Abstract
Background Partial bladder outlet obstruction due to neurogenic bladder or mechanical obstruction is common amongst the population and can cause bladder injury and dysfunction. Bladder Smooth Muscle Cells (BSMCs) undergo phenotypic changes such as hyper-proliferation, de-differentiation and altered expression of integrins and ECM proteins.[1] Extracellular matrix changes are often crucial inciting events for fibroproliferative disease.[2] Epigenetic change, specifically DNA methylation, may be important factors underlying the persistent fibroproliferative phenotype. Previously, damaged matrix (heat-denatured collagen, DNC) induced hyper-proliferation of bladder smooth muscle cells (BSMC) and the phenotype was not reverted upon a return to normal matrix. [3] We examined the dependency of matrix-induced fibroproliferation and SMC phenotype on DNA methyltransferase activity. The cooperativity of matrix with other inciting stimuli (growth factors, hypoxia and strain) associated with bladder obstruction was also examined.
Highlights
Partial bladder outlet obstruction due to neurogenic bladder or mechanical obstruction is common amongst the population and can cause bladder injury and dysfunction
DNC exposure significantly increased the translocalization of DNA methyltransferase 3A (DNMT3A) into the nucleus of Bladder Smooth Muscle Cells (BSMCs), in contrast to native collagen (NC) cells, which expressed only cytoplasmic DNMT3A
The increase in nuclear expression of DNMT3A was coupled with decreased expression level of a-Smooth muscle actin (a-SMA)
Summary
Partial bladder outlet obstruction due to neurogenic bladder or mechanical obstruction is common amongst the population and can cause bladder injury and dysfunction. Bladder Smooth Muscle Cells (BSMCs) undergo phenotypic changes such as hyper-proliferation, de-differentiation and altered expression of integrins and ECM proteins.[1] Extracellular matrix changes are often crucial inciting events for fibroproliferative disease.[2] Epigenetic change, DNA methylation, may be important factors underlying the persistent fibroproliferative phenotype. Damaged matrix (heat-denatured collagen, DNC) induced hyper-proliferation of bladder smooth muscle cells (BSMC) and the phenotype was not reverted upon a return to normal matrix. [3] We examined the dependency of matrix-induced fibroproliferation and SMC phenotype on DNA methyltransferase activity. The cooperativity of matrix with other inciting stimuli (growth factors, hypoxia and strain) associated with bladder obstruction was examined
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