PMID- 30521964
OWN - NLM
STAT- MEDLINE
DCOM- 20190503
LR  - 20211028
IS  - 1878-1705 (Electronic)
IS  - 1567-5769 (Linking)
VI  - 66
DP  - 2019 Jan
TI  - Long non-coding RNA THRIL promotes LPS-induced inflammatory injury by 
      down-regulating microRNA-125b in ATDC5 cells.
PG  - 354-361
LID - S1567-5769(18)31226-8 [pii]
LID - 10.1016/j.intimp.2018.11.038 [doi]
AB  - BACKGROUND: Osteoarthritis is an age-related disorder of bone-joint that causes 
      pain and disability in middle and older people. This study aimed to investigate 
      the potential effects of long non-coding RNA (lncRNA) THRIL on lipopolysaccharide 
      (LPS)-induced osteoarthritis cell injury model (ATDC5 cell inflammatory injury), 
      as well as the possible internal molecular mechanisms. METHODS: Cell viability 
      and apoptosis were assessed using CCK-8 assay and Guava Nexin assay, 
      respectively. Cell transfection was conducted to change the expression of THRIL 
      and microRNA-125b (miR-125b) in ATDC5 cells. qRT-PCR was performed to detect the 
      expression of THRIL, miR-125b and pro-inflammatory cytokines IL-6, TNF-alpha and 
      monocyte chemotactic protein 1 (MCP-1) in ATDC5 cells. ELISA was used to measure 
      the concentrations of IL-6, TNF-alpha and MCP-1 in culture supernatant of ATDC5 
      cells. Finally, the protein expression of key factors involved in cell apoptosis, 
      inflammatory response, JAK1/STAT3 and NF-kappaB pathways were evaluated using western 
      blotting. RESULTS: LPS significantly induced ATDC5 cell inflammatory injury and 
      up-regulated the expression of THRIL. Overexpression of THRIL aggravated the 
      LPS-induced ATDC5 cell inflammatory injury. Suppression of THRIL had opposite 
      effects. Moreover, THRIL negatively regulated the expression of miR-125b in ATDC5 
      cells. miR-125b participated in the effects of THRIL overexpression on 
      LPS-induced ATDC5 cell inflammatory injury. Furthermore, overexpression of THRIL 
      enhanced the LPS-induced JAK1/STAT3 and NF-kappaB pathways activation by 
      down-regulating miR-125b. CONCLUSION: THRIL exerted pro-inflammatory roles in 
      LPS-induced osteoarthritis cell injury model. Overexpression of THRIL promoted 
      LPS-induced ATDC5 cell inflammatory injury by down-regulating miR-125b and then 
      activating JAK1/STAT3 and NF-kappaB pathways.
CI  - Copyright (c) 2018. Published by Elsevier B.V.
FAU - Liu, Guangyao
AU  - Liu G
AD  - Department of Orthopaedics, China-Japan Union Hospital of Jilin University, 
      Changchun 130033, China.
FAU - Wang, Yongkun
AU  - Wang Y
AD  - Department of Orthopaedics, China-Japan Union Hospital of Jilin University, 
      Changchun 130033, China.
FAU - Zhang, Mingran
AU  - Zhang M
AD  - Department of Orthopaedics, China-Japan Union Hospital of Jilin University, 
      Changchun 130033, China.
FAU - Zhang, Qiao
AU  - Zhang Q
AD  - Department of Orthopaedics, China-Japan Union Hospital of Jilin University, 
      Changchun 130033, China. Electronic address: qiaozhang0094@sina.com.
LA  - eng
PT  - Journal Article
DEP - 20181204
PL  - Netherlands
TA  - Int Immunopharmacol
JT  - International immunopharmacology
JID - 100965259
RN  - 0 (Lipopolysaccharides)
RN  - 0 (MicroRNAs)
RN  - 0 (Mirn125 microRNA, mouse)
RN  - 0 (NF-kappa B)
RN  - 0 (RNA, Long Noncoding)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 2.7.10.2 (Janus Kinase 1)
SB  - IM
ECI - Int Immunopharmacol. 2021 Nov;100:107944. PMID: 34702570
MH  - Apoptosis
MH  - Cell Line
MH  - Cell Survival
MH  - Chondrocytes/*physiology
MH  - Down-Regulation
MH  - Humans
MH  - Inflammation/*genetics
MH  - Janus Kinase 1/metabolism
MH  - Lipopolysaccharides/immunology
MH  - MicroRNAs/*genetics
MH  - NF-kappa B/metabolism
MH  - Osteoarthritis/*genetics
MH  - RNA, Long Noncoding/*genetics
MH  - Signal Transduction
MH  - Tumor Necrosis Factor-alpha/metabolism
OTO - NOTNLM
OT  - Cell inflammation
OT  - JAK1/STAT3 and NF-kappaB pathways
OT  - Lipopolysaccharide
OT  - Long non-coding RNA THRIL
OT  - MicroRNA-125b
OT  - Osteoarthritis
EDAT- 2018/12/07 06:00
MHDA- 2019/05/06 06:00
CRDT- 2018/12/07 06:00
PHST- 2018/08/02 00:00 [received]
PHST- 2018/11/09 00:00 [revised]
PHST- 2018/11/23 00:00 [accepted]
PHST- 2018/12/07 06:00 [pubmed]
PHST- 2019/05/06 06:00 [medline]
PHST- 2018/12/07 06:00 [entrez]
AID - S1567-5769(18)31226-8 [pii]
AID - 10.1016/j.intimp.2018.11.038 [doi]
PST - ppublish
SO  - Int Immunopharmacol. 2019 Jan;66:354-361. doi: 10.1016/j.intimp.2018.11.038. Epub 
      2018 Dec 4.