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Siewiera 2016 Abstract IOC109

From Bioblast
Siewiera K, Kassassir H, Watala C (2016) Potential role of mitochondria as modulators of blood platelet activation and reactivity in diabetes. Mitochondr Physiol Network 21.01.

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Siewiera K, Kassassir H, Watala C (2016)

Event: IOC109

Numerous studies have shown that cardiovascular complications are one of the major consequences of diabetes mellitus. They are responsible for two of three death events among this group of patients. Blood platelet dysfunctions are strongly involved in the development of the micro- and macrovascular complications in types 1 and 2 diabetes mellitus. However, mechanisms of abnormal platelet activation and their hypersensitivity in diabetes are still far from complete understanding. We believe that the changes in the functioning of the platelet mitochondria may largely underlie such phenomena.

WHAT WE KNOW: Platelet mitochondria provide energy that may be used for platelet activation and platelet-mediated blood clotting. Both platelet activation and intraplatelet granule secretion are energy-dependent processes. Moreover, in the course of platelet activation the rates of both glycolysis and oxidative phosphorylation increase, thus reflecting the increased energy requirements for the functioning of blood platelets [1]. The role of mitochondria as a supplier of ATP is so important in the course of platelet response to stimulating agents, that the inhibition of mitochondrial respiration has been found to reduce dense granule secretion and aggregation of platelets [2]. Therefore, the impaired functioning of platelet mitochondria may lead to altered platelet reactivity profile and relevantly altered responses of stimulated platelets.

OUR RESULTS AND CONCLUSIONS: Greater activation of circulating (resting) blood platelets was observed in streptozotocin-diabetic rats compared to their non-diabetic littermates. Diabetic platelets were also characterized by significantly elevated mitochondria mass, increased mitochondrial membrane potential and enhanced respiration, although the respiration control ratios appear to remain unchanged. Moreover, higher mitochondrial membrane potential and elevated mitochondrial respiration were closely related to the excessive activation of circulating platelets in diabetic animals. Interestingly, diabetic and healthy blood platelets differed also in response to insulin treatment. The incubation of diabetic platelets with insulin resulted in the elevated mitochondrial respiration, whereas no changes were observed in healthy platelets [3]. Our results indicate that long-term untreated diabetes may change blood platelet bioenergetics. These phenomena may be the result of the adaptation of blood platelets to much higher availability of energy substrates in diabetes. Observed alterations may be a potential underlying cause of abnormal platelet functioning in diabetes mellitus, however further research to validate this conclusion seems mandatory.


β€’ O2k-Network Lab: PL Lodz Watala C


Labels: MiParea: Respiration, mt-Biogenesis;mt-density, mt-Membrane  Pathology: Diabetes 

Organism: Rat  Tissue;cell: Blood cells, Platelet 





Affiliation

Dept Haemostasis and Haemostatic Disorders, Chair of Biomedical Sc, Med Univ Lodz, Poland. - [email protected]

References

  1. Zharikov S, Shiva S (2013) Platelet mitochondrial function: from regulation of thrombosis to biomarker of disease. Biochem Soc Trans 41:118-23.
  2. Barile CJ, Herrmann PC, Tyvoll DA, Collman JP, Decreau RA, Bull BS (2012) Inhibiting platelet-stimulated blood coagulation by inhibition of mitochondrial respiration. Proc Natl Acad Sci U S A 109:2539-43.
  3. Siewiera K, Kassassir H, Talar M, Wieteska L, Watala C (2016) Higher mitochondrial potential and elevated mitochondrial respiration are associated with excessive activation of blood platelets in diabetic rats. Life Sci 10. Bioblast Link