Ischemia/Reperfusion Effects on Bladder Muscle and Mucosa Cell Contractile Regulatory Proteins

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Ischemia/reperfusion (I/R) has been shown to be the major etiologic factor in animal models in a variety of bladder dysfunctions. Herein we investigate the direct effect of I/R on rabbit bladder contractile regulatory proteins.


Male rabbit bladders were subjected to IR. The contractile responses were recorded and the protein levels of rho-kinase (ROK), caldesmon (CaD) and myosin light chain kinase (MLCK) were analyzed in both bladder muscle and mucosa.


For the mucosa layer, ROK was unchanged after ischemia, but increased significantly after 1 week of reperfusion. MLCK increased after ischemia and then significantly increased after 1 and 2 weeks of reperfusion. In the muscle layer, ROK increased at 2 h of reperfusion, decreased significantly following 1 week of reperfusion, then returned to control level by 2 weeks of reperfusion. MLCK expression significantly decreased as early as ischemia alone and did not recover after reperfusion. For CaD expression in the mucosa layer, both CaD isoforms significantly increased at 1 week of reperfusion, then progressively decreased at 2 weeks of reperfusion. In the muscle layer, both CaD isoforms had different expressions. In the muscle layer, smooth muscle caldesmon (h-CaD) decreased at ischemia alone and at 2 h of reperfusion, but significantly increased at 2 weeks of reperfusion; whereas non-muscle caldesmon (l-CaD) significantly decreased at 2 weeks of reperfusion.


As bladder muscle and mucosa have markedly different purposes, it is not surprising that they respond differently to I/R. Bladder mucosa and muscle have different kinds of alternations on contractile regulatory proteins.

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