Jianmin Xue1,2, Baoyang Hu1,2, Wenhua Xing2, Feng Li2, Zhi Huang2, Wenkai Zheng2, Bo Wang1,2, Yong Zhu3, Xuejun Yang4. 1. Graduate School of Inner Mongolia Medical University, Hohhot City, 010059, Inner Mongolia, China. 2. Department of Thoracolumbar Spine Surgery, The Second Affiliated Hospital of Inner Mongolia Medical University, No. 1 Yingfang Road, Hohhot City, 010059, Inner Mongolia, China. 3. Department of Thoracolumbar Spine Surgery, The Second Affiliated Hospital of Inner Mongolia Medical University, No. 1 Yingfang Road, Hohhot City, 010059, Inner Mongolia, China. 1036227632@qq.com. 4. Department of Thoracolumbar Spine Surgery, The Second Affiliated Hospital of Inner Mongolia Medical University, No. 1 Yingfang Road, Hohhot City, 010059, Inner Mongolia, China. yangxuejun2004@126.com.
Abstract
BACKGROUND: Intervertebral disk degeneration (IDD) is a degenerative disease characterized by cytoplasm loss and extracellular matrix degradation. Numerous evidence reported that miRNAs participated in IDD development. Nevertheless, the function of miR-142-3p in IDD development remains unknown. This study mainly explored the potential role and function of miR-142-3p in IDD development. METHODS: One percent fetal bovine serum was used to induce the degeneration of ATDC5 cells, and miR-142-3p level was examined by qRT-PCR. Then, miR-142-3p mimic/inhibitor and its corresponding negative control were transfected into ATDC5 normal and degenerative cells. Viability, migration, invasion, apoptosis, cycle, Bax, Bcl-2, P62, and Beclin1 expression levels were assessed using CCK8, wound healing assay, annexin V-FITC/PI staining, western blot, and qRT-PCR, respectively. RESULTS: The results revealed that the expression levels of MMP13, ADAMTS5, MMP3, and Col-X were increased as well as the expression levels of SOX-9 and Col-II were reduced in ATDC5 degenerative cells, indicating the degeneration model was constructed. We observed that miR-142-3p was decreased in ATDC5 degenerative cells and its suppression could promote ATDC5 cell degeneration. However, miR-142-3p overexpression could reverse the cell viability inhibition, as well as apoptosis and autophagy enhancement in ATDC5 degenerative cells. CONCLUSIONS: Our results proved that miR-142-3p may play an important role in disk degeneration. Further animal study is needed to illustrate the role of the miR-142-3p in IDD development.
BACKGROUND: Intervertebral disk degeneration (IDD) is a degenerative disease characterized by cytoplasm loss and extracellular matrix degradation. Numerous evidence reported that miRNAs participated in IDD development. Nevertheless, the function of miR-142-3p in IDD development remains unknown. This study mainly explored the potential role and function of miR-142-3p in IDD development. METHODS: One percent fetal bovine serum was used to induce the degeneration of ATDC5 cells, and miR-142-3p level was examined by qRT-PCR. Then, miR-142-3p mimic/inhibitor and its corresponding negative control were transfected into ATDC5 normal and degenerative cells. Viability, migration, invasion, apoptosis, cycle, Bax, Bcl-2, P62, and Beclin1 expression levels were assessed using CCK8, wound healing assay, annexin V-FITC/PI staining, western blot, and qRT-PCR, respectively. RESULTS: The results revealed that the expression levels of MMP13, ADAMTS5, MMP3, and Col-X were increased as well as the expression levels of SOX-9 and Col-II were reduced in ATDC5 degenerative cells, indicating the degeneration model was constructed. We observed that miR-142-3p was decreased in ATDC5 degenerative cells and its suppression could promote ATDC5 cell degeneration. However, miR-142-3p overexpression could reverse the cell viability inhibition, as well as apoptosis and autophagy enhancement in ATDC5 degenerative cells. CONCLUSIONS: Our results proved that miR-142-3p may play an important role in disk degeneration. Further animal study is needed to illustrate the role of the miR-142-3p in IDD development.
Entities:
Keywords:
Cell behavior; Intervertebral disk degeneration; miR-142-3p