PMID- 34183035
OWN - NLM
STAT- MEDLINE
DCOM- 20211027
LR  - 20211027
IS  - 1749-799X (Electronic)
IS  - 1749-799X (Linking)
VI  - 16
IP  - 1
DP  - 2021 Jun 28
TI  - Knockdown of long noncoding RNA HOTAIR inhibits osteoarthritis chondrocyte injury 
      by miR-107/CXCL12 axis.
PG  - 410
LID - 10.1186/s13018-021-02547-7 [doi]
LID - 410
AB  - BACKGROUND: Osteoarthritis (OA) is a joint disease characterized via destruction 
      of cartilage. Chondrocyte damage is associated with cartilage destruction during 
      OA. Long noncoding RNAs (lncRNAs) are implicated in the regulation of chondrocyte 
      damage in OA progression. This study aims to investigate the role and underlying 
      mechanism of lncRNA homeobox antisense intergenic RNA (HOTAIR) in OA chondrocyte 
      injury. METHODS: Twenty-three OA patients and healthy controls without OA were 
      recruited. Chondrocytes were isolated from OA cartilage tissues. HOTAIR, 
      microRNA-107 (miR-107) and C-X-C motif chemokine ligand 12 (CXCL12) levels were 
      measured by quantitative real-time polymerase chain reaction and western blot. 
      Cell proliferation, apoptosis and extracellular matrix (ECM) degradation were 
      measured using cell counting kit-8, flow cytometry and western blot. The target 
      interaction was explored by bioinformatics, luciferase reporter and RNA 
      immunoprecipitation assays. RESULTS: HOTAIR expression was enhanced, and miR-107 
      level was reduced in OA cartilage samples. HOTAIR overexpression inhibited cell 
      proliferation, but induced cell apoptosis and ECM degradation in chondrocytes. 
      HOTAIR knockdown caused an opposite effect. MiR-107 was sponged and inhibited via 
      HOTAIR, and knockdown of miR-107 mitigated the effect of HOTAIR silence on 
      chondrocyte injury. CXCL12 was targeted by miR-107. CXCL12 overexpression 
      attenuated the roles of miR-107 overexpression or HOTAIR knockdown in the 
      proliferation, apoptosis and ECM degradation. CXCL12 expression was decreased by 
      HOTAIR silence, and restored by knockdown of miR-107. CONCLUSION: HOTAIR 
      knockdown promoted chondrocyte proliferation, but inhibited cell apoptosis and 
      ECM degradation in OA chondrocytes by regulating the miR-107/CXCL12 axis.
FAU - Lu, Jipeng
AU  - Lu J
AD  - Department of Orthopedics, Yan'an Hospital Affiliated to Kunming Medical 
      University, No. 245 Renmin East Road, Panlong District, Kunming, 650051, Yunnan, 
      China.
FAU - Wu, Zhongxiong
AU  - Wu Z
AD  - Department of Orthopedics, Yan'an Hospital Affiliated to Kunming Medical 
      University, No. 245 Renmin East Road, Panlong District, Kunming, 650051, Yunnan, 
      China. spring_beginning@163.com.
FAU - Xiong, Ying
AU  - Xiong Y
AD  - Department of Orthopedics, Yan'an Hospital Affiliated to Kunming Medical 
      University, No. 245 Renmin East Road, Panlong District, Kunming, 650051, Yunnan, 
      China.
LA  - eng
PT  - Journal Article
DEP - 20210628
PL  - England
TA  - J Orthop Surg Res
JT  - Journal of orthopaedic surgery and research
JID - 101265112
RN  - 0 (CXCL12 protein, human)
RN  - 0 (Chemokine CXCL12)
RN  - 0 (MIRN107 microRNA, human)
RN  - 0 (MicroRNAs)
RN  - 0 (RNA, Long Noncoding)
SB  - IM
MH  - Apoptosis/genetics
MH  - Cartilage, Articular/cytology
MH  - Case-Control Studies
MH  - Cell Proliferation/genetics
MH  - Cells, Cultured
MH  - Chemokine CXCL12/*genetics
MH  - Chondrocytes/*metabolism
MH  - Extracellular Matrix/genetics
MH  - Female
MH  - Gene Knockdown Techniques
MH  - Genes, Homeobox/*genetics
MH  - Humans
MH  - Male
MH  - MicroRNAs/*genetics
MH  - Middle Aged
MH  - Osteoarthritis/*genetics
MH  - RNA, Long Noncoding/*genetics
MH  - Signal Transduction/genetics
PMC - PMC8237457
OTO - NOTNLM
OT  - CXCL12
OT  - Chondrocyte
OT  - HOTAIR
OT  - Osteoarthritis
OT  - miR-107
COIS- The authors declare that they have no competing interests.
EDAT- 2021/06/30 06:00
MHDA- 2021/10/28 06:00
PMCR- 2021/06/28
CRDT- 2021/06/29 05:41
PHST- 2021/03/16 00:00 [received]
PHST- 2021/06/08 00:00 [accepted]
PHST- 2021/06/29 05:41 [entrez]
PHST- 2021/06/30 06:00 [pubmed]
PHST- 2021/10/28 06:00 [medline]
PHST- 2021/06/28 00:00 [pmc-release]
AID - 10.1186/s13018-021-02547-7 [pii]
AID - 2547 [pii]
AID - 10.1186/s13018-021-02547-7 [doi]
PST - epublish
SO  - J Orthop Surg Res. 2021 Jun 28;16(1):410. doi: 10.1186/s13018-021-02547-7.