Upregulation of microRNA‑140‑3p mediates dachshund family transcription factor 1 expression in immunoglobulin A nephropathy through cell cycle‑dependent mechanisms.

Immunoglobulin A nephropathy (IgAN) is a kidney disease and one of the commonest forms of glomerulonephritis worldwide. The present study investigated the role of dachshund family transcription factor 1 (DACH1) in IgAN and identified one of its binding microRNAs (miRNAs). The expression of DACH1 in human mesangial cells (HMCs) incubated with polymeric IgA (pIgA) isolated and purified from the serum of patients with IgAN or healthy individuals was evaluated by reverse transcription‑quantitative (RT‑q) PCR and western blotting. Cell proliferation and cell cycle assays were performed in DACH1‑overexpressing HMCs to identify the role of DACH1 in IgAN and enzyme‑linked immunosorbent assay was carried out to verify the release of inflammatory factors from HMCs. The target miRNAs of DACH1 were predicted using bioinformatics software and miR‑140‑3p was identified as a target of DACH1 by luciferase report assay, RT‑qPCR and western blotting. The results demonstrated that DACH1 was downregulated in HMCs cultured with pIgA‑IgAN at both mRNA and protein levels. Overexpression of DACH1 suppressed HMC growth and inhibited inflammatory cytokine release from HMCs cultured with pIgA‑IgAN. The expression of DACH1 was negatively regulated by miR‑140‑3p in IgAN and miR‑140‑3p inhibition suppressed HMC growth and inhibited inflammatory cytokine release from HMCs cultured with pIgA‑IgAN. The findings of the present study demonstrated that DACH1 decreased HMC growth and the release of inflammatory cytokines from HMCs may be targeted by miR‑140‑3p. The results suggested that DACH1 could be associated with the progression of IgAN and provide a potential target for further studies related to the mechanism of IgAN.