PMID- 29434702
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220330
IS  - 1792-0981 (Print)
IS  - 1792-1015 (Electronic)
IS  - 1792-0981 (Linking)
VI  - 15
IP  - 1
DP  - 2018 Jan
TI  - miR-4262 regulates chondrocyte viability, apoptosis, autophagy by targeting SIRT1 
      and activating PI3K/AKT/mTOR signaling pathway in rats with osteoarthritis.
PG  - 1119-1128
LID - 10.3892/etm.2017.5444 [doi]
AB  - The present study aimed to investigate the effect and underlying mechanism of 
      microRNA (miR)-4262 in the development of osteoarthritis (OA) in rats. Primary 
      chondrocytes were separated from Sprague-Dawley rats and then treated with tumor 
      necrosis factor-alpha (TNF-alpha). The level of miR-4262 was detected in TNF-alpha-treated 
      chondrocytes, and then the miR-4262 or its target gene sirtuin type 1 (SIRT1) 
      level was overexpressed, or knocked down. Furthermore, cell viability, cell 
      apoptosis, cell autophagy and matrix synthesis, as well as the expressions of 
      proteins associated with the phosphoinositide 3-kinase (PI3K)/protein kinase B 
      (AKT)/mammalian target of rapamycin (mTOR) signaling pathway were detected. 
      miR-4262 was significantly overexpressed in TNF-alpha-treated chondrocytes compared 
      with untreated cells (P<0.05). TNF-alpha treatment or miR-4262 overexpression 
      significantly decreased cell viability, autophagy-related proteins levels and 
      matrix synthesis-related proteins levels, as well as increased the apoptotic rate 
      in chondrocytes (P<0.05). Overexpression of SIRT1 significantly increased cell 
      viability, autophagy-related proteins levels and matrix synthesis-related 
      proteins levels, as well as decreased the apoptotic rate in TNF-alpha-treated 
      chondrocytes (P<0.05). In addition, the effects of miR-4262 on cell viability, 
      cell apoptosis, cell autophagy and matrix synthesis were inhibited by SIRT1 
      (P<0.05). Furthermore, upregulated miR-4262 remarkably increased the expressions 
      of phosphorylated (p)-PI3K, p-AKT and p-mTOR (P<0.05) in TNF-alpha treated 
      chondrocytes. The present study revealed that the upregulation of miR-4262 may 
      promote the occurrence and development of OA in rats by regulating cell 
      viability, cell apoptosis, cell autophagy, and matrix synthesis. Furthermore, 
      these roles of miR-4262 may be associated with PI3K/AKT/mTOR signaling pathway.
FAU - Sun, Wencai
AU  - Sun W
AD  - Department of Orthopaedics, The Third Hospital Affiliated to Qiqihar Medical 
      College, Qiqihar, Heilongjiang 161006, P.R. China.
FAU - Li, Yintai
AU  - Li Y
AD  - Department of Rehabilitation, Baoji Traditional Chinese Medicine Hospital, Baoji, 
      Shaanxi 721000, P.R. China.
FAU - Wei, Suizhuan
AU  - Wei S
AD  - Department of Orthopaedics, Baoji Traditional Chinese Medicine Hospital, Baoji, 
      Shaanxi 721000, P.R. China.
LA  - eng
PT  - Journal Article
DEP - 20171106
PL  - Greece
TA  - Exp Ther Med
JT  - Experimental and therapeutic medicine
JID - 101531947
PMC - PMC5772979
OTO - NOTNLM
OT  - PI3K/AKT/mTOR signaling pathway
OT  - cell autophagy
OT  - matrix synthesis
OT  - miR-4262
OT  - osteoarthritis
EDAT- 2018/02/13 06:00
MHDA- 2018/02/13 06:01
PMCR- 2017/11/06
CRDT- 2018/02/14 06:00
PHST- 2017/05/16 00:00 [received]
PHST- 2017/10/16 00:00 [accepted]
PHST- 2018/02/14 06:00 [entrez]
PHST- 2018/02/13 06:00 [pubmed]
PHST- 2018/02/13 06:01 [medline]
PHST- 2017/11/06 00:00 [pmc-release]
AID - ETM-0-0-5444 [pii]
AID - 10.3892/etm.2017.5444 [doi]
PST - ppublish
SO  - Exp Ther Med. 2018 Jan;15(1):1119-1128. doi: 10.3892/etm.2017.5444. Epub 2017 Nov 
      6.