IGF-1 siRNA transfection was used to investigate whether SCF
expression was affected by endogenous IGF-1 expression in smooth muscle cells, and IGF-1 induced SCF expression effects were studied. The effect of high H 89 order glucose on the expression of endogenous IGF-1 and SCF was also investigated. Results: Diabetic rats showed prolonged colonic transit time (252 ± 16 vs 168 ± 9 min, P < 0.01) and weakness of circular muscle contraction (0.81 ± 0.09 g vs 2.48 ± 0.23 g, P < 0.01) compared with the control group. Endogenous IGF-1 and SCF protein expression were significantly reduced in the diabetic colonic muscle tissues. IGF-1 and SCF mRNA expression also showed a paralleled reduction in diabetic rats. In the IGF-1 siRNA transfected smooth muscle cells, SCF mRNA and protein Rucaparib nmr expression were significantly decreased. IGF-1 could induce SCF expression in a concentration and time-dependent manner, mainly through the ERK1/2 signal pathway. High glucose inhibited endogenous IGF-1 and SCF expression, while the addition of IGF-1 to the medium reversed the SCF expression. Conclusion: Myopathy may resolve in colonic motility dysfunction in diabetic rats. Deficiency of endogenous IGF-1 in colonic smooth muscle cells caused reduction of SCF expression. Key Word(s): 1. diabetes; 2. smooth muscle cells; 3. IGF-1; 4. stem cell factor; Presenting
Author: YUN WANG Additional Authors: LIN LIN, QINGE WANG Corresponding Author: YUN WANG Affiliations: The first affiliated hospital
of Nanjing Medical University Objective: Smooth muscle dysfunction could impair the gastrointestinal motility. Advanced glycation end products (AGEs) participates diabetic complications. But no studies have reported AGEs is involved in diabetic colonic smooth muscle medroxyprogesterone pathologies. The aim of present study was to describe detailed ultrastructural abnormalities in colonic smooth muscle of diabetic patients, determine AGEs levels in these patients’ colon and the expression levels of smooth muscle cells (SMCs) specific proteins, and if there are correlation between AGEs levels and SMCs specific proteins. Methods: Colonic muscle tissues were collected from patients with colon surgical, and samples were resected 10 cm away from the edge of the colon lesions. Nε-carboxymethyl lysine (CML), an AGEs marker, in colonic muscle tissues samples was tested. Transmission electron microscopy was used to determine ultrastructural abnormalities in SMCs of diabetic patients. SMCs specific proteins in diabetic colon were measured and correlation between CML and these specific proteins was analyzed. Results: Fifteen cases were included in control and diabetic group respectively. CML levels increased in colon muscle layer of diabetic patients. Ultrastructural abnormalities in colonic SMCs are: swollen mitochondrial, increased dense band and dense body, increased caeolae and broken gap junction. There were no redundant collagen fibers in intercellular space.