ArticleWorld journal of urology2025
Exploring the therapeutic potential of PACAP in Hunner-type Interstitial Cystitis.
Article in World journal of urology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Transient Receptor Potential Melastatin 4 (TRPM4) is associated with an immuno-stimulatory TME and better prognosis in BLCA.Discover oncology · 2025Article
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Authors and funding
4 authors.
Funding
Abstract
purposeThis study aims to elucidate the role of pituitary adenylate cyclase-activating polypeptide (PACAP) in Hunner-type Interstitial Cystitis (HIC) and evaluate its potential as a therapeutic target.
methodsBladder tissue samples were obtained from HIC patients and normal bladder tissue from bladder cancer patients. PACAP expression was assessed through immunohistochemistry. An in vitro HIC model was established using LPS-induced SV-HUC1 cells. PACAP knockdown was performed using siRNA. The expression of inflammatory markers (IL-6, IL-1β, TNF-α) and fibrotic markers (fibronectin 1, TGF-β1, collagen I) was evaluated via qPCR, Western blot, and ELISA. Cell migration and proliferation were analyzed using wound healing and CCK-8 assays. Transcriptomic profiling was conducted to identify differentially expressed genes (DEGs) and explore their functional significance.
resultsPACAP expression was significantly elevated in the bladder tissues of HIC patients. LPS stimulation of SV-HUC1 cells induced PACAP expression alongside increased levels of inflammatory cytokines, validating the inflammatory model. PACAP knockdown markedly suppressed IL-6, IL-1β, and TNF-α expression and attenuated LPS-induced fibrosis by reducing fibronectin 1, TGF-β1, and collagen I levels. Additionally, PACAP knockdown inhibited LPS-induced cell migration and proliferation, as evidenced by wound healing and CCK-8 assays. Transcriptomic analysis revealed distinct molecular alterations in HIC tissues, including PACAP upregulation, implicating it in HIC pathogenesis.
conclusionPACAP plays a pivotal role in the inflammatory and fibrotic pathways of HIC. PACAP knockdown alleviates LPS-induced pathological responses, highlighting its potential as a novel therapeutic target. Further research is warranted to investigate PACAP's precise mechanisms in HIC and its translational application in clinical settings.
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