Effects of microRNA-27a Targeting Smad1 on Intervertebral Disc Degeneration and Biological Characteristics of Nucleus Pulposus Cells

Abstract

Objective: The present study aimed to analyze the expression of microRNA-27a (miR-27a) in intervertebral disc degeneration (IDD) and its effect on the biological characteristics of nucleus pulposus (NP) cells. Methods: An IDD rat model was established, and the expression of miR-27a and Smad1 in the intervertebral disc tissue was detected. An oxygen and glucose deprivation (OGD) NP cell model was established to simulate the IDD microenvironment, and the effects of downregulated miR-27a on the proliferation, apoptosis, inflammatory response, and extracellular matrix (ECM) proteins of OGD-NP cells were analyzed. The target relationship of miR-27a and Smad1 was verified by luciferase reporter assays, and siRNA-Smad1 was transfected to reverse the experiment. Results: The level of miR-27a in the IDD model group was significantly increased, whereas that of Smad1 was decreased compared with the sham group (P<0.05). Inhibition of miR-27a improved cell proliferation, and inhibited apoptosis, degradation of the ECM, and inflammatory response of OGD-NP cells compared with the OGD group (P<0.05). The results of the double luciferase reporter assays indicated that Smad1 was the target gene of miR-27a. Smad1 silencing reversed the increase in ECM proteins induced by inhibition of miR-27a; However, it did not affect cell proliferation and apoptosis. Conclusion: The expression levels of miR-27a were upregulated in IDD and it may be involved in the progression of IDD by promoting the apoptosis of NP cells and ECM degradation by targeting Smad1.