PMID- 35942891
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220914
IS  - 2046-3758 (Print)
IS  - 2046-3758 (Electronic)
IS  - 2046-3758 (Linking)
VI  - 11
IP  - 8
DP  - 2022 Aug
TI  - Long noncoding RNA H19 alleviates inflammation in osteoarthritis through 
      interactions between TP53, IL-38, and IL-36 receptor.
PG  - 594-607
LID - 10.1302/2046-3758.118.BJR-2021-0188.R1 [doi]
AB  - AIMS: Osteoarthritis (OA) is a common degenerative joint disease characterized by 
      chronic inflammatory articular cartilage degradation. Long noncoding RNAs 
      (lncRNAs) have been previously indicated to play an important role in 
      inflammation-related diseases. Herein, the current study set out to explore the 
      involvement of lncRNA H19 in OA. METHODS: Firstly, OA mouse models and 
      interleukin (IL)-1beta-induced mouse chondrocytes were established. Expression 
      patterns of IL-38 were determined in the synovial fluid and cartilage tissues 
      from OA patients. Furthermore, the targeting relationship between lncRNA H19, 
      tumour protein p53 (TP53), and IL-38 was determined by means of dual-luciferase 
      reporter gene, chromatin immunoprecipitation, and RNA immunoprecipitation assays. 
      Subsequent to gain- and loss-of-function assays, the levels of cartilage damage 
      and proinflammatory factors were further detected using safranin O-fast green 
      staining and enzyme-linked immunosorbent assay (ELISA) in vivo, respectively, 
      while chondrocyte apoptosis was measured using Terminal deoxynucleotidyl 
      transferase dUTP Nick-End Labeling (TUNEL) in vitro. RESULTS: IL-38 was highly 
      expressed in lentivirus vector-mediated OA mice. Meanwhile, injection of 
      exogenous IL-38 to OA mice alleviated the cartilage damage, and reduced the 
      levels of proinflammatory factors and chondrocyte apoptosis. TP53 was responsible 
      for lncRNA H19-mediated upregulation of IL-38. Furthermore, it was found that the 
      anti-inflammatory effects of IL-38 were achieved by its binding with the IL-36 
      receptor (IL-36R). Overexpression of H19 reduced the expression of inflammatory 
      factors and chondrocyte apoptosis, which was abrogated by knockdown of IL-38 or 
      TP53. CONCLUSION: Collectively, our findings evidenced that upregulation of 
      lncRNA H19 attenuates inflammation and ameliorates cartilage damage and 
      chondrocyte apoptosis in OA by upregulating TP53, IL-38, and by activating 
      IL-36R.Cite this article: Bone Joint Res 2022;11(8):594-607.
FAU - Zhou, Yeli
AU  - Zhou Y
AD  - Department of Orthopedics, The First Affiliated Hospital of Wenzhou Medical 
      University, Wenzhou, China.
FAU - Li, Jing
AU  - Li J
AD  - Department of Orthopedics, The First Affiliated Hospital of Wenzhou Medical 
      University, Wenzhou, China.
FAU - Xu, Feng
AU  - Xu F
AD  - Surgical Department, Wuhan Pulmonary Hospital, Wuhan, China.
FAU - Ji, Encheng
AU  - Ji E
AD  - Department of Orthopedics, The Second Affiliated Hospital of Wenzhou Medical 
      University, Wenzhou, China.
FAU - Wang, Chenglong
AU  - Wang C
AD  - Department of Orthopedics, The First Affiliated Hospital of Wenzhou Medical 
      University, Wenzhou, China.
FAU - Pan, Zheer
AU  - Pan Z
AUID- ORCID: 0000-0003-1279-9609
AD  - Department of Orthopedics, The First Affiliated Hospital of Wenzhou Medical 
      University, Wenzhou, China.
LA  - eng
PT  - Journal Article
PL  - England
TA  - Bone Joint Res
JT  - Bone & joint research
JID - 101586057
PMC - PMC9396924
OTO - NOTNLM
OT  - Inflammatory response
OT  - Interleukin-36 receptor
OT  - Interleukin-38
OT  - Long noncoding RNA H19
OT  - Osteoarthritis
OT  - Tumour protein p53
EDAT- 2022/08/10 06:00
MHDA- 2022/08/10 06:01
PMCR- 2022/08/17
CRDT- 2022/08/09 05:13
PHST- 2022/08/09 05:13 [entrez]
PHST- 2022/08/10 06:00 [pubmed]
PHST- 2022/08/10 06:01 [medline]
PHST- 2022/08/17 00:00 [pmc-release]
AID - BJR-11-594 [pii]
AID - 10.1302/2046-3758.118.BJR-2021-0188.R1 [doi]
PST - ppublish
SO  - Bone Joint Res. 2022 Aug;11(8):594-607. doi: 
      10.1302/2046-3758.118.BJR-2021-0188.R1.