PMID- 21191105
OWN - NLM
STAT- MEDLINE
DCOM- 20110420
LR  - 20211203
IS  - 1522-1563 (Electronic)
IS  - 0363-6143 (Linking)
VI  - 300
IP  - 3
DP  - 2011 Mar
TI  - Prostaglandin F2α stimulates PI3K/ERK/mTOR signaling and skeletal myotube 
      hypertrophy.
PG  - C671-82
LID - 10.1152/ajpcell.00549.2009 [doi]
AB  - Cyclooxygenase (COX) enzymes mediate the synthesis of proinflammatory 
      prostaglandin (PG) species from cellular arachidonic acid. COX/PGs have been 
      implicated in skeletal muscle growth/regeneration; however, the mechanisms by 
      which PGs influence skeletal muscle adaptation are poorly understood. The present 
      study aimed to investigate PGF(2alpha) signaling and its role in skeletal myotube 
      hypertrophy. PGF(2alpha) or the FP receptor agonist fluprostenol increased C2C12 
      myotube diameter. This effect was abolished by the FP receptor antagonist AL8810 
      and mammalian target of rapamycin (mTOR) inhibition. PGF(2alpha) stimulated time- and 
      dose-dependent increases in the phosphorylation of extracellular receptor kinase 
      (ERK)1/2 (Thr202/Tyr204), p70S6 kinase (p70S6K) (Thr389 and Thr421/Ser424), and 
      eukaryotic initiation factor 4G (eIF4G) (Ser1108) without influencing Akt 
      (Ser473). Pretreatment with the phosphoinositide 3-kinase (PI3K) inhibitor 
      LY294002 and the ERK inhibitor PD98059 blocked F prostanoid receptor signaling 
      responses, whereas rapamycin blocked heightened p70S6K/eIF4G phosphorylation 
      without influencing ERK1/2 phosphorylation. These data suggest that activation of 
      the F prostanoid receptor is coupled to C2C12 myotube growth and intracellular 
      signaling via a PI3K/ERK/mTOR-dependent pathway.
FAU - Markworth, James F
AU  - Markworth JF
AD  - School of Exercise and Nutrition Sciences, Deakin Univ., 221 Burwood Highway, 
      Burwood, Victoria 3125, Australia.
FAU - Cameron-Smith, David
AU  - Cameron-Smith D
LA  - eng
PT  - Journal Article
DEP - 20101229
PL  - United States
TA  - Am J Physiol Cell Physiol
JT  - American journal of physiology. Cell physiology
JID - 100901225
RN  - EC 2.7.1.1 (mTOR protein, mouse)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
SB  - IM
MH  - Animals
MH  - Cell Differentiation/physiology
MH  - Cell Line
MH  - Cell Movement/physiology
MH  - Extracellular Signal-Regulated MAP Kinases/*physiology
MH  - Hypertrophy
MH  - MAP Kinase Signaling System/physiology
MH  - Mice
MH  - Muscle Fibers, Skeletal/enzymology/*metabolism/pathology
MH  - Muscle, Skeletal/enzymology/*metabolism/*pathology
MH  - Myoblasts/enzymology/metabolism/pathology
MH  - Phosphatidylinositol 3-Kinases/*physiology
MH  - Signal Transduction/*physiology
MH  - TOR Serine-Threonine Kinases/*physiology
EDAT- 2010/12/31 06:00
MHDA- 2011/04/22 06:00
CRDT- 2010/12/31 06:00
PHST- 2010/12/31 06:00 [entrez]
PHST- 2010/12/31 06:00 [pubmed]
PHST- 2011/04/22 06:00 [medline]
AID - ajpcell.00549.2009 [pii]
AID - 10.1152/ajpcell.00549.2009 [doi]
PST - ppublish
SO  - Am J Physiol Cell Physiol. 2011 Mar;300(3):C671-82. doi: 
      10.1152/ajpcell.00549.2009. Epub 2010 Dec 29.