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Smooth muscle-specific deletion of MnSOD exacerbates diabetes-induced bladder dysfunction in mice.

Bladder dysfunction in diabetes progresses gradually over time. However, the mechanisms of the development are not clear. We test the hypothesis that oxidative stress plays a key role in the development of diabetic bladder dysfunction, using an inducible smooth muscle (SM)-specific Sod2 gene knockout (SM-Sod2 KO) mouse model. Eight-week-old male Sod2lox/lox, SM-CreERT2(ki)Cre/+ mice and wild-type mice were assigned to diabetic or control groups. 4-hydroxytamoxifen was injected into Sod2lox/lox, SM-CreERT2(ki)Cre/+ mice to activate CreERT2-mediated deletion of Sod2. Diabetes was induced by injection of streptozotocin while control mice were injected with vehicle. Nine weeks later, bladder function was evaluated and bladders were harvested for immunoblotting analysis. Wild-type diabetic mice presented compensated bladder function, along with increased nitrotyrosine and manganese superoxide dismutase in detrusor muscle. Induction of diabetes in SM-Sod2 knockout mice caused deteriorated bladder function and even greater increases in nitrotyrosine compared with wild-type diabetic mice. The expression levels of Bax and cleaved caspase-3 were increased, but Bcl-2 was decreased in detrusor muscle of both diabetic groups, with more pronounced effects in SM-Sod2 knockout diabetic mice. Our findings demonstrate that exaggerated oxidative stress can accelerate the development of bladder dysfunction in diabetic mice, and the enhanced activation of apoptotic pathways in the bladder may be involved in the process.