PMID- 32050156
OWN - NLM
STAT- MEDLINE
DCOM- 20210106
LR  - 20210106
IS  - 1878-1705 (Electronic)
IS  - 1567-5769 (Linking)
VI  - 81
DP  - 2020 Apr
TI  - UFL1 attenuates IL-1beta-induced inflammatory response in human osteoarthritis 
      chondrocytes.
PG  - 106278
LID - S1567-5769(19)32589-5 [pii]
LID - 10.1016/j.intimp.2020.106278 [doi]
AB  - Osteoarthritis (OA) is a chronic inflammatory joint disease characterized by 
      degradation of articular cartilage. Ubiquitin-fold modifier 1 (UFM1)-specific 
      ligase 1 (UFL1) is an UFM1 E3 ligase that has been identified as a regulator of 
      inflammatory response. However, the role of UFL1 in OA remains unknown. The aim 
      of the present study was to explore the function of UFL1 in an in vitro OA system 
      in chondrocytes. Our results showed that UFL1 was lowly expressed in both OA 
      articular tissues and chondrocytes with IL-1beta induction. Ectopic expression of 
      UFL1 improved cell viability of IL-1beta-induced chondrocytes. UFL1 suppressed the 
      production of NO and PGE2, as well the expression levels of iNOS and COX-2 in 
      IL-1beta-induced chondrocytes. The IL-1beta-induced increases in TNF-alpha and IL-6 levels 
      were attenuated by UFL1. Ectopic expression of UFL1 inhibited the production of 
      extracellular matrix (ECM) degrading enzymes including matrix metalloproteinase 3 
      (MMP-3), MMP-13, ADAMTS-4 and ADAMTS-5 in chondrocytes with IL-1beta induction. 
      Additionally, UFL1 suppressed IL-1beta-induced activation of NF-kappaB signaling pathway 
      in chondrocytes. In conclusion, these findings indicated that UFL1 exerted 
      protective effect on IL-1beta-induced chondrocytes. Thus, UFL1 might be a potential 
      target for the treatment of OA.
CI  - Copyright (c) 2020 Elsevier B.V. All rights reserved.
FAU - Yang, Guangjie
AU  - Yang G
AD  - Department of Orthopedics, The First Affiliated Hospital of Henan University, 
      Kaifeng 475000, Henan Province, China.
FAU - Wang, Yongsheng
AU  - Wang Y
AD  - Department of Orthopedics, The First Affiliated Hospital of Henan University, 
      Kaifeng 475000, Henan Province, China.
FAU - Chen, You
AU  - Chen Y
AD  - Department of Orthopedics, The First Affiliated Hospital of Henan University, 
      Kaifeng 475000, Henan Province, China.
FAU - Huang, Rong
AU  - Huang R
AD  - Department of Neurology, The First Affiliated Hospital of Henan University, 
      Kaifeng 475000, Henan Province, China. Electronic address: huang_rong2@126.com.
LA  - eng
PT  - Journal Article
DEP - 20200209
PL  - Netherlands
TA  - Int Immunopharmacol
JT  - International immunopharmacology
JID - 100965259
RN  - 0 (Inflammation Mediators)
RN  - 0 (Interleukin-1beta)
RN  - 0 (Interleukin-6)
RN  - 0 (NF-kappa B)
RN  - 0 (Proteins)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (UFM1 protein, human)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - EC 2.3.2.27 (Ubiquitin-Protein Ligases)
RN  - EC 6.3.2.- (UFL1 protein, human)
RN  - K7Q1JQR04M (Dinoprostone)
SB  - IM
MH  - Cells, Cultured
MH  - Chondrocytes/*physiology
MH  - Dinoprostone/metabolism
MH  - Extracellular Matrix/metabolism
MH  - Female
MH  - Humans
MH  - Inflammation Mediators/metabolism
MH  - Interleukin-1beta/*metabolism
MH  - Interleukin-6/metabolism
MH  - Male
MH  - NF-kappa B/metabolism
MH  - Nitric Oxide/metabolism
MH  - Osteoarthritis/*metabolism
MH  - Proteins/metabolism
MH  - Signal Transduction
MH  - Tumor Necrosis Factor-alpha/metabolism
MH  - Ubiquitin-Protein Ligases/*metabolism
OTO - NOTNLM
OT  - Chondrocytes
OT  - IL-1beta
OT  - Inflammation
OT  - NF-kappaB signaling pathway
OT  - Osteoarthritis (OA)
OT  - Ubiquitin-fold modifier 1 (UFM1)-specific ligase 1 (UFL1)
COIS- Declaration of Competing Interest The authors declare that they have no known 
      competing financial interests or personal relationships that could have appeared 
      to influence the work reported in this paper.
EDAT- 2020/02/13 06:00
MHDA- 2021/01/07 06:00
CRDT- 2020/02/13 06:00
PHST- 2019/11/13 00:00 [received]
PHST- 2020/01/29 00:00 [revised]
PHST- 2020/02/01 00:00 [accepted]
PHST- 2020/02/13 06:00 [pubmed]
PHST- 2021/01/07 06:00 [medline]
PHST- 2020/02/13 06:00 [entrez]
AID - S1567-5769(19)32589-5 [pii]
AID - 10.1016/j.intimp.2020.106278 [doi]
PST - ppublish
SO  - Int Immunopharmacol. 2020 Apr;81:106278. doi: 10.1016/j.intimp.2020.106278. Epub 
      2020 Feb 9.