-1, basic fibroblast 
      growth factor (bFGF), hepatocyte growth factor (HGF), and Akt were measured at 7, 
      14, and 30 days. FO resulted in hypertrophy in both genotypes, but fiber sizes 
      were 13% and 23% smaller after 14 and 30 days, respectively, and mass 15% less 
      after 30 days in skmVEGF(-/-) than WT. FO increased isometric force after 30 days 
      in WT and decreased in skmVEGF(-/-) after 7 and 14 days. FO also resulted in a 
      reduction in specific force and this differed between genotypes at 14 days. 
      Fatigue resistance improved only in 14-day WT mice. Capillary density was 
      decreased by FO in both genotypes. However, capillary-to-fiber ratios were 19% 
      and 15% lower in skmVEGF(-/-) than WT at the 14- and 30-day time points, 
      respectively. IGF-1 was increased by FO at all time points and was 45% and 40% 
      greater in skmVEGF(-/-) than WT after 7 and 14 days, respectively. bFGF, HGF, 
      total Akt, and phospho-Akt, independent of VEGF expression, and VEGF levels in WT 
      were increased after 7 days of FO. These findings suggest VEGF-dependent 
      capillary maintenance supports muscle growth and function in overloaded muscle 
      and is not rescued by compensatory IGF-1 expression.
CI  - Copyright (c) 2016 the American Physiological Society.
FAU - Huey, Kimberly A
AU  - Huey KA
AD  - College of Pharmacy and Health Sciences, Drake University, Des Moines, Iowa; and 
      kimberly.huey@drake.edu.
FAU - Smith, Sophia A
AU  - Smith SA
AD  - College of Pharmacy and Health Sciences, Drake University, Des Moines, Iowa; and.
FAU - Sulaeman, Alexis
AU  - Sulaeman A
AD  - Department of Medicine, University of California-San Diego, La Jolla, California.
FAU - Breen, Ellen C
AU  - Breen EC
AD  - Department of Medicine, University of California-San Diego, La Jolla, California.
LA  - eng
GR  - R15-AR-060469/AR/NIAMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20151105
PL  - United States
TA  - J Appl Physiol (1985)
JT  - Journal of applied physiology (Bethesda, Md. : 1985)
JID - 8502536
RN  - 0 (Vascular Endothelial Growth Factor A)
RN  - 0 (vascular endothelial growth factor A, mouse)
RN  - 62031-54-3 (Fibroblast Growth Factors)
RN  - 67256-21-7 (Hepatocyte Growth Factor)
RN  - 67763-96-6 (Insulin-Like Growth Factor I)
SB  - IM
MH  - Adaptation, Physiological/*physiology
MH  - Animals
MH  - Capillaries/metabolism/physiology
MH  - Fibroblast Growth Factors/metabolism
MH  - Hepatocyte Growth Factor/metabolism
MH  - Hypertrophy/metabolism/physiopathology
MH  - Insulin-Like Growth Factor I/metabolism
MH  - Male
MH  - Mice
MH  - Muscle Contraction/*physiology
MH  - Muscle Development/*physiology
MH  - Muscle Fibers, Skeletal/*metabolism/*physiology
MH  - Vascular Endothelial Growth Factor A/*metabolism
PMC - PMC4719059
OTO - NOTNLM
OT  - VEGF
OT  - functional overload
OT  - muscle force
OT  - plantaris
EDAT- 2015/11/07 06:00
MHDA- 2016/10/12 06:00
PMCR- 2017/01/15
CRDT- 2015/11/07 06:00
PHST- 2015/07/27 00:00 [received]
PHST- 2015/10/21 00:00 [accepted]
PHST- 2015/11/07 06:00 [entrez]
PHST- 2015/11/07 06:00 [pubmed]
PHST- 2016/10/12 06:00 [medline]
PHST- 2017/01/15 00:00 [pmc-release]
AID - japplphysiol.00638.2015 [pii]
AID - JAPPL-00638-2015 [pii]
AID - 10.1152/japplphysiol.00638.2015 [doi]
PST - ppublish
SO  - J Appl Physiol (1985). 2016 Jan 15;120(2):188-95. doi: 
      10.1152/japplphysiol.00638.2015. Epub 2015 Nov 5.