PMID- 28732288
OWN - NLM
STAT- MEDLINE
DCOM- 20180221
LR  - 20220614
IS  - 1878-1705 (Electronic)
IS  - 1567-5769 (Linking)
VI  - 50
DP  - 2017 Sep
TI  - LncRNA HOTAIR alleviates rheumatoid arthritis by targeting miR-138 and 
      inactivating NF-kappaB pathway.
PG  - 283-290
LID - S1567-5769(17)30243-6 [pii]
LID - 10.1016/j.intimp.2017.06.021 [doi]
AB  - Rheumatoid arthritis (RA) is a chronic and autoimmune-mediated inflammatory 
      disease. We aimed to investigate the regulation of lncRNA HOTAIR in LPS-treated 
      chondrocytes and RA mouse. Our results showed that HOTAIR expression was 
      significantly reduced in LPS-treated chondrocytes. The HOTAIR was then 
      over-expressed in chondrocytes by transfecting recombinant lentivirus carrying 
      sequences encoding HOTAIR. The LPS-induced reduction of cell proliferation rate 
      and production of two inflammatory factors interleukin (IL)-17, IL-23 were 
      markedly inhibited. Enforced expression of HOTAIR also led to the upregulation of 
      proliferation-related protein Ki67 and proliferating cell nuclear antigen (PCNA). 
      Moreover, a negative correlation was detected between the expression of HOTAIR 
      and microRNA (miR)-138, and the expression of miR-138 was significantly increased 
      in LPS-induced chondrocytes. The effects of HOTAIR over-expression on the 
      proliferation and inflammation were partly reversed by miR-138 overexpression. 
      Furthermore, the overexpression of HOTAIR significantly inhibited the activation 
      of nuclear transcription factor-kappaB (NF-kappaB) in LPS-treated chondrocytes by 
      suppressing p65 to cell nucleus, resulting in the down-regulation of IL-1beta and 
      tumor necrosis factor (TNF)-alpha. In addition, the in vivo experiments exhibited 
      that overexpression of HOTAIR increased cell proliferation and inhibited 
      inflammation in RA rats, which were demonstrated by upregulation of Ki67 and 
      PCNA, reduced CD4(+)IL-17(+),CD4(+)IL-23(+) cells, and down-regulation of p-p65, 
      IL-1beta and TNF-alpha. In summary, our study suggests HOTAIR plays a protective role in 
      RA by increasing proliferation rate and inhibiting inflammation, which may be 
      related with the regulation of miR-138 expression and NF-kappaB signaling pathway. 
      These results suggest that the regulation of HOTAIR may be a promising 
      therapeutic strategy for RA.
CI  - Copyright (c) 2017. Published by Elsevier B.V.
FAU - Zhang, Hong-Ju
AU  - Zhang HJ
AD  - Department of Rheumatology, ZiBo Central Hospital, Zibo 255036, Shandong 
      Province, PR China.
FAU - Wei, Qiao-Feng
AU  - Wei QF
AD  - Department of Rheumatology, ZiBo Central Hospital, Zibo 255036, Shandong 
      Province, PR China.
FAU - Wang, Shu-Jun
AU  - Wang SJ
AD  - Department of Rheumatology, ZiBo Central Hospital, Zibo 255036, Shandong 
      Province, PR China.
FAU - Zhang, Hong-Jie
AU  - Zhang HJ
AD  - The Disease Prevention and Control Center of Zibo, Zibo 255000, Shandong 
      Province, PR China.
FAU - Zhang, Xiu-Ying
AU  - Zhang XY
AD  - Department of Rheumatology, ZiBo Central Hospital, Zibo 255036, Shandong 
      Province, PR China.
FAU - Geng, Qin
AU  - Geng Q
AD  - Department of Rheumatology, ZiBo Central Hospital, Zibo 255036, Shandong 
      Province, PR China.
FAU - Cui, Yan-Hui
AU  - Cui YH
AD  - Department of Rheumatology, ZiBo Central Hospital, Zibo 255036, Shandong 
      Province, PR China.
FAU - Wang, Xiu-Hua
AU  - Wang XH
AD  - Department of Rheumatology, The Qianfoshan Hospital Affiliated to Shandong 
      University, Jinan 250014, Shandong Province, PR China. Electronic address: 
      xiuhuawangxhw@sina.com.
LA  - eng
PT  - Journal Article
PT  - Retracted Publication
DEP - 20170718
PL  - Netherlands
TA  - Int Immunopharmacol
JT  - International immunopharmacology
JID - 100965259
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Cytokines)
RN  - 0 (MIRN138 microRNA, rat)
RN  - 0 (MicroRNAs)
RN  - 0 (NF-kappa B)
RN  - 0 (RNA, Long Noncoding)
SB  - IM
RIN - Int Immunopharmacol. 2021 Jun;95:107500. PMID: 33674214
MH  - Animals
MH  - Anti-Inflammatory Agents/chemistry/*metabolism
MH  - Arthritis, Rheumatoid/genetics/*therapy
MH  - Cell Proliferation
MH  - Cells, Cultured
MH  - Chondrocytes/*physiology
MH  - Cytokines/metabolism
MH  - Gene Expression Regulation
MH  - Inflammation/genetics/*therapy
MH  - Male
MH  - MicroRNAs/*genetics
MH  - NF-kappa B/metabolism
MH  - RNA, Long Noncoding/*genetics
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Signal Transduction
OTO - NOTNLM
OT  - HOTAIR
OT  - Inflammation
OT  - NF-kappaB signaling pathway
OT  - Proliferation
OT  - Rheumatoid arthritis
OT  - miR-138
EDAT- 2017/07/22 06:00
MHDA- 2018/02/22 06:00
CRDT- 2017/07/22 06:00
PHST- 2017/02/15 00:00 [received]
PHST- 2017/05/31 00:00 [revised]
PHST- 2017/06/20 00:00 [accepted]
PHST- 2017/07/22 06:00 [pubmed]
PHST- 2018/02/22 06:00 [medline]
PHST- 2017/07/22 06:00 [entrez]
AID - S1567-5769(17)30243-6 [pii]
AID - 10.1016/j.intimp.2017.06.021 [doi]
PST - ppublish
SO  - Int Immunopharmacol. 2017 Sep;50:283-290. doi: 10.1016/j.intimp.2017.06.021. Epub 
      2017 Jul 18.