Differential perturbation of the interstitial cystitis-associated genes of bladder and urethra in rat model

Abstract

Interstitial cystitis (IC) is a chronic bladder dysfunction characterized as urinary frequency, urgency, nocturia, and pelvic pain. The changes in urethra may wind up with the bladder changes in structure and functions, however, the functions of the urethra in IC remains elusive. The aim of this study was to understand the perturbed gene expression in urethra, compared with urinary bladder, associated with the defected urodynamics. Using female IC mimic rats, a comprehensive RNA-sequencing combined with a bioinformatics analysis was performed and revealed that IC-specific genes in bladder or urethra. Gene ontology analysis suggested that the cell adhesion or extracellular matrix regulation, intracellular signaling cascade, cardiac muscle tissue development, and second messenger-mediated signaling might be the most enriched cellular processes in IC context. Further study of the effects of these bladder- or urethra-specific genes may suggest underlying mechanism of lower urinary tract function and novel therapeutic strategies against IC.

Alpha-oxoglutarate inhibits the proliferation of immortalized normal bladder epithelial cells via an epigenetic switch involving ARID1A

“…Our previous study on RNA-sequencing analysis of a IC rat mimic model revealed significant association of cell adhesion and IC context 30 . In addition, gene expression changes of chromatin remodeling genes were identified in human bladder epithelial cells from patients with IC 30 . We thus focused on cell-cell adhesion and chromatin remodeling.…”

Notch controls urothelial integrity in the mouse bladder

“…Enriched GO networks based on the differentially (primarily downregulated) expressed transcripts indicated 3 major hubs: ECM organization/extracellular structure organization, epithelial cell proliferation, and regulation of vasculature development/regulation of angiogenesis (Supplemental Figure 3). Of interest, RNA-Seq experiments on chemical-induced rat models of IC indicate that processes and pathways associated with ECM organization, blood vessel formation, antigen processing and presentation, immune response, and others are similarly affected (29).…”