PMID- 38254314
OWN - NLM
STAT- MEDLINE
DCOM- 20240212
LR  - 20240212
IS  - 1607-842X (Electronic)
IS  - 0891-6934 (Linking)
VI  - 57
IP  - 1
DP  - 2024 Dec
TI  - Circ_0011058 alleviates RA pathology through the circ_0011058/miR-335-5p/CUL4B 
      signal axis.
PG  - 2299587
LID - 10.1080/08916934.2023.2299587 [doi]
AB  - Our previous study found that Cullin 4B (CUL4B) inhibited rheumatoid arthritis 
      (RA) pathology through glycogen synthase kinase-3beta (GSK3beta)/canonical Wnt 
      signalling pathway. In this work, pre-experiment and bioinformatics analysis 
      suggested that circ_0011058 may lead to the up-regulation of CUL4B expression by 
      inhibiting miR-335-5p. Therefore, we studied whether circ_0011058 can promote the 
      expression of CUL4B through sponging the miR-335-5p and further promote the 
      pathological development of RA. Bioinformatics prediction, real-time quantitative 
      PCR (RT-qPCR), western blot (WB), double luciferase reporter gene and other 
      relevant methods were used to study the inhibition of circ_0011058 on RA 
      pathology and its molecular mechanism. Results showed that the expression of 
      circ_0011058 was significantly increased in adjuvant arthritis (AA) rats and RA 
      fibroblast-like synoviocytes (FLS). The knockout of circ_0011058 inhibited the 
      proliferation of AA FLS and RA FLS, decreased the levels of interleukin-1 beta 
      (IL-1beta), interleukin 6 (IL-6), interleukin 8 (IL-8), and inhibited the expression 
      of matrix metalloproteinase 3 (MMP3), fibronectin, which showed that circ_0011058 
      had a strong role in promoting RA pathology. Furthermore, miR-335-5p expression 
      was reduced in AA rats and RA FLS. The highly expressed circ_0011058 directly 
      sponged the miR-335-5p, which led to the increase of CUL4B expression and 
      promoted the activation of the GSK3beta/canonical signalling pathway. Finally, we 
      confirmed that miR-335-5p mediated the roles of circ_0011058 in promoting RA 
      pathological development, which showed that the circ_0011058/miR-335-5p/CUL4B 
      signal axis was involved in RA pathology. This work was of great significance for 
      clarifying the roles of circ_0011058 in RA pathology, and further work was needed 
      to establish whether circ_0011058 was a potential therapeutic target or 
      diagnostic marker for RA.
FAU - Wang, Xiaomei
AU  - Wang X
AD  - Department of Humanistic Nursing, School of Nursing, Anhui University of Chinese 
      Medicine, Hefei, China.
FAU - Xue, Qiuyun
AU  - Xue Q
AD  - Department of Pharmacology, School of Integrated Chinese and Western Medicine, 
      Anhui University of Chinese Medicine, Hefei, China.
FAU - Duan, Qiangjun
AU  - Duan Q
AD  - Department of Experimental Teaching Center, School of Integrated Chinese and 
      Western Medicine, Anhui University of Chinese Medicine, Hefei, China.
FAU - Sun, Ziyi
AU  - Sun Z
AD  - Department of Scientific Research Technology Center, Anhui University of Chinese 
      Medicine, Hefei, China.
FAU - Wu, Yajie
AU  - Wu Y
AD  - Department of Pharmacology, School of Integrated Chinese and Western Medicine, 
      Anhui University of Chinese Medicine, Hefei, China.
FAU - Yang, Shuo
AU  - Yang S
AD  - Department of Orthopaedics, the First Affiliated Hospital of Anhui Medical 
      University, Hefei, China.
AD  - Anhui Public Health Clinical Center, Hefei, China.
FAU - Xu, Pengfei
AU  - Xu P
AD  - Department of Orthopaedics, the First Affiliated Hospital of Anhui Medical 
      University, Hefei, China.
AD  - Anhui Public Health Clinical Center, Hefei, China.
FAU - Cao, Huibo
AU  - Cao H
AD  - Chuzhou Integrated Traditional Chinese and Western Medicine Hospital, Anhui 
      University of Chinese Medicine, Chuzhou, China.
FAU - Liao, Faxue
AU  - Liao F
AD  - Department of Orthopaedics, the First Affiliated Hospital of Anhui Medical 
      University, Hefei, China.
AD  - Anhui Public Health Clinical Center, Hefei, China.
FAU - Wang, Xiao
AU  - Wang X
AD  - Department of Clinical Nursing, School of Nursing, Anhui University of Chinese 
      Medicine, Hefei, China.
FAU - Miao, Chenggui
AU  - Miao C
AD  - Department of Pharmacology, School of Integrated Chinese and Western Medicine, 
      Anhui University of Chinese Medicine, Hefei, China.
AD  - Institute of Rheumatism, Anhui University of Chinese Medicine, Hefei, China.
LA  - eng
PT  - Journal Article
DEP - 20240122
PL  - England
TA  - Autoimmunity
JT  - Autoimmunity
JID - 8900070
RN  - EC 2.7.11.1 (Glycogen Synthase Kinase 3 beta)
RN  - 0 (Interleukin-6)
RN  - 0 (RNA, Circular)
RN  - 0 (MIRN335 microRNA, human)
RN  - 0 (CUL4B protein, human)
RN  - 0 (Cullin Proteins)
RN  - 0 (MicroRNAs)
SB  - IM
MH  - Animals
MH  - Rats
MH  - *Arthritis, Experimental
MH  - *Arthritis, Rheumatoid/genetics
MH  - Computational Biology
MH  - Fibroblasts
MH  - Glycogen Synthase Kinase 3 beta/genetics
MH  - Interleukin-6
MH  - *RNA, Circular/genetics/metabolism
MH  - *Cullin Proteins
MH  - Humans
MH  - *MicroRNAs/genetics/metabolism
OTO - NOTNLM
OT  - CUL4B
OT  - Rheumatoid arthritis
OT  - canonical wnt signalling pathway
OT  - circ_0011058
OT  - miR-335-5p
EDAT- 2024/01/23 06:43
MHDA- 2024/01/24 06:43
CRDT- 2024/01/23 00:33
PHST- 2024/01/24 06:43 [medline]
PHST- 2024/01/23 06:43 [pubmed]
PHST- 2024/01/23 00:33 [entrez]
AID - 10.1080/08916934.2023.2299587 [doi]
PST - ppublish
SO  - Autoimmunity. 2024 Dec;57(1):2299587. doi: 10.1080/08916934.2023.2299587. Epub 
      2024 Jan 22.