Dysregulation of LINC01094 is involved in the pathogenesis of pulpitis by regulating the miR-340-5p expression.

Abstract

Pulpitis seriously affects people's living standards and dental health, so identifying effective therapeutic targets is crucial for pulpitis. The research aimed to explore the underlying regulatory mechanism of LINC01094 and miR-340-5p in pulpitis. The study involved a total of 173 subjects (97 pulpitis and 76 healthy individuals). The expression of LINC01094 and miR-340-5p were evaluated through the polymerase chain reaction (PCR). The association linking LINC01094 and miR-340-5p expression was assessed by Pearson correlation analysis. The Human dental pulp cells (HDPCs) injury model was conducted by lipopolysaccharide (LPS). Cell proliferation was examined through the Cell Counting Kit-8 assay and flow cytometry. Cell apoptosis was also evaluated by flow cytometry. The caspase-3 levels and inflammatory cytokines were quantified using an enzyme-linked immunosorbent assay (ELISA). Upregulated LINC01094 and downregulated miR-340-5p expression were observed in pulpitis and LPS-induced HDPC injury models. A negative correlation was observed between miR-340-5p and LINC01094 expression in pulpitis. LPS could suppress proliferation and promote apoptosis of HDPCs. The TNF-α, IL-6, and IL-1β levels in LPS-induced HDPCs were also elevated. The HDPC injury induced by LPS could be aggravated by the LINC01094 overexpression. MiR-340-5p showed a relieved effect on HDPC injury and could alleviate the HDPC injury aggravated by LINC01094 overexpression. In summary, upregulated LINC01094 and downregulated miR-340-5p expression was observed in pulpitis. LINC01094 could accelerate the pulpitis progression via targeting miR-340-5p.