Inhibition of microRNA‐132 attenuates inflammatory response and detrusor fibrosis in rats with interstitial cystitis via the JAK‐STAT signaling pathway

Interstitial cystitis (IC) is a heterogeneous syndrome with unknown etiology, and microRNAs (miRs) were found to be involved in IC. In our study, we aim to explore the role of miR‐132 in the inflammatory response and detrusor fibrosis in IC through the Janus kinase‐signal transducer and activator of transcription (JAK‐STAT) signaling pathway in rat models. A rat model of IC was established and treated with the miR‐132 mimic, miR‐132 inhibitor, and/or JAK‐STAT signaling pathway inhibitor AG490. Enzyme‐linked immunosorbent assay was applied to measure the expression of interleukin (IL)‐6, IL‐10, interferon‐γ (IFN‐γ), and tumor necrosis factor‐α (TNF‐α), and intercellular adhesion molecule‐1 (ICAM‐1). The urodynamic test was performed to assess urodynamic parameters, and reverse transcription quantitative polymerase chain reaction and Western blot analysis for the expression of miR‐132, STAT4, suppressors of cytokine signaling 3 (SOCS3), JAK2, vascular endothelial growth factor (VEGF), IFN‐γ, and TNF‐α. IC rats treated with miR‐132 inhibitor and AG490 had decreased collagen fiber, inflammatory cell infiltration, and mast cells, lower expression of IL‐6, IL‐10, IFN‐γ, TNF‐α, ICAM‐1, collagens I and III, and alleviated urodynamic parameters and decreased expression of STAT4, VEGF, JAK2, IFN‐γ, TNF‐α, and increased expression of SOCS3. Taken together, our data indicate that downregulation of miR‐132 alleviates inflammatory response and detrusor fibrosis in IC via the inhibition of the JAK‐STAT signaling pathway. Taken together, our data indicate that downregulation of miR‐132 alleviates inflammatory response and detrusor fibrosis in interstitial cystitis via the inhibition of the Janus kinase‐signal transducer and activator of transcription signaling pathway