Sonkar 2013 Abstract MiP2013
|Sonkar VK, Dash D, Kulkarn PP (2013) Platelets, amyloid beta and mitochondrial respiration. Mitochondr Physiol Network 18.08.|
Platelets or thrombocytes are the key players in hemostasis and contain >90% of the circulating amyloid precursor protein, which upon proteolytic cleavage by β-secretase BACE1 (β-site APP cleaving enzyme 1) and the presenilin-containing γ-secretase complex produces amyloid beta peptide (Aβ). Aβ, a major mediator of neuronal death, is also cytotoxic to cerebral endothelial cells, vascular smooth muscle cells and can accumulate in the cerebral blood vessels leading to cerebral amyloid angiopathy. In this report we have evaluated the effect of Aβ active fragment containing amino acid sequence 25-35 (Aβ25-35) on platelet activity and mitochondrial respiration. Exogenous Aβ25-35 was found to induce platelet aggregation, PAC-1binding and P-selectin exposure in washed human platelets, which was comparable to that induced by other physiological agonists. Aβ25-35 also induced ATP release indicative of secretion from platelet dense granules. High-resolution respirometry (HRR) showed that Aβ25-35 elicited sharp rise in mitochondrial respiration in intact platelets. Thus, Aβ induced platelet activation that was associated with an increase in oxygen consumption rate.
• Keywords: Platelets, Amyloid beta (Aβ25-35)
• O2k-Network Lab: IN Varanasi Dash D
Labels: MiParea: Respiration, mt-Medicine Pathology: Alzheimer's, Neurodegenerative
Organism: Human Tissue;cell: Blood cells Preparation: Intact cells
Regulation: ATP Coupling state: ROUTINE
Department of Biochemistry, Institute of Medical Sciences, Banaras Hindu University, Varanasi, India.
- Corresponding author: email@example.com
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