EAU 2018: The Mechanism of Diabetes Mellitus-induced Ureteral Smooth Muscle Cell Proliferation Using a Murine Model
To investigate this claim, Dr. Taesoo and his cohort used twenty 15-week-old mice in and in vivo experimental analysis. Ten of these mice were left normal as a control while the remaining 10 were induced with diabetes mellitus. After euthanasia of the mice, the proximal, mid, and distal ureteral smooth muscle thickness was recorded and the differences between each of the ureteral section was analyzed and compared between the two cohorts. Using a western blot analysis, the ureteral specimens were tested to detect protein expression of phospho-ERK (P-ERK), phospho-JNK (P-JNK), VEGF, and PKC, which are important cellular factors used for cell regulation.
Upon completion of the study, it was observed that all three sections of the ureter for diabetes mellitus mice were consistently and significantly thicker than the control mice. In these animals, there was significant hyperproliferation of ureteral smooth in the diabetes mice which may have provoked reduced peristalsis. From the western blot analysis, it was shown that the expression of P-ERK, P-JNK, VEGF, and PKC were all significantly higher in the diabetic group compared to the control. This information clearly shows that ureteral lumen diameter is greatly reduced which would make expulsion of stones significantly more difficult in patients affected by diabetes mellitus. Additionally, Dr. Taesoo suggests that the pathways mediated by P-ERK, P-JNK, VEGF, and PKC may play an important role in pathological ureteral conditions. In closing, he briefly mentioned that this may be a viable field of study that requires future experimentation.
Speaker: C. Taesoo
Authors: Taesoo C., Kim Y.B., Lee Y., Jeon S.H., Lee S-J., Lee H-L., Yoo K.H.
Written by: Zachary Valley, Department of Urology, University of California-Irvine, at the 2018 European Association of Urology Meeting EAU18, 16-20 March, 2018 Copenhagen, Denmark