OBJECTIVE: To explore the roles of stem cell factor (SCF) on the loss of interstitial cells (ICCs) in the bladder of diabetic rats, which have not been investigated. METHODS: The rats were assigned to 3 groups: normal control rats, diabetic rats, and SCF-treated diabetic rats. The diabetic rat model was created using a streptozotocin (60 mg/kg) intraperitoneal injection. The SCF and c-kit levels in bladder tissue were determined using reverse transcriptase-polymerase chain reaction and Western blot analysis. The quantity of ICCs as represented by c-kit-positive cells was examined by image analysis of immunofluorescence staining. RESULTS: Compared with the control rats, the diabetic rats exhibited a significant decrease in the SCF levels and c-kit expression and number of ICCs in the bladder tissues. All these impaired parameters were effectively restored to the control level after exogenous SCF treatment. CONCLUSION: These findings suggest that the loss of ICCs in the bladder tissue of diabetic rats can be attributed to a deficiency in endogenous SCF. The beneficial effect of exogenous SCF on diabetic depletion of ICCs could provide a theoretical rationale for the use of SCF as a potential therapeutic drug in treating patients with diabetes-related voiding dysfunction.
OBJECTIVE: To explore the roles of stem cell factor (SCF) on the loss of interstitial cells (ICCs) in the bladder of diabeticrats, which have not been investigated. METHODS: The rats were assigned to 3 groups: normal control rats, diabeticrats, and SCF-treated diabeticrats. The diabeticrat model was created using a streptozotocin (60 mg/kg) intraperitoneal injection. The SCF and c-kit levels in bladder tissue were determined using reverse transcriptase-polymerase chain reaction and Western blot analysis. The quantity of ICCs as represented by c-kit-positive cells was examined by image analysis of immunofluorescence staining. RESULTS: Compared with the control rats, the diabeticrats exhibited a significant decrease in the SCF levels and c-kit expression and number of ICCs in the bladder tissues. All these impaired parameters were effectively restored to the control level after exogenous SCF treatment. CONCLUSION: These findings suggest that the loss of ICCs in the bladder tissue of diabeticrats can be attributed to a deficiency in endogenous SCF. The beneficial effect of exogenous SCF on diabetic depletion of ICCs could provide a theoretical rationale for the use of SCF as a potential therapeutic drug in treating patients with diabetes-related voiding dysfunction.