title: Higher mitochondrial potential and elevated mitochondrial respiration are associated with excessive activation of blood platelets in diabetic rats.
abstract: OBJECTIVE
  The high glucose concentration observed in diabetic patients is a recognized factor of mitochondrial damage in various cell types. Its impact on mitochondrial bioenergetics in blood platelets remains largely vague. The aim of the study was to determine how the metabolism of carbohydrates, which has been impaired by streptozotocin-induced diabetes may affect the functioning of platelet mitochondria.
  
  
  METHODS
  Diabetes was induced in Sprague Dawley rats by intraperitoneal injection of streptozotocin. Platelet mitochondrial respiratory capacity was monitored as oxygen consumption (high-resolution respirometry). Mitochondrial membrane potential was assessed using a fluorescent probe, JC-1. Activation of circulating platelets was monitored by flow cytometry measuring of the expressions of CD61 and CD62P on a blood platelet surface. To determine mitochondrial protein density in platelets, Western Blot technique was used.
  
  
  RESULTS
  The results indicate significantly elevated mitochondria mass, increased mitochondrial membrane potential (ΔΨm) and enhanced respiration in STZ-diabetic animals, although the respiration control ratios appear to remain unchanged. Higher ΔΨm and elevated mitochondrial respiration were closely related to the excessive activation of circulating platelets in diabetic animals.
  
  
  CONCLUSIONS
  Long-term diabetes can result in increased mitochondrial mass and may lead to hyperpolarization of blood platelet mitochondrial membrane. These alterations may be a potential underlying cause of abnormal platelet functioning in diabetes mellitus and hence, a potential target for antiplatelet therapies in diabetes.
authors.affiliation: Department of Haemostasis and Haemostatic Disorders, Medical University of Lodz, Mazowiecka 6/8, 92-215 Lodz, Poland. Electronic address: ksiewiera@gmail.com.
authors.forename: Karolina
authors.initials: K
authors.lastname: Siewiera
authors.affiliation: Department of Haemostasis and Haemostatic Disorders, Medical University of Lodz, Mazowiecka 6/8, 92-215 Lodz, Poland.
authors.forename: Hassan
authors.initials: H
authors.lastname: Kassassir
authors.affiliation: Department of Haemostasis and Haemostatic Disorders, Medical University of Lodz, Mazowiecka 6/8, 92-215 Lodz, Poland.
authors.forename: Marcin
authors.initials: M
authors.lastname: Talar
authors.affiliation: Department of Medical Biochemistry, Medical University of Lodz, Mazowiecka 6/8, 92-215 Lodz, Poland.
authors.forename: Lukasz
authors.initials: L
authors.lastname: Wieteska
authors.affiliation: Department of Haemostasis and Haemostatic Disorders, Medical University of Lodz, Mazowiecka 6/8, 92-215 Lodz, Poland.
authors.forename: Cezary
authors.initials: C
authors.lastname: Watala
mesh_terms: D000818:Animals; D001792:Blood Platelets / Q000378:metabolism*; D019069:Cell Respiration / Q000502:physiology; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism*; D008297:Male; D053078:Membrane Potential, Mitochondrial / Q000502:physiology*; D008928:Mitochondria / Q000378:metabolism*; D010101:Oxygen Consumption / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley
keywords: Blood platelets; Diabetes mellitus; Mitochondrial membrane potential; Mitochondrial respiration; Platelet activation and reactivity