Sonkar 2013 Abstract MiP2013: Difference between revisions

From Bioblast
No edit summary
No edit summary
Line 10: Line 10:
}}
}}
{{Labeling
{{Labeling
|tissues=Blood Cell; Suspension Culture
|tissues=Blood cells
|preparations=Intact cells
|preparations=Intact cells
|instruments=Oxygraph-2k
|instruments=Oxygraph-2k

Revision as of 09:14, 9 August 2013

Sonkar VK, Dash D, Kulkarn PP (2013) Platelets, amyloid beta and mitochondrial respiration. Mitochondr Physiol Network 18.08.

Link:

Sonkar VK, Dash D, Kulkarn PP (2013)

Event: MiP2013

Vijay K Sonkar

Platelets or thrombocytes are the key players in hemostasis and contain >90% of the circulating amyloid precursor protein, which upon proteolytic cleavage by Ξ²-secretase BACE1 (Ξ²-site APP cleaving enzyme 1) and the presenilin-containing Ξ³-secretase complex produces amyloid beta peptide (AΞ²). AΞ², 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 AΞ² active fragment containing amino acid sequence 25-35 (AΞ²25-35) on platelet activity and mitochondrial respiration. Exogenous AΞ²25-35 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. AΞ²25-35 also induced ATP release indicative of secretion from platelet dense granules. High-resolution respirometry (HRR) showed that AΞ²25-35 elicited sharp rise in mitochondrial respiration in intact platelets. Thus, AΞ² induced platelet activation that was associated with an increase in oxygen consumption rate.

β€’ Keywords: Platelets, Amyloid beta (AΞ²25-35), ATP, Mitochondrial respiration

β€’ O2k-Network Lab: IN Varanasi Dash D


Labels:


Tissue;cell: Blood cells  Preparation: Intact cells 



HRR: Oxygraph-2k 



Affiliations and author contributions

Department of Biochemistry, Institute of Medical Sciences, Banaras Hindu University, Varanasi, India.

Email: [email protected]

References

  1. Smith CCT (1997) Stimulated release of the b-amyloid protein of Alzheimer’s disease by normal human platelets. Neurosci Lett 235: 157–159.
  2. Hsu MJ, Hsu CY, Chen BC, Chen MC, Ou G, Lin CH, (2007) Apoptosis signal regulating kinase 1 in amyloid beta peptide-induced cerebral endothelial cell apoptosis. J Neurosci 27: 5719–5729.
  3. Shen MY, Hsiao G, Fong TH, Chen HM, Chou DS, Lin CH, Sheu JR, Hsu CY (2008) Amyloid beta peptide-activated signal pathways in human platelets. Euro J Pharmacol 588: 259-266
Cookies help us deliver our services. By using our services, you agree to our use of cookies.