miR-1737 targets TAK1 to mediate the BMP-Smad signaling pathway to regulate the molecular mechanism of chicken tibial chondrodysplasia.

Abstract

Tibial dyschondroplasia (TD) is a prevalent skeletal disorder in the modern broiler poultry industry. MicroRNAs (miRNAs) regulate various biological processes. Our previous studies suggest miR-1737 plays a role in cartilage development, but its mechanism in TD remains unclear. This study found that miR-1737 promotes chondrocyte proliferation and differentiation in TD chickens (P < 0.05), accelerating disease progression. Bioinformatics analysis predicted transforming growth factor &#x3b2;-activated kinase 1 (TAK1) as a target gene of miR-1737, which was confirmed through luciferase assays, qRT-PCR, and rescue experiments. TAK1 was shown to inhibit chondrocyte proliferation and differentiation (P < 0.05). Additionally, miR-1737 markedly upregulated the mRNA expression levels of Smad 1/5/8, key components of the BMP-Smad signaling pathway, and enhanced their phosphorylation, whereas TAK1 exhibited opposing effects. In conclusion, miR-1737 promotes TD chondrocyte proliferation and differentiation in vitro by targeting TAK1 and activating the BMP-Smad signaling pathway. These findings enhance our understanding of TD and suggest new molecular targets for its prevention and treatment.