PMID- 37424166
OWN - NLM
STAT- MEDLINE
DCOM- 20230804
LR  - 20230804
IS  - 1756-185X (Electronic)
IS  - 1756-1841 (Linking)
VI  - 26
IP  - 8
DP  - 2023 Aug
TI  - The study of the effect of HLA-B27 on THP-1 monocytic cells survival and its 
      mechanism.
PG  - 1474-1484
LID - 10.1111/1756-185X.14758 [doi]
AB  - OBJECTIVE: Previous studies have shown that human leukocyte antigen (HLA)-B27 
      induces the accumulation of unfolded proteins in the endoplasmic reticulum (ER) 
      to cause ER stress, resulting in the unfold protein response (UPR), apoptosis and 
      autophagy. However, it is still unknown whether it affects the survival of 
      monocytes. In this study, we attempted to examine the effect of HLA-B27 gene 
      knockout on the proliferation and apoptosis of THP-1 monocytic cell line and its 
      potential mechanism. METHODS: HLA-B27 gene knockout THP-1 cell line was 
      constructed by lentivirus infection, and knockout efficiency was detected by 
      immunofluorescence, quantitative reverse transcription - polymerase chain 
      reaction (qRT-PCR) and western blot. Cell Counting Kit-8 (CCK-8) method and 
      Annexin-V/PI double staining were used to detect the proliferation and apoptosis 
      of the constructed THP-1 cell line, respectively. qRT-PCR was used to detect the 
      effect of HLA-B27 inhibition on the expressions of ER molecular chaperone binding 
      immunoglobulin protein (BiP) and genes about the UPR pathway. The proliferation 
      rate of human BiP protein-stimulated THP-1 cells was detected by CCK-8 method. 
      RESULTS: HLA-B27 gene knockout THP-1 cells were successfully constructed by 
      lentivirus infection. Knockout of HLA-B27 effectively promoted the proliferation 
      of THP-1 cells and inhibited the apoptosis induced by cisplatin. qRT-PCR showed 
      that BiP was synchronously increased, while activation of UPR pathway was 
      inhibited. Stimulation with human BiP promoted the proliferation of THP-1 cells 
      in a concentration-dependent manner. CONCLUSIONS: HLA-B27 inhibition can promote 
      the proliferation and inhibit the apoptosis of THP-1 cells. The inhibition 
      function may be achieved through promotion of BiP and inhibition of UPR pathway 
      activation.
CI  - (c) 2023 The Authors. International Journal of Rheumatic Diseases published by Asia 
      Pacific League of Associations for Rheumatology and John Wiley & Sons Australia, 
      Ltd.
FAU - Gui, Lian
AU  - Gui L
AUID- ORCID: 0000-0002-6750-142X
AD  - Department of Rheumatology, The Third Affiliated Hospital of Sun Yat-sen 
      University, Guangzhou, China.
FAU - Gu, Jieruo
AU  - Gu J
AD  - Department of Rheumatology, The Third Affiliated Hospital of Sun Yat-sen 
      University, Guangzhou, China.
LA  - eng
GR  - Guangdong Clinical Research Center of Immune Disease (2020B1111170008)/
PT  - Journal Article
DEP - 20230709
PL  - England
TA  - Int J Rheum Dis
JT  - International journal of rheumatic diseases
JID - 101474930
RN  - 0 (HLA-B27 Antigen)
SB  - IM
MH  - Humans
MH  - *HLA-B27 Antigen/genetics
MH  - *Monocytes
MH  - *Spondylitis, Ankylosing
MH  - THP-1 Cells
OTO - NOTNLM
OT  - HLA-B*27:04
OT  - THP-1 cells
OT  - UPR
OT  - ankylosing spondylitis
OT  - cell proliferation
EDAT- 2023/07/10 06:42
MHDA- 2023/08/02 06:42
CRDT- 2023/07/10 02:01
PHST- 2023/05/11 00:00 [revised]
PHST- 2023/05/01 00:00 [received]
PHST- 2023/05/17 00:00 [accepted]
PHST- 2023/08/02 06:42 [medline]
PHST- 2023/07/10 06:42 [pubmed]
PHST- 2023/07/10 02:01 [entrez]
AID - 10.1111/1756-185X.14758 [doi]
PST - ppublish
SO  - Int J Rheum Dis. 2023 Aug;26(8):1474-1484. doi: 10.1111/1756-185X.14758. Epub 
      2023 Jul 9.