Integrin-linked kinase acts as a pro-survival factor against high glucose-associated osmotic stress in human mesangial cells.
BACKGROUND: Integrin-linked kinase (ILK) is a protein that plays an important role in extracellular matrix-mediated signalling. Recent studies implicated ILK dysregulation in the development of diabetic nephropathy. However, little is known about the significance of ILK up-regulation in response to high glucose in mesangial cells. METHODS: The ILK messenger (m)RNA and protein expression in human mesangial cells were analysed with quantitative real-time polymerase chain reaction (PCR) and western blotting after exposure to either 100, 200, or 500 mg/dl glucose, or 100 mg/dl glucose + 400 mg/dl mannitol. Activation of protein Kinase B (PKB)/Akt was also determined by western blot analysis. Cells were transfected with ILK siRNA to determine the effects of ILK knockdown on PKB/Akt activation and cell death following treatment with high glucose or mannitol. RESULTS: High concentrations of glucose or mannitol for three days significantly up-regulated ILK mRNA and protein expression (P < 0.05 vs 100 mg/dl glucose). In contrast, ILK expression in cells exposed to the same conditions for seven days was unaffected. The time course of PKB/Akt phosphorylation was similar to that of ILK protein expression. The siRNA-mediated down-regulation of ILK expression inhibited the elevation of PKB/Akt phosphorylation induced by high glucose treatment. Furthermore, the inhibition of ILK expression promoted high glucose- or mannitol-induced apoptosis. CONCLUSION: The ILK may act as a pro-survival factor and play a role in protecting mesangial cells from hyperglycaemic osmotic stress.[1]References
- Integrin-linked kinase acts as a pro-survival factor against high glucose-associated osmotic stress in human mesangial cells. Ohnishi, M., Hasegawa, G., Yamasaki, M., Obayashi, H., Fukui, M., Nakajima, T., Ichida, Y., Ohse, H., Mogami, S., Yoshikawa, T., Nakamura, N. Nephrol. Dial. Transplant. (2006) [Pubmed]
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