Store-operated Ca2+ entry and tyrosine kinase pp60src hyperactivity are modulated by hyperglycemia in platelets from patients with non insulin-dependent diabetes mellitus

We have investigated the involvement of store-operated Ca2+ entry (SOCE) in the abnormal platelet Ca2+ homeostasis in patients with non insulin-dependent diabetes mellitus (NIDDM). In a medium containing 180 mg/dL glucose, platelets from NIDDM patients showed an increased SOCE compared to controls. We found that tyrosine phosphorylation was elevated in platelets from NIDDM patients. Consistent with this, the activity of the tyrosine kinase pp60src is enhanced in platelets from diabetic patients. When the experiments were performed in a medium containing 90 mg/dL both, SOCE and pp60src activity, were similar to those found in control platelets. Our results indicate that SOCE is altered in platelets from NIDDM patients probably due to the increased activity of the tyrosine kinase pp60src. Both, SOCE and pp60src activity in platelets from NIDDM patients are more susceptible to the extracellular glucose concentration, which seems to be involved in the dysfunction of these mechanisms.