Long non-coding RNA cyclin-dependent kinase inhibitor 2B antisense ribonucleic acid 1 is associated with in-stent restenosis and promotes human carotid artery smooth muscle cell proliferation and migration by sponging miR-143-3p.

Carotid angioplasty and stenting (CAS) is an efficient therapeutic approach for carotid stenosis. However, in-stent restenosis (ISR) frequently occurs and seriously affects the therapeutic efficacy of CAS. Certain non-coding (nc)RNAs serve potential roles in ISR development and progression. Thus, the goals of the present study were to investigate novel biomarkers for ISR development and to further uncover the mechanisms underlying the progression of ISR. The expression of long ncRNA cyclin-dependent kinase inhibitor (CDKN)2B-antisense 1 (AS1) and microRNA (miR)-143-3p in patients with ISR and human carotid artery smooth muscle cells (hHCtASMCs) was analyzed using reverse transcription-quantitative PCR. A luciferase reporter assay was performed to examine the interaction between CDKN2B-AS1 and miR-143-3p. The effects of the CDKN2B/miR-143-3p axis on hHCtASMC proliferation and migration were assessed using Cell Counting Kit-8 and Transwell assays. The results indicated that serum CDKN2B-AS1 was increased and miR-143-3p was decreased in patients with ISR as compared with that in patients with no ISR (all P<0.001). CDKN2B-AS1 and miR-143-3p were identified as risk factors for ISR onset (all P<0.05) and knockdown of CDKN2B-AS1 in hHCtASMCs led to inhibited cell proliferation and migration. Furthermore, the luciferase reporter assay and expression analysis indicated that miR-143-3p is a target of CDKN2B-AS1 and may mediate the effects of CDKN2B-AS1 on hHCtASMC proliferation and migration. In conclusion, dysregulation of CDKN2B-AS1 and miR-143-3p may represent risk factors for the occurrence of ISR. The results suggested that the CDKN2B-AS1/miR-143-3p axis may regulate the proliferation and migration of hHCtASMCs, indicating its potential to be developed as a target for preventative measures and therapies for ISR.