PMID- 23444088
OWN - NLM
STAT- MEDLINE
DCOM- 20140507
LR  - 20211203
IS  - 1439-3964 (Electronic)
IS  - 0172-4622 (Linking)
VI  - 34
IP  - 9
DP  - 2013 Sep
TI  - The fibrotic role of phosphatidylinositol-3-kinase/Akt pathway in injured 
      skeletal muscle after acute contusion.
PG  - 789-94
LID - 10.1055/s-0032-1333284 [doi]
AB  - Transforming growth factor beta (TGF-beta) is a multifunctional cytokine with 
      fibrogenic properties. Previous studies demonstrated that Phosphatidylinositol 
      3-Kinase (PI3K)/Akt/ mammalian target of Ramycin (mTOR), a non-Smad TGF-beta 
      pathway, plays an important role in the fibrotic pathogenesis of different organs 
      such as the lung, kidney, skin and liver. However, the role of PI3k-Akt pathway 
      in fibrosis in injured skeletal muscle is still unclear. In this study, we 
      determined the fibrotic role of PI3K-Akt pathway in injured skeletal muscle. We 
      established a mouse model for acute muscle contusion. Western blotting analysis 
      showed that TGF-beta, phosphorylated Akt and phosphorylated mTOR were increased in 
      muscles after acute contusion, which indicated that the PI3K-Akt- mTOR pathway 
      was activated in skeletal muscle after acute contusion. The pathway was inhibited 
      by a PI3K inhibitor, LY294002. Moreover, the expression of fibrosis markers 
      vimentin, alpha SMA and collagen I and the area of scar decreased in injured skeletal 
      muscle after PI3K pathway was blocked. The muscle function improved in terms of 
      both fast-twitch and tetanic strength after PI3K/Akt pathway was inhibited in 
      injured skeletal muscle. In conclusion, activation of PI3K-Akt-mTOR pathway might 
      promote collagen production and scar formation in the acute contused skeletal 
      muscle. Blocking of PI3K-Akt-mTOR pathway could improve the function of injured 
      skeletal muscle.
CI  - (c) Georg Thieme Verlag KG Stuttgart . New York.
FAU - Li, H-Y
AU  - Li HY
AD  - Department of Sports Medicine, Huashan Hospital, Sports Medicine Center of Fudan 
      University, Shanghai, China.
FAU - Zhang, Q-G
AU  - Zhang QG
FAU - Chen, J-W
AU  - Chen JW
FAU - Chen, S-Q
AU  - Chen SQ
FAU - Chen, S-Y
AU  - Chen SY
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130226
PL  - Germany
TA  - Int J Sports Med
JT  - International journal of sports medicine
JID - 8008349
RN  - 0 (Chromones)
RN  - 0 (Morpholines)
RN  - 0 (Phosphoinositide-3 Kinase Inhibitors)
RN  - 0 (Transforming Growth Factor beta)
RN  - 31M2U1DVID (2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one)
RN  - 9007-34-5 (Collagen)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
SB  - IM
MH  - Animals
MH  - Athletic Injuries/etiology/pathology
MH  - Blotting, Western
MH  - Chromones/pharmacology
MH  - Cicatrix/metabolism
MH  - Collagen/metabolism
MH  - Contusions/etiology/pathology
MH  - Disease Models, Animal
MH  - Fibrosis
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Morpholines/pharmacology
MH  - Muscle, Skeletal/*pathology
MH  - Phosphatidylinositol 3-Kinases/*metabolism
MH  - Phosphoinositide-3 Kinase Inhibitors
MH  - Proto-Oncogene Proteins c-akt/*metabolism
MH  - TOR Serine-Threonine Kinases/metabolism
MH  - Transforming Growth Factor beta/*metabolism
EDAT- 2013/02/28 06:00
MHDA- 2014/05/08 06:00
CRDT- 2013/02/28 06:00
PHST- 2013/02/28 06:00 [entrez]
PHST- 2013/02/28 06:00 [pubmed]
PHST- 2014/05/08 06:00 [medline]
AID - 10.1055/s-0032-1333284 [doi]
PST - ppublish
SO  - Int J Sports Med. 2013 Sep;34(9):789-94. doi: 10.1055/s-0032-1333284. Epub 2013 
      Feb 26.