Inhibition of DNA methylation during chronic obstructive bladder disease (COBD) improves function, pathology and expression.

ABSTRACT: Partial bladder outlet obstruction due to prostate hyperplasia or posterior urethral valves, is a widespread cause of urinary dysfunction, patient discomfort and also responsible for immense health care costs. Even after removal or relief of obstruction, the functional and pathologic aspects of obstruction remain as a chronic obstructive bladder disease (COBD). Epigenetic changes, such as DNA methylation, contribute to the persistent character of many chronic diseases, and may be altered in COBD. We tested whether candidate genes and pathways and the pathophysiology of COBD were affected by a hypomethylating agent, decitabine (DAC). COBD was created in female Sprague-Dawley rats by surgical ligation of the urethra for 6 weeks, followed by removal of the suture. Sham ligations were performe

SUBMITTER: Sidler M 

PROVIDER: S-EPMC8397724 | biostudies-literature | 2021 Aug

REPOSITORIES: biostudies-literature