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W. Amoaku, A.C. Browning, A. Alibhai, A. Rotchford; The Effect of Diabetes Mellitis and Hyperglycaemia on the Proliferation of Human Tenon's Fibroblasts . Invest. Ophthalmol. Vis. Sci. 2003;44(13):1194.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: We have previously shown that proliferation of Human Tenon’s fibroblasts (HTCFs) from diabetic patients is reduced. The aim of this study was to determine the effect hyperglycaemia on the previously noted changes in proliferation of HTCFs from diabetic and non-diabetic patients. We also determined the expression of cell surface receptors required for control of cellular proliferation in the diabetic and control patients. Methods: Tenon’s capsule fibroblasts from 7 diabetic and 7 non-diabetic patients were exposed to normo- (5mmol/L) and hyperglycaemic (25mmol/L) conditions and their proliferation determined by 3H thymidine incorporation. The possession of cell surface receptors (PDGF and TGF RII) and intracellular signalling molecules (TGF-ß1, ERK1/2 and MAPK) was determined on lysed and non-lysed cells by direct immunoblotting. Results: Human Tenon’s capsule fibroblasts (HTCF) derived from diabetic patients exposed to a glucose concentration of 5mmol/L exhibited a significantly reduced rate of proliferation compared with non-diabetic control samples (p=< 0.00001). HTCFs derived from diabetic patients and cultured in a high concentration of glucose (25mmol/L) for 24 hours did not show any significant difference in proliferation compared with paired samples incubated with 5mmol/L of glucose (Student’s paired t test, p=0.95). However, human Tenon’s capsule fibroblasts derived from age matched control patients cultured in a high concentration of glucose (25mmol/L) showed a significant inhibition in proliferation after 24 hours when compared with paired samples incubated with 5mmol/L of glucose (student’s paired t test, p=0.0008). All diabetic and non-diabetic samples were positive for PDGF receptor and intracellular ERK1/2 and MAPK, however diabetic cells showed reduced expression of TGF-ß1. Conclusions HTCFs from diabetic patients show reduced proliferation at normo-glycaemic glucose concentrations when compared to non-diabetics. High glucose concentrations suppressed the proliferation of non-diabetic HTCFs. This reduction in proliferation was associated with reduced levels of TGF-ß1 expression.
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