PMID- 30546417
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200929
IS  - 1792-0981 (Print)
IS  - 1792-1015 (Electronic)
IS  - 1792-0981 (Linking)
VI  - 16
IP  - 6
DP  - 2018 Dec
TI  - MicroRNA-182-5p contributes to the protective effects of thrombospondin 1 against 
      lipotoxicity in INS-1 cells.
PG  - 5272-5279
LID - 10.3892/etm.2018.6883 [doi]
AB  - The dysfunction of beta cells serves an important role in the pathogenesis of 
      type 2 diabetes mellitus (T2DM). An improved understanding of the molecular 
      mechanisms underlying beta cell mass and failure will be useful for identifying 
      novel approaches toward preventing and treating this disease. Recent studies have 
      indicated that free fatty acids (FFAs) can cause beta cell dysfunction. In the 
      present study, palmitate (Pal) was used as a FFA and its functions on cell 
      viability and apoptosis were detected. MTT assay and flow cytometry were used and 
      the results revealed that incubation of INS-1 cells with Pal significantly 
      decreased cell viability and increased cell apoptosis. However, a co-incubation 
      with thrombospondin 1 (THBS-1) protected the cells against Pal-induced toxicity. 
      Numerous studies have demonstrated that microRNAs (miRs) are involved in fatty 
      acid-induced beta cell dysfunction. Various studies have reported that miR-182-5p 
      is associated with a number of diseases, including cancer, heart disease, and 
      leukemia. However, to the best of our knowledge miR-182-5p has never been 
      reported to be associated with diabetes. In the present study, miR-182-5p, which 
      is predicted to target the 3'-untranslated region (UTR) of THBS-1, was detected 
      using reverse transcription-quantitative polymerase chain reaction in INS-1 cells 
      in response to Pal. miR-182-5p was significantly increased in Pal-treated cells 
      compared with the control cells. Furthermore, miR-182-5p mimics significantly 
      decreased cell viability and increased Pal-induced apoptosis in INS-1 cells. 
      However, cell viability was increased and Pal-induced apoptosis was decreased in 
      cells that were treated with miR-182-5p inhibitors. The present findings also 
      revealed that overexpression of THBS-1 counteracted the effect of miR-182-5p on 
      cell viability and apoptosis. These results suggested that miR-182-5p is involved 
      in the mechanism of THBS 1 on the modulation of beta cell survival.
FAU - Liu, Ying
AU  - Liu Y
AD  - Department of Pediatrics, West China Second University Hospital, Sichuan 
      University, Chengdu, Sichuan 610041, P.R. China.
AD  - Laboratory of Birth Defects and Related Disease of Women and Children, Sichuan 
      University, Ministry of Education, Chengdu, Sichuan 610041, P.R. China.
FAU - Dong, Jiayue
AU  - Dong J
AD  - Department of Traditional Chinese Medicine, College of Pharmacy, Chengdu 
      University, Chengdu, Sichuan 610106, P.R. China.
FAU - Ren, Bo
AU  - Ren B
AD  - Department of Traditional Chinese Medicine, College of Pharmacy, Chengdu 
      University, Chengdu, Sichuan 610106, P.R. China.
LA  - eng
PT  - Journal Article
DEP - 20181019
PL  - Greece
TA  - Exp Ther Med
JT  - Experimental and therapeutic medicine
JID - 101531947
PMC - PMC6256972
OTO - NOTNLM
OT  - apoptosis
OT  - beta cells
OT  - diabetes
OT  - microRNAs
OT  - palmitate
EDAT- 2018/12/14 06:00
MHDA- 2018/12/14 06:01
PMCR- 2018/10/19
CRDT- 2018/12/15 06:00
PHST- 2018/03/02 00:00 [received]
PHST- 2018/07/26 00:00 [accepted]
PHST- 2018/12/15 06:00 [entrez]
PHST- 2018/12/14 06:00 [pubmed]
PHST- 2018/12/14 06:01 [medline]
PHST- 2018/10/19 00:00 [pmc-release]
AID - ETM-0-0-6883 [pii]
AID - 10.3892/etm.2018.6883 [doi]
PST - ppublish
SO  - Exp Ther Med. 2018 Dec;16(6):5272-5279. doi: 10.3892/etm.2018.6883. Epub 2018 Oct 
      19.