BOO induces fibrosis and EMT in urothelial cells which can be recapitulated in vitro through elevated storage and voiding pressure cycles

Dunton, Cody L.; Purves, J. Todd; Hughes, Francis M.; Nagatomi, Jiro

doi:10.1007/s11255-021-02942-3

Cited by 5 publications

(2 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…BOO is a common chronic disease of the urinary system that is caused by various bladder outflow tract obstructions and causes related lower urinary tract symptoms 27 . Long‐term obstruction can lead to progressive bladder tissue remodeling and may even severely impair kidney function.…”

Section: Discussionmentioning

confidence: 99%

“…BOO is a common chronic disease of the urinary system that is caused by various bladder outflow tract obstructions and causes related lower urinary tract symptoms. 27 Long‐term obstruction can lead to progressive bladder tissue remodeling and may even severely impair kidney function. A large number of studies have shown that in the pathophysiological process of bladder remodeling, increased intravesical pressure, which is mechanical stress, is an important stimulator of hypertrophy and the proliferation of bladder wall muscle layer cells.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Serum/glucocorticoid‐regulated kinase 1‐targeted transient receptor potential oxalate subtype 1 regulates bladder smooth muscle cell proliferation due to bladder outlet obstruction in mice via activated T cell nuclear factor transcription factor 2

Yang

Chen

et al. 2022

IUBMB Life

View full text Add to dashboard Cite

Bladder outlet obstruction (BOO) is a type of chronic disease that is mainly caused by benign prostatic hyperplasia. Previous studies discovered the involvements of both serum/glucocorticoid-regulated kinase 1 (SGK1) and activated T cell nuclear factor transcription factor 2 (NFAT2) in the proliferation of smooth muscle cells after BOO. However, the relationship between these two molecules is yet to be explored. Thus, this study explored the specific mechanism of the SGK1-NFAT2 signaling pathway in mouse BOO-mediated bladder smooth muscle cell proliferation in vivo and in vitro. In vivo experiments were performed by suturing 1/2 of the external urethra of female BALB/C mice to cause BOO for 2 weeks. In vitro, mouse bladder smooth muscle cells (MBSMCs) were treated with dexamethasone (Dex) or dexamethasone + SB705498 for 12 h and were transfected with SGK1 siRNA for 48 h. The expression and distribution of SGK1, transient receptor potential oxalate subtype 1 (TRPV1), NFAT2, and proliferating cell nuclear antigen (PCNA) were measured by Western blotting, polymerase chain reaction, and immunohistochemistry. The relationship between SGK1 and TRPV1 was analyzed by coimmunoprecipitation. The proliferation of MBSMCs was examined by 5-ethynyl-2 0 -deoxyuridine and cell counting kit 8 assays. Bladder weight, smooth muscle thickness, and collagen deposition in mice after 2 weeks of BOO were examined. Bladder weight, smooth muscle thickness, the

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%