Vasopressin activates Akt/mTOR pathway in smooth muscle cells cultured in high glucose concentration.
Biochem Biophys Res Commun
; 441(4): 923-8, 2013 Nov 29.
Article
in En
| MEDLINE
| ID: mdl-24216105
ABSTRACT
Mammalian target of rapamycin (mTOR) complex is a key regulator of autophagy, cell growth and proliferation. Here, we studied the effects of arginine vasopressin (AVP) on mTOR activation in vascular smooth muscle cells cultured in high glucose concentration. AVP induced the mTOR phosphorylation in A-10 cells grown in high glucose, in contrast to cells cultured in normal glucose; wherein, only basal phosphorylation was observed. The AVP-induced mTOR phosphorylation was inhibited by a PI3K inhibitor. Moreover, the AVP-induced mTOR activation inhibited autophagy and increased thymidine incorporation in cells grown in high glucose. This increase was abolished by rapamycin which inhibits the mTORC1 complex formation. Our results suggest that AVP stimulates mTOR phosphorylation by activating the PI3K/Akt signaling pathway and, subsequently, inhibits autophagy and raises cell proliferation in A-10 cells maintained in high glucose concentration.
Key words
AMP-activated protein kinase; AMPK; AVP; Akt; ERK; PI3-kinase; PI3K; PKC; PLD; Rheb; TSC1/TSC2; Vascular remodeling; Vasopressin; arginine vasopressin; extracellular regulated-kinase; mTOR; mTOR complex 1; mTORC1; mammalian target of rapamycin; phosphatidyl inositol-3 kinase; phospholipase D; protein kinase C, Akt or protein kinase B; ras homolog enriched in brain; tubero sclerosis protein 1 and 2
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Arginine Vasopressin
/
Myocytes, Smooth Muscle
/
Multiprotein Complexes
/
Proto-Oncogene Proteins c-akt
/
TOR Serine-Threonine Kinases
/
Glucose
/
Hyperglycemia
Limits:
Animals
Language:
En
Journal:
Biochem Biophys Res Commun
Year:
2013
Document type:
Article
Affiliation country:
Chile