• Xiangxin Li.
• Department of Pain Management, The Affiliated Hospital to Changchun University of Chinese Medicine, Changchun City, Jilin Province, China.
• Shock. 2022 Nov 1; 58 (5): 384392384-392.

AbstractIntervertebral disc degeneration is a multifactorial pathological disease. miR-199a-5p is exceedingly implicated in regulating degenerative nucleus pulposus cell (DNPC). We explored the roles of miR-199a-5p in DNPCs. Cell morphology and Collagen II-positive expression were observed. Cell proliferation, apoptosis, and Bax and Bcl-2 levels were assessed. miR-199a-5p inhibitor, pcDNA3.1-CDKN1B, or si-CDKN1B was transfected into DNPCs. miR-199a-5p and CDKN1B expressions were detected. The binding relationship between miR-199a-5p and CDKN1B was verified. DNPCs with silenced miR-199a-5p and CDKN1B were treated with PDTC. The nuclear factor-κB (NF-κB) pathway-related protein levels were detected. DNPCs showed decreased proliferation and promoted apoptosis. miR-199a-5p was highly expressed in DNPCs. miR-199a-5p knockdown increased DNPC proliferation and inhibited apoptosis. CDKN1B was repressed in DNPCs. miR-199a-5p targeted CDKN1B. CDKN1B knockdown partially abrogated the effects of miR-199a-5p inhibition on DNPC proliferation and apoptosis. In DNPCs, p65 was translocated to the nucleus, IκB protein phosphorylation level was increased, and the NF-κB pathway was activated. miR-199a-5p knockdown or CDKN1B overexpression repressed the NF-κB pathway activation. NF-κB pathway inhibitor promoted DNPC proliferation and inhibited apoptosis. Briefly, miR-199a-5p was upregulated in DNPCs. We discovered for the first time that miR-199a-5p silencing repressed the NF-κB pathway by promoting CDKN1B transcription, thus promoting DNPC proliferation and inhibiting apoptosis.Copyright © 2022 by the Shock Society.

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