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Transcriptome profiling of urothelial cells after exposure to low-grade oxidative stress

ABSTRACT: In this study, we aimed to determine the overall effect of glucose oxidase (GO) on transcriptomic profile of urothelial cells using RNA sequencing. Our study represents a reference database that could lead to a better understanding of the link between oxidative stress and innate immune response of urothelial cells leading to continuous cycle of inflammation in IC/BPS pathology. Furthermore, the study sets grounds for future studies exploring potential biomarkers and therapeutic targets for IC/PBS diagnosis and treatment.

ORGANISM(S): Homo sapiens

PROVIDER: GSE288905 | GEO | 2025/03/26

REPOSITORIES: GEO

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Project description:The pathogenesis of interstitial cystitis/bladder pain syndrome (IC/BPS) remains incompletely understood. Bladder fibrosis is a significant histopathological feature of IC/BPS, particularly in non-Hunner-type IC (NHIC). Transient receptor potential cation channel subfamily C member 3 (TRPC3) is known to play a crucial role in myocardial and renal fibrosis. This study investigates the involvement of TRPC3 in bladder fibrosis associated with IC/BPS. A rat model of IC/BPS was established using cyclophosphamide (CYP, 50 mg/kg, intraperitoneally, every 3 days for 3 doses). Bulk RNA sequencing was used to identify differentially expressed transient receptor potential (TRP) channel genes in CYP-induced cystitis rats, whereas single-cell RNA sequencing was utilized to pinpoint the cell type predominantly expressing transient receptor potential cation channel subfamily C member 3 (TRPC3) . TRPC3 inhibition was achieved through intraperitoneal injection of Pyrazole 3 (Pyr3, 0.1 mg/kg or 1 mg/kg). Suprapubic mechanical allodynia was assessed using up-down method with von Frey filaments and micturition frequency was assessed by cystometry. The expression of TRPC3 and components of the transforming growth factor beta (TGF-β)/Smad signaling pathway (TGF-β, p-Smad2, and p-Smad3) in the bladder was analyzed by Western blot. Bladder fibrosis was assessed through Masson’s staining and detection of fibrosis markers (Vimentin, Collagen I, and Collagen III) using Western blot. The RNA and protein expression of TRPC3 was up-regulated in CYP-induced cystitis rats. TRPC3 inhibition led to significant improvements in suprapubic mechanical allodynia and reduced micturition frequency in CYP-induced cystitis rats. Western blot analyses revealed that markers of bladder fibrosis (Vimentin, Collagen I, and Collagen III) were markedly upregulated in CYP-induced cystitis rats. Masson’s staining showed an increased area of collagen fibers. Additionally, inhibition of TRPC3 resulted in significant downregulation of the TGF-β/Smad signaling pathway (TGF-β, p-Smad2, and p-Smad3) in CYP-induced cystitis rats. TRPC3 activation contributes to bladder fibrosis in IC/BPS. Inhibition of TRPC3 ameliorates suprapubic mechanical allodynia and micturition frequency in CYP-induced cystitis rats by downregulating the TGF-β/Smad pathway. TRPC3 represents a potential therapeutic target for managing bladder fibrosis in IC/BPS.

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Transcriptome profiling of urothelial cells after exposure to low-grade oxidative stress

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