PMID- 34192661
OWN - NLM
STAT- MEDLINE
DCOM- 20220117
LR  - 20220117
IS  - 1878-1705 (Electronic)
IS  - 1567-5769 (Linking)
VI  - 98
DP  - 2021 Sep
TI  - Blocking HOTAIR protects human chondrocytes against IL-1beta-induced cell apoptosis, 
      ECM degradation, inflammatory response and oxidative stress via regulating 
      miR-222-3p/ADAM10 axis.
PG  - 107903
LID - S1567-5769(21)00539-7 [pii]
LID - 10.1016/j.intimp.2021.107903 [doi]
AB  - BACKGROUND: Long non-coding RNA (lncRNA) HOX transcript antisense RNA (HOTAIR) 
      contributes to cartilage damages including osteoarthritis (OA). While, its role 
      and mechanism in chondrocytes is incompletely clear. METHODS: HOTAIR, microRNA 
      (miR)-222-3p and ADAM metalloproteinase-like domain 10 (ADAM10) expressions were 
      detected by real-time quantitative PCR and western blotting. The interaction 
      between miR-222-3p and HOTAIR or ADAM10 was confirmed by dual-luciferase reporter 
      assay. Cell injury was measured by MTS method, flow cytometry, western blotting, 
      enzyme-linked immunosorbent assay for collagen Type II, type X, sex determining 
      region Y-box 9 (SOX9), matrix metalloproteinase (MMP)-13, interleukin (IL)-6, 
      IL-10, and tumor necrosis factor (TNF)-alpha, and special assay kits for 
      malondialdehyde (MDA), reactive oxygen species (ROS) and superoxide dismutase 
      (SOD). RESULTS: HOTAIR was highly expressed in human OA cartilages and 
      IL-1beta-induced OA model in immortalized chondrocytes (C-28/I2). Under IL-1beta 
      stress, blocking HOTAIR was responsible to high mitochondrial activity and low 
      early apoptosis rate, accompanied with increased B cell lymphoma (Bcl)-2 and 
      LC3B-II/I proteins, boosted IL-10 and SOD productions, suppressed cleaved 
      caspase-3 and p62 proteins, and decreased MDA and ROS levels, as well as elevated 
      secretions of Type II collagen, Type X collagen, SOX9, MMP-13, IL-6, and TNF-alpha. 
      Moreover, miR-222-3p was a target of HOTAIR, and its overexpression and knockdown 
      could suppress and aggravate IL-1beta-induced chondrocytes injury. Furthermore, 
      restoring ADAM10, a target gene of miR-222-3p, counteracted the protective role 
      of miR-222-3p upregulation. CONCLUSION: HOTAIR might contribute to IL-1beta-induced 
      chondrocytes death, inflammation, extracellular matrix degradation, and oxidative 
      stress in OA via miR-222-3p/ADAM10 axis.
CI  - Copyright (c) 2021 Elsevier B.V. All rights reserved.
FAU - Wang, Jinliang
AU  - Wang J
AD  - Department of Joint Disease, Zhengzhou Orthopaedic Hospital, Zhengzhou, China.
FAU - Luo, Xiaofei
AU  - Luo X
AD  - Department of Joint Disease, Zhengzhou Orthopaedic Hospital, Zhengzhou, China.
FAU - Cai, Songtao
AU  - Cai S
AD  - Department of Joint Disease, Zhengzhou Orthopaedic Hospital, Zhengzhou, China.
FAU - Sun, Jingtao
AU  - Sun J
AD  - Department of Joint Disease, Zhengzhou Orthopaedic Hospital, Zhengzhou, China.
FAU - Wang, Shaohua
AU  - Wang S
AD  - Department of Joint Disease, Zhengzhou Orthopaedic Hospital, Zhengzhou, China.
FAU - Wei, Xuan
AU  - Wei X
AD  - Department of Joint Disease, Zhengzhou Orthopaedic Hospital, Zhengzhou, China. 
      Electronic address: jiajiawaers@126.com.
LA  - eng
PT  - Journal Article
DEP - 20210627
PL  - Netherlands
TA  - Int Immunopharmacol
JT  - International immunopharmacology
JID - 100965259
RN  - 0 (HOTAIR long untranslated RNA, human)
RN  - 0 (IL1B protein, human)
RN  - 0 (Interleukin-1beta)
RN  - 0 (MIRN222 microRNA, human)
RN  - 0 (Membrane Proteins)
RN  - 0 (MicroRNAs)
RN  - 0 (RNA, Long Noncoding)
RN  - 0 (Recombinant Proteins)
RN  - EC 3.4.- (Amyloid Precursor Protein Secretases)
RN  - EC 3.4.24.81 (ADAM10 Protein)
RN  - EC 3.4.24.81 (ADAM10 protein, human)
SB  - IM
MH  - ADAM10 Protein/*genetics
MH  - Amyloid Precursor Protein Secretases/*genetics
MH  - Apoptosis/genetics/immunology
MH  - Cell Line
MH  - Chondrocytes/immunology/metabolism/pathology
MH  - Cohort Studies
MH  - Extracellular Matrix/pathology
MH  - Gene Expression Regulation/immunology
MH  - Humans
MH  - Inflammation/genetics/immunology/pathology
MH  - Interleukin-1beta/metabolism
MH  - Membrane Proteins/*genetics
MH  - MicroRNAs/*metabolism
MH  - Osteoarthritis, Knee/genetics/*immunology/pathology
MH  - Oxidative Stress/genetics/immunology
MH  - RNA, Long Noncoding/antagonists & inhibitors/genetics/*metabolism
MH  - Recombinant Proteins/metabolism
MH  - Signal Transduction/genetics
OTO - NOTNLM
OT  - ADAM10
OT  - Chondrocytes
OT  - HOTAIR
OT  - Osteoarthritis
OT  - miR-222-3p
EDAT- 2021/07/01 06:00
MHDA- 2022/01/18 06:00
CRDT- 2021/06/30 20:25
PHST- 2021/02/20 00:00 [received]
PHST- 2021/06/16 00:00 [revised]
PHST- 2021/06/16 00:00 [accepted]
PHST- 2021/07/01 06:00 [pubmed]
PHST- 2022/01/18 06:00 [medline]
PHST- 2021/06/30 20:25 [entrez]
AID - S1567-5769(21)00539-7 [pii]
AID - 10.1016/j.intimp.2021.107903 [doi]
PST - ppublish
SO  - Int Immunopharmacol. 2021 Sep;98:107903. doi: 10.1016/j.intimp.2021.107903. Epub 
      2021 Jun 27.