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
- Ji Zhang
- Haoran Jiang
- Min Li
- Lixiang Ding
Affiliations: Department of Spine Surgery, Beijing Shijitan Hospital, Capital Medical University, Beijing 100089, P.R. China, Department of Clinical Medicine, Mudanjiang Medical University, Mudanjiang, Heilongjiang 157011, P.R. China
- Published online on: July 29, 2022 https://doi.org/10.3892/etm.2022.11544
Copyright: © Zhang
et al. This is an open access article distributed under the
terms of Creative
Commons Attribution License.
Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
This article is mentioned in:
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‑1β 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‑1β was found to elevate the level of TREM1 in NPCs. TREM1 knockdown reversed the observed effects of IL‑1β on cell viability, ECM degradation, inflammation, apoptosis of NPCs, ERS and TLR4/NF‑κB signaling. Subsequently, the TLR4 and ERS agonists were found to reverse the effect of TREM1 knockdown on NPCs, indicating that the TLR4/NF‑κB 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‑κB signaling pathway, inhibited ERS and reduced the levels of ECM degradation and apoptosis of NPCs induced by IL‑1β.