Long non-coding RNA TPT1-AS1 alleviates cell injury and promotes the production of extracellular matrix by targeting the microRNA-324-5p/CDK16 axis in human dermal fibroblasts after thermal injury.

Long non-coding RNAs (lncRNAs) are associated with the healing of burn wounds in the dermis. The present study aimed to probe the role and regulatory network of the lncRNA TPT1 antisense RNA 1 (TPT1-AS1) in human dermal fibroblasts (HDFs) following thermal injury. A model of thermally injured cells was constructed with HDFs. The levels of TPT1-AS1, microRNA (miR)-324-5p and cyclin-dependent kinase (CDK)16 were determined through reverse transcription-quantitative PCR. Cell viability, cell cycle distribution, cell apoptosis rate and extracellular matrix (ECM) synthesis were assessed with a series of gain-of-function experiments and MTT, flow cytometry and western blot analyses. The binding ability of miR-324-5p and TPT1-AS1 (or the 3' untranslated region of CDK16) was identified via bioinformatics analysis and luciferase reporter assay. It was found that TPT1-AS1 and CDK16 were downregulated, but miR-324-5p was upregulated, in the HDFs after thermal injury. TPT1-AS1 elevation induced cell viability and ECM synthesis but attenuated cell cycle arrest at the G/G stage and decreased the cell apoptosis rate of thermally injured HDFs. In addition, TPT1-AS1 sponged miR-324-5p to modulate CDK16 expression. Moreover, silencing CDK16 weakened the impacts of TPT1-AS1 upregulation on cell function and ECM synthesis in heat-treated HDFs. In summary, TPT1-AS1 relieved cell injury and induced ECM synthesis by sponging miR-324-5p and targeting CDK16 in the HDFs after thermal injury, implying a protective role for TPT1-AS1 in the burn wound healing process.