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Attenuated store-operated divalent cation entry and association between STIM1, Orai1, hTRPC1 and hTRPC6 in platelets

Isaac Jardín1, Jose J López, Hanene Zbidi

  • 1Department of Physiology, Cell Physiology Research Group, University of Extremadura, Cáceres. Spain.

Blood Cells, Molecules & Diseases
|February 10, 2011
PubMed

Insights

Store-operated calcium entry is reduced in platelets of type 2 diabetic patients. This impairment in calcium signaling may contribute to altered platelet function and cardiovascular risks in diabetes.

Area of Science:

  • Cardiovascular Biology
  • Diabetology
  • Platelet Physiology

Background:

  • Type 2 diabetes is associated with altered platelet responsiveness and increased cardiovascular complications.
  • Agonist-evoked calcium (Ca2+) entry in platelets is reportedly enhanced in diabetic patients.
  • Store-operated divalent cation entry represents a significant pathway for Ca2+ influx into platelets.

Purpose of the Study:

  • To investigate alterations in store-operated divalent cation entry in platelets from type 2 diabetic patients.
  • To determine the role of STIM1, Orai1, hTRPC1, and hTRPC6 in diabetic platelet dysfunction.

Main Methods:

  • Estimating store-operated divalent cation entry via manganese (Mn2+) influx assays.
  • Utilizing co-immunoprecipitation and Western blotting to detect protein-protein interactions.
  • Employing thapsigargin (TG) to induce store-operated Ca2+ entry and thrombin as an agonist.

Main Results:

  • Thapsigargin-induced Mn2+ entry was significantly reduced in platelets from diabetic donors compared to healthy controls.
  • The association of STIM1 with Orai1, hTRPC1, and hTRPC6 was enhanced by TG or thrombin in healthy platelets but reduced in diabetic platelets.
  • Impaired STIM1-channel subunit interaction suggests a mechanism for reduced store-operated calcium entry in diabetic platelets.

Conclusions:

  • Store-operated divalent cation entry is diminished in platelets from type 2 diabetic subjects.
  • This reduction is likely due to impaired association between STIM1 and channel subunits (Orai1, hTRPC1, hTRPC6).
  • The findings suggest a potential role in the pathogenesis of altered platelet responsiveness in diabetes.

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