PMID- 23403698
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20211021
IS  - 1792-0981 (Print)
IS  - 1792-1015 (Electronic)
IS  - 1792-0981 (Linking)
VI  - 5
IP  - 3
DP  - 2013 Mar
TI  - Mechanism underlying the inhibitory effect of Apelin-13 on glucose 
      deprivation-induced autophagy in rat cardiomyocytes.
PG  - 797-802
AB  - The aim of the present study was to investigate the effect of Apelin-13 on 
      cardiomyocyte autophagy and to determine the underlying mechanism of this effect. 
      To establish an autophagic model system, the cardiomyocytes of Sprague Dawley 
      rats (postnatal day 3) were cultured and divided into five groups: normal control 
      (Co), glucose deprivation (GD), GD+Apelin-13, GD+Apelin-13 treated with the 
      Akt-specific inhibitor triciribine (GD+Apelin-13+Triciribine) and triciribine 
      alone (Triciribine). The intracellular autophagosomes were then observed using 
      transmission electron microscopy (TEM) and the expression levels of cellular 
      autophagy-related protein microtubule-associated protein 1 light chain 3 (LC3), 
      phosphatidylinositol-3-kinase (PI3K) and mammalian target of rapamycin (mTOR) 
      protein were measured using western blotting. Compared with the Co group, the 
      ratio of LC3-II/LC3-I increased significantly in all treatment groups, with the 
      exception of the Triciribine group (P<0.05). Compared with the GD group, the 
      ratio of LC3-II/LC3-I was significantly decreased, and the PI3K and mTOR 
      expression was significantly enhanced in the GD+Apelin-13 and 
      GD+Apelin-13+Triciribine groups (P<0.05). Compared with the GD+Apelin-13 group, 
      the ratio of LC3-II/LC3-I increased significantly (P<0.05) and the PI3K 
      expression remained unchanged in the GD+Apelin-13+Triciribine group (P>0.05), but 
      mTOR expression was significantly reduced (P<0.05). GD led to increased numbers 
      of autophagosomes and augmented the LC3-II/LC3-I ratio (P<0.05). Apelin-13 
      pretreatment attenuated GD-induced cardiomyocte injury, decreased the 
      autophagosome number and the ratio of LC3-II/LC3-I (P<0.05), enhanced PI3K 
      activity (P<0.05) and upregulated the phosphorylation levels of the Akt and mTOR 
      proteins (P<0.05). The Akt-specific inhibitor triciribine weakened the protective 
      role of Apelin-13 (P<0.05). To a certain extent, Apelin-13 inhibited GD-induced 
      cardiomyocyte autophagy, which may be related in part to the activation of the 
      PI3K/Akt/mTOR signaling pathway.
FAU - Jiao, Hui
AU  - Jiao H
AD  - Department of Cardiology, The Third Affilated Hospital of Liaoning Medical 
      University, Jinzhou 121001, P.R. China.
FAU - Zhang, Zhi
AU  - Zhang Z
FAU - Ma, Qinghua
AU  - Ma Q
FAU - Fu, Wei
AU  - Fu W
FAU - Liu, Zidong
AU  - Liu Z
LA  - eng
PT  - Journal Article
DEP - 20130117
PL  - Greece
TA  - Exp Ther Med
JT  - Experimental and therapeutic medicine
JID - 101531947
PMC - PMC3570085
OTO - NOTNLM
OT  - Apelin-13
OT  - PI3K/Akt/mTOR pathway
OT  - autophagy
OT  - cardiomyocytes
OT  - glucose deprivation
OT  - light chain 3
EDAT- 2013/02/14 06:00
MHDA- 2013/02/14 06:01
PMCR- 2013/01/17
CRDT- 2013/02/14 06:00
PHST- 2012/11/02 00:00 [received]
PHST- 2013/01/08 00:00 [accepted]
PHST- 2013/02/14 06:00 [entrez]
PHST- 2013/02/14 06:00 [pubmed]
PHST- 2013/02/14 06:01 [medline]
PHST- 2013/01/17 00:00 [pmc-release]
AID - etm-05-03-0797 [pii]
AID - 10.3892/etm.2013.902 [doi]
PST - ppublish
SO  - Exp Ther Med. 2013 Mar;5(3):797-802. doi: 10.3892/etm.2013.902. Epub 2013 Jan 17.