MIR-199A-5P REGULATES THE PROLIFERATION AND APOPTOSIS OF DEGENERATIVE NUCLEUS PULPOSUS CELLS THROUGH THE CDKN1B/NF-ΚB AXIS

Intervertebral 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.