PMID- 36160910
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220928
IS  - 1792-1015 (Electronic)
IS  - 1792-0981 (Print)
IS  - 1792-0981 (Linking)
VI  - 24
IP  - 4
DP  - 2022 Oct
TI  - Knockdown of triggering receptor expressed on myeloid cells 1 (TREM1) inhibits 
      endoplasmic reticulum stress and reduces extracellular matrix degradation and the 
      apoptosis of human nucleus pulposus cells.
PG  - 607
LID - 10.3892/etm.2022.11544 [doi]
LID - 607
AB  - According to the linear model of microarray data analysis, triggering receptor 
      expressed on myeloid cells 1 (TREM1) has been shown to have a significantly 
      different expression profile between intervertebral disc degeneration (IDD) 
      samples and associated control samples. The purpose of the present study was to 
      explore the probable role and underlying mechanism of TREM1 in IDD. To accomplish 
      this, an in vitro model of IDD was established by using IL-1beta to stimulate human 
      nucleus pulposus cells (NPCs). After the level of TREM1 had been determined, its 
      functions in terms of the viability of the NPCs, extracellular matrix (ECM) 
      degradation, inflammation, apoptosis and endoplasmic reticulum stress (ERS) were 
      assessed. The downstream target of TREM1 was predicted to be Toll-like receptor-4 
      (TLR-4) and its roles were then studied, incorporating experiments featuring an 
      ERS agonist. IL-1beta was found to elevate the level of TREM1 in NPCs. TREM1 
      knockdown reversed the observed effects of IL-1beta on cell viability, ECM 
      degradation, inflammation, apoptosis of NPCs, ERS and TLR4/NF-kappaB signaling. 
      Subsequently, the TLR4 and ERS agonists were found to reverse the effect of TREM1 
      knockdown on NPCs, indicating that the TLR4/NF-kappaB signaling pathway and ERS were 
      responsible for mediating the regulation of TREM1. In conclusion, the present 
      study showed that TREM1 knockdown blocked the TLR4/NF-kappaB signaling pathway, 
      inhibited ERS and reduced the levels of ECM degradation and apoptosis of NPCs 
      induced by IL-1beta.
CI  - Copyright: (c) Zhang et al.
FAU - Zhang, Ji
AU  - Zhang J
AD  - Department of Spine Surgery, Beijing Shijitan Hospital, Capital Medical 
      University, Beijing 100089, P.R. China.
FAU - Jiang, Haoran
AU  - Jiang H
AD  - Department of Spine Surgery, Beijing Shijitan Hospital, Capital Medical 
      University, Beijing 100089, P.R. China.
FAU - Li, Min
AU  - Li M
AD  - Department of Clinical Medicine, Mudanjiang Medical University, Mudanjiang, 
      Heilongjiang 157011, P.R. China.
FAU - Ding, Lixiang
AU  - Ding L
AD  - Department of Spine Surgery, Beijing Shijitan Hospital, Capital Medical 
      University, Beijing 100089, P.R. China.
LA  - eng
PT  - Journal Article
DEP - 20220729
PL  - Greece
TA  - Exp Ther Med
JT  - Experimental and therapeutic medicine
JID - 101531947
PMC - PMC9468837
OTO - NOTNLM
OT  - Toll-like receptor 4
OT  - endoplasmic reticulum stress
OT  - human nucleus pulposus cells
OT  - intervertebral disc degeneration
OT  - triggering receptor expressed on myeloid cells 1
COIS- The authors declare that they have no competing interests.
EDAT- 2022/09/27 06:00
MHDA- 2022/09/27 06:01
PMCR- 2022/07/29
CRDT- 2022/09/26 17:57
PHST- 2022/04/02 00:00 [received]
PHST- 2022/07/15 00:00 [accepted]
PHST- 2022/09/26 17:57 [entrez]
PHST- 2022/09/27 06:00 [pubmed]
PHST- 2022/09/27 06:01 [medline]
PHST- 2022/07/29 00:00 [pmc-release]
AID - ETM-24-4-11544 [pii]
AID - 10.3892/etm.2022.11544 [doi]
PST - epublish
SO  - Exp Ther Med. 2022 Jul 29;24(4):607. doi: 10.3892/etm.2022.11544. eCollection 
      2022 Oct.