Volume 29, Issue 3
DOI: 10.24205/03276716.2020.941
LncRNA SNHG1 improves chondrocyte apoptosis and inflammation microenvironment by down-regulating miR-195-5p
Abstract
Background: Osteoarthritis (OA) is a chronic progressive bone disease, which still lacks effective treatment strategies. Many evidences show that long non-coding RNA (LncRNA) is closely related to the progression of OA. However, the effect of small nucleolar RNA host gene 1 (SNHG1) on OA apoptosis and inflammatory microenvironment have not been described in detail.
Methods: Firstly, the expression levels of SNHG1 and miR-195-5p in cartilage tissue and normal cartilage tissue of OA patients and rats were detected. Secondly, the effects of SNHG1 and miR-195-5p on apoptosis, inflammation and proliferation of OA chondrocytes were studied through a series of cell function experiments. Next, the relationship between SNHG1 and miR-195-5p was studied. Finally, SNHG1 promoter and miR-195-5p inhibitor were injected to explore the in vivo effects on OA rat models.
Results: We found that the SNHG1 expression was down-regulated and the miR-195-5p expression was up-regulated in OA tissue. In addition, increasing SNHG1 or knocking down miR-195-5p expression can reduce apoptosis rate, improve inflammatory microenvironment of OA chondrocytes, and restore cell proliferation. Besides, we clarified that SNHG1 could act as a molecular sponge for miR-195-5p. Finally, we found that SNHG1 promoter and miR195-5p inhibitor could reduce apoptosis and inflammatory reaction in OA rat models.
Conclusion: Adjusting the SNHG1-miR-195-5p axis, increasing SNHG1 or knocking down miR195-5p is beneficial to improving the apoptosis and inflammatory microenvironment of chondrocytes and provides new insights for the mechanism of OA progression.
Keywords
osteoarthritis, SNHG1, miR-195-5p, apoptosis, inflammatory microenvironment