Multiple sclerosis (MS) affects the brain and nervous system’s functioning. Mice with MS showed significant fibrosis in their bladders. The scarring and thickening of bladder walls lead to urinary incontinence and upper tract damage. The protein fibronectin 1 (FN1) plays a key role in tissue damage. This study investigates the relationship between fibrosis, FN1, and its regulator mRNAs.

Immunohistochemistry determined smooth muscle fibrosis degree. FN1 expression for different fibrosis grades was determined using quantitative real-time polymerase chain reaction (RT-qPCR) and Western blotting. Bioinformatics analysis showed FN1 synthesis could get inhibited by miR-219c-5p, miR-199a-3p, and miR-3572-3p. These non-coding molecules decreased or overexpressed in BSMCs.

RT-qPCR detected FN1 knockdown efficiencies and respective transfection, and only miR-219c-5p gave exact results. A dual-luciferase reporter assay determined the targeting association between miR-219c-5p and FN1. Flow CCK-8 experiments confirmed that miR-219c-5p decreased FN1 expression and BSMCs. The in vivo transfected agomir and anagomir with miR-219c-5p reduced and worsened the fibrosis, respectively.

The study associates FN1 up-regulation with bladder fibrosis development. The miR-219c-5p plays a significant role in down-regulating FN1 expression. This research proposes a new antifibrotic property of miR-219c-5p. It can be a potential diagnostic and treatment target for this disease.