TREM-2 negatively regulates LPS-mediated inflammatory response in rat bone marrow-derived MSCs
- Authors:
- Published online on: August 10, 2017 https://doi.org/10.3892/mmr.2017.7212
- Pages: 4777-4783
-
Copyright: © Ye et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
Metrics: Total
Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
Abstract
To the best of our knowledge, our previous study demonstrated the expression of triggering receptor expressed on myeloid cells 2 (TREM‑2) in human bone marrow mesenchymal stem cells (MSCs) for the first time. However, the inflammation regulatory role of TREM‑2 in MSCs remain elusive. The aim of the present study was to investigate the immune regulation and the underlying mechanism of TREM‑2 in rat bone marrow MSCs. MSCs were divided into three groups: NullMSCs, TREM‑2MSCs, and NormMSCs. TREM‑2 was expressed in MSCs at the mRNA and protein level. Following stimulation by lipopolysaccharide (LPS), the gene transcription levels of TREM‑2 and inflammatory cytokines were increased. The expression levels of inflammatory cytokines, including tumor necrosis factor‑α (TNF‑α) and interleukin‑1β (IL‑1β), in the TREM‑2MSCs lentiviral vector group were significantly downregulated, and the expression of IL‑10 was significantly upregulated compared with the controls. Western blot analysis revealed that TREM‑2 downregulated the LPS‑induced inflammatory response in MSCs, which was probably associated with regulating AKT serine/threonine kinase and p38 mitogen‑activated protein kinase downstream signaling proteins. The results of the current study demonstrated that TREM‑2 negatively regulates the LPS‑mediated inflammatory response in MSCs suggesting that TREM‑2 is a potential target of immune regulation in rat MSCs.
