| Experiment Id | GSE218946 | Name | Differential Gene Expression in Bladders of Wild-Type Mice Compared to Mice Lacking miroRNA-29a/b1 |
| Experiment Type | RNA-Seq | Study Type | WT vs. Mutant |
| Source | GEO | Curation Date | 2023-07-27 |
| description | Lower urinary tract symptoms (LUTS) refer to a spectrum of urological diseases, and incomplete bladder emptying is common among affected patients. The etiology of LUTS is largely unknown and evidence arising from epidemiologic, clinical, and basic research suggests that bladder fibrosis is an important contributing factor to pathogenesis of LUTS. MicroRNAs (miRNAs) are short (~22 nucleotides), non-coding RNAs that repress target gene expression by a combination of mRNA degradation and translation inhibition. The miR-29 family is best known for its anti-fibrotic role in various organs. Recent studies have reported decreased miR-29 in bladders of patients with outlet obstruction and in a rat model of bladder outlet obstruction, suggesting that miR-29 may be associated with impaired bladder function subsequent to tissue fibrosis. In the present study, we characterized bladder function in male mice lacking expression of MIR29A and MIR29B1 (miR-29a/b1). We found that lack of miR-29a/b1 resulted in severe urinary retention, increased urination duration with reduced flow rate, and these mice failed to void or voided irregularly during anesthetized cytometry. Collagens and elastin were increased in the bladder walls of mice lacking miR-29a/b1. These findings reveal an important role of mir-29 in bladder homeostasis and suggest therapeutic potential of miR-29 to improve symptoms in patients with LUTS. Total RNA was isolated from bladders of wild-type mice and age matched mice lacking expression of microRNA-29a/b1. Mice lacking expression of microRNA 29-a/b1 were sacrificed when bladder enlargement and dysfunction were observed. RNAseq was performed. |
