MP67-11 DIABETES MELLITUS PROMOTES URETERAL SMOOTH MUSCLE CELL PROLIFERATION: A RESEARCH ON THE MECHANISM.

INTRODUCTION AND OBJECTIVES: The aim of our study was to evaluate the role of underlying diabetes mellitus (DM) that was proved to be a significant factor effecting on spontaneous stone expulsion by preceding research. We investigated the influence of DM on the ureter using a mouse-model system. METHODS: The mouse-model arm of this study used 20 15week-old mice, including 10 normal (control) mice and 10 DM mice. We measured the proximal, middle and distal ureteral smooth muscle thickness of each mouse and the differences among each ureteral section were analyzed. Mouse ureteral specimens were also analyzed via Western blotting to detect relative protein expressions. RESULTS: In the mouse model, we saw significant hyperproliferation of ureteral smooth muscle in DM mice compared to normal mice, which might provoke reduced peristalsis among DM mice. The ureteral smooth muscle of DM mice was obviously thicker than that of normalmice in all ureteral tissues: proximal (p1⁄40.040), mid (p1⁄40.010) and distal (p1⁄40.028). The expressions of P-ERK (p1⁄40.005), and P-JNK (p1⁄40.001) in the diabetic group had high expression levels compared to the normal group. High glucose also induced up-regulation of VEGF (p1⁄40.002) protein expression, and correlated PKC (p1⁄40.001) expression. CONCLUSIONS: One explanation for the higher risk of stonepassage failure among DM patient may be decreased ureteral peristalsis resulting in the hyperproliferation of ureteral smoothmuscle. JNKandERK pathways may play an important role in the pathologic manifestation.