PMID- 30747215
OWN - NLM
STAT- MEDLINE
DCOM- 20190531
LR  - 20220408
IS  - 1791-244X (Electronic)
IS  - 1107-3756 (Print)
IS  - 1107-3756 (Linking)
VI  - 43
IP  - 3
DP  - 2019 Mar
TI  - MicroRNA-101 inhibits autophagy to alleviate liver ischemia/reperfusion injury 
      via regulating the mTOR signaling pathway.
PG  - 1331-1342
LID - 10.3892/ijmm.2019.4077 [doi]
AB  - Liver ischemia/reperfusion injury (LIRI) is a common complication of liver 
      surgery, and affects liver function post‑transplantation. However, the precise 
      mechanism underlying LIRI has not yet been completely elucidated. Previous 
      studies have demonstrated the involvement of a number of microRNAs (miRNAs/miRs) 
      in liver pathophysiology. The objective of the present study was to determine the 
      potential function and mechanism of miR‑101‑mediated regulation of autophagy in 
      LIRI. Compared with the sham‑treated group, a significant decrease in miR‑101 and 
      mechanistic target of rapamycin (mTOR) expression levels following 
      ischemia/reperfusion (IR) were observed, along with an increased number of 
      autophagosomes (P<0.001). The exogenous overexpression of miR‑101 has been 
      demonstrated to inhibit autophagy during the LIRI response and the levels of mTOR 
      and phosphorylated (p)‑mTOR expression are correspondingly elevated. However, 
      compared with the miR‑NC group, miR‑101 silencing was associated with reduced 
      mTOR and p‑mTOR levels and increased autophagy, as indicated by the gradual 
      increase in the levels of the microtubule‑associated protein 1 light II (LC3II). 
      The peak levels of LC3II were observed 12 h subsequent to reperfusion, which 
      coincided with the lowest levels of miR‑101. In addition, inhibition of autophagy 
      by 3‑methyladenine significant enhanced the protective effect of miR‑101 against 
      LIRI, compared with the IR group (P<0.001). Altogether, miR‑101 attenuates LIRI 
      by inhibiting autophagy via activating the mTOR pathway.
FAU - Song, Hu
AU  - Song H
AD  - First Central Clinical College, Tianjin Medical University, Tianjin 300070, P.R. 
      China.
FAU - Du, Chenyang
AU  - Du C
AD  - First Central Clinical College, Tianjin Medical University, Tianjin 300070, P.R. 
      China.
FAU - Wang, Xingxing
AU  - Wang X
AD  - First Central Clinical College, Tianjin Medical University, Tianjin 300070, P.R. 
      China.
FAU - Zhang, Jianjun
AU  - Zhang J
AD  - First Central Clinical College, Tianjin Medical University, Tianjin 300070, P.R. 
      China.
FAU - Shen, Zhongyang
AU  - Shen Z
AD  - First Central Clinical College, Tianjin Medical University, Tianjin 300070, P.R. 
      China.
LA  - eng
PT  - Journal Article
DEP - 20190124
PL  - Greece
TA  - Int J Mol Med
JT  - International journal of molecular medicine
JID - 9810955
RN  - 0 (MIRN101 microRNA, mouse)
RN  - 0 (MicroRNAs)
RN  - EC 2.6.1.1 (Aspartate Aminotransferases)
RN  - EC 2.6.1.2 (Alanine Transaminase)
RN  - EC 2.7.1.1 (mTOR protein, mouse)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
SB  - IM
EIN - Int J Mol Med. 2019 Jun;43(6):2532. PMID: 31017258
MH  - Alanine Transaminase/blood
MH  - Animals
MH  - Apoptosis/genetics
MH  - Aspartate Aminotransferases/blood
MH  - *Autophagy/genetics
MH  - Cell Proliferation
MH  - Liver/*metabolism
MH  - Male
MH  - Mice, Inbred C57BL
MH  - MicroRNAs/genetics/*metabolism
MH  - Reperfusion Injury/blood/*genetics/*pathology
MH  - *Signal Transduction
MH  - TOR Serine-Threonine Kinases/*metabolism
PMC - PMC6365072
EDAT- 2019/02/13 06:00
MHDA- 2019/06/01 06:00
PMCR- 2019/01/24
CRDT- 2019/02/13 06:00
PHST- 2018/09/08 00:00 [received]
PHST- 2019/01/17 00:00 [accepted]
PHST- 2019/02/13 06:00 [pubmed]
PHST- 2019/06/01 06:00 [medline]
PHST- 2019/02/13 06:00 [entrez]
PHST- 2019/01/24 00:00 [pmc-release]
AID - ijmm-43-03-1331 [pii]
AID - 10.3892/ijmm.2019.4077 [doi]
PST - ppublish
SO  - Int J Mol Med. 2019 Mar;43(3):1331-1342. doi: 10.3892/ijmm.2019.4077. Epub 2019 
      Jan 24.