Abstract
Bladder outlet obstruction (BOO) often results in lower urinary tract symptoms (LUTSs) and negatively affects quality of life. Here, we evaluated gene expression patterns in the urinary bladder during tissue remodeling due to BOO. We divided BOO model rats into two groups according to the degree of hypertrophy of smooth muscle in the bladder. The strong muscular hypertrophy group, which exhibited markedly increased bladder smooth muscle proportion and HIF1α mRNA levels compared with the control group, was considered a model for the termination of hypertrophy, whereas the mild muscular hypertrophy group was considered a model of the initiation of hypertrophy. Some genes related to urinary function showed different expression patterns between the two groups. Furthermore, we found that several genes, including D-box binding PAR bZIP transcription factor (DBP), were upregulated only in the mild muscular hypertrophy group. DBP expression levels were increased in bladder smooth muscle cells in response to hypoxic stress. DBP associated with enhancer and promoter regions of NOS3 gene locus and upregulated NOS3 gene expression under hypoxic conditions. These findings suggested that the regulatory systems of gene expression were altered during tissue remodeling following BOO. Furthermore, circadian clock components might be involved in control of urinary function via transcriptional gene regulation in response to hypoxic stimuli.
Highlights
Components are involved in controlling urinary functions[8,9]
We categorized Bladder outlet obstruction (BOO) model rats into two groups according to the degree of hypertrophy of smooth muscular cells : the strong muscular hypertrophy (SH) group and the mild hypertrophy (MH) group
Our findings suggested that BOO modulated signaling pathways by regulation of gene expression in the bladder
Summary
Components are involved in controlling urinary functions[8,9]. The mechanisms through which clock components mediated urinary functions have not been fully elucidated. The effects of BOO on the roles of clock components in urinary functions are unclear. We aimed to elucidate the mechanisms regulating gene expression at the initiation of bladder tissue remodeling in BOO. Our findings demonstrated that gene expression patterns were altered during BOOdependent bladder remodeling. We found that D-box binding PAR bZIP transcription factor (DBP), a circadian clock component, was upregulated in response to hypoxic stress and functioned as a regulator of a urinary function-related gene
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