Lack of expression of miR-29a/b1 impairs bladder function in male mice.
Zunyi Y WangRobert SpitzChad M VezinaJianghui HouDale E BjorlingPublished in: Disease models & mechanisms (2023)
Lower urinary tract symptoms (LUTS) refer to various urological diseases, and incomplete bladder emptying is common among affected patients. Etiology of LUTS is largely unknown, and investigations of LUTS suggest that bladder fibrosis contributes 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. miR-29 was decreased in bladders of patients with outlet obstruction and a rat model of bladder outlet obstruction, suggesting that miR-29 may contribute to impaired bladder function subsequent to tissue fibrosis. We characterized bladder function in male mice lacking expression of MIR29A and MIR29B1 (miR-29a/b1). Lack of miR-29a/b1 resulted in severe urinary retention, increased voiding duration with reduced flow rate, and these mice failed to void or voided irregularly during anesthetized cytometry. Collagens and elastin were increased in bladders 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.
Keyphrases
- long non coding rna
- cell proliferation
- lower urinary tract symptoms
- long noncoding rna
- spinal cord injury
- poor prognosis
- gene expression
- benign prostatic hyperplasia
- urinary tract
- physical activity
- ejection fraction
- depressive symptoms
- genome wide
- skeletal muscle
- early onset
- newly diagnosed
- binding protein
- systemic sclerosis