PMID- 36278814
OWN - NLM
STAT- MEDLINE
DCOM- 20221221
LR  - 20221221
IS  - 2410-8650 (Electronic)
IS  - 1607-551X (Linking)
VI  - 38
IP  - 12
DP  - 2022 Dec
TI  - circRNA-MSR regulates the expression of FBXO21 to inhibit chondrocyte autophagy 
      by targeting miR-761 in osteoarthritis.
PG  - 1168-1177
LID - 10.1002/kjm2.12604 [doi]
AB  - Osteoarthritis (OA) is a chronic degenerative joint disease and is the most 
      prevalent and disabling form of arthritis worldwide. Autophagy plays a vital role 
      in OA. This study aimed to explore whether covalently closed circular RNA MSR 
      (circRNA-MSR) could affect the F-box Only Protein 21 (FBXO21) expression by 
      targeting microRNA-761 (miR-761), thereby affecting the autophagy in OA 
      chondrocytes. Clinical OA tissues were collected, and circRNA-MSR, miR-761, and 
      FBXO21 expressions were detected via quantitative real-time polymerase chain 
      reaction (qRT-PCR). An in vitro OA model was constructed by treating C28/I2 cells 
      with LPS and treating them with overexpression or knockdown vector of 
      circRNA-MSR, miR-761, and FBXO21, and autophagy inhibitor 3-MA. Fluorescence in 
      situ hybridization (FISH) determined the location of circRNA-MSR and miR-761. 
      Dual-luciferase assay assessed circRNA-MSR and miR-761, along with the bindings 
      of miR-761 and FBXO21. Cell viability was detected by 
      3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. LC3 
      II/I, p62 and beclin 1 expressions were detected via the western blot. 
      circRNA-MSR and FBXO21 levels were elevated in OA, but miR-761 level was 
      inhibited. Suppressing circRNA-MSR promoted the autophagy of LPS-treated cells. 
      circRNA-MSR could bind to miR-761 and inhibit its expression. MiR-761 inhibition 
      reversed the promoted autophagy caused by circRNA-MSR knockdown in LPS-treated 
      C28/I2 cells. Moreover, miR-761 could target FBXO21 and inhibit its expression. 
      FBXO21 overexpression reversed the increased autophagy caused by miR-761 
      overexpression in LPS-treated C28/I2 cells. circRNA-MSR could affect FBXO21 level 
      via targeting miR-761, thereby repressing autophagy in OA chondrocytes, providing 
      a new target and strategy for OA treatment.
CI  - (c) 2022 The Authors. The Kaohsiung Journal of Medical Sciences published by John 
      Wiley & Sons Australia, Ltd on behalf of Kaohsiung Medical University.
FAU - Jia, Zhen
AU  - Jia Z
AD  - Joint Surgery and Sport Medicine Department, Hunan Provincial People's Hospital 
      (The First Affiliated Hospital of Hunan Normal University), Changsha, Hunan 
      Province, People's Republic of China.
FAU - Liu, Jia
AU  - Liu J
AD  - Joint Surgery and Sport Medicine Department, Hunan Provincial People's Hospital 
      (The First Affiliated Hospital of Hunan Normal University), Changsha, Hunan 
      Province, People's Republic of China.
FAU - Wang, Jing
AU  - Wang J
AUID- ORCID: 0000-0002-3458-9736
AD  - Joint Surgery and Sport Medicine Department, Hunan Provincial People's Hospital 
      (The First Affiliated Hospital of Hunan Normal University), Changsha, Hunan 
      Province, People's Republic of China.
LA  - eng
GR  - 20200519/Key Project from Health Commission of Hunan Province, China/
PT  - Journal Article
DEP - 20221024
PL  - China (Republic : 1949- )
TA  - Kaohsiung J Med Sci
JT  - The Kaohsiung journal of medical sciences
JID - 100960562
RN  - 0 (Lipopolysaccharides)
RN  - 0 (microRNA761 microRNA, human)
RN  - 0 (MicroRNAs)
RN  - 0 (RNA, Circular)
RN  - 0 (FBXO21 protein, human)
RN  - 0 (F-Box Proteins)
SB  - IM
MH  - Humans
MH  - Apoptosis/genetics
MH  - Autophagy/genetics
MH  - Chondrocytes/metabolism
MH  - In Situ Hybridization, Fluorescence
MH  - Lipopolysaccharides
MH  - *MicroRNAs/genetics
MH  - *Osteoarthritis/genetics/drug therapy/metabolism
MH  - RNA, Circular/genetics
MH  - *F-Box Proteins/genetics
OTO - NOTNLM
OT  - FBXO21
OT  - autophagy
OT  - circRNA-MSR
OT  - miR-761
OT  - osteoarthritis
EDAT- 2022/10/25 06:00
MHDA- 2022/12/16 06:00
CRDT- 2022/10/24 07:42
PHST- 2022/08/22 00:00 [revised]
PHST- 2022/06/07 00:00 [received]
PHST- 2022/09/06 00:00 [accepted]
PHST- 2022/10/25 06:00 [pubmed]
PHST- 2022/12/16 06:00 [medline]
PHST- 2022/10/24 07:42 [entrez]
AID - 10.1002/kjm2.12604 [doi]
PST - ppublish
SO  - Kaohsiung J Med Sci. 2022 Dec;38(12):1168-1177. doi: 10.1002/kjm2.12604. Epub 
      2022 Oct 24.