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  • Title: Integrin-linked kinase acts as a pro-survival factor against high glucose-associated osmotic stress in human mesangial cells.
    Author: Ohnishi M, Hasegawa G, Yamasaki M, Obayashi H, Fukui M, Nakajima T, Ichida Y, Ohse H, Mogami S, Yoshikawa T, Nakamura N.
    Journal: Nephrol Dial Transplant; 2006 Jul; 21(7):1786-93. PubMed ID: 16611685.
    Abstract:
    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.
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