Sonkar 2013 Abstract MiP2013: Difference between revisions
No edit summary |
No edit summary |
||
| Line 1: | Line 1: | ||
{{Abstract | {{Abstract | ||
|title=Sonkar VK, Dash D, Kulkarn PP (2013) Platelets, amyloid beta and mitochondrial respiration. Mitochondr Physiol Network 18.08. | |title=Sonkar VK, Dash D, Kulkarn PP (2013) Platelets, amyloid beta and mitochondrial respiration. Mitochondr Physiol Network 18.08. | ||
|info=[http://www.mitophysiology.org/?MiP2013 MiP2013], [[Laner 2013 Mitochondr Physiol Network MiP2013|Book of Abstracts Open Access]] | |info=[[File:SonkarV.jpg|150px|right|Vijay K Sonkar]] [http://www.mitophysiology.org/?MiP2013 MiP2013], [[Laner 2013 Mitochondr Physiol Network MiP2013|Book of Abstracts Open Access]] | ||
|authors=Sonkar VK, Dash D, Kulkarn PP | |authors=Sonkar VK, Dash D, Kulkarn PP | ||
|year=2013 | |year=2013 | ||
|event=MiP2013 Programme | |event=MiP2013 Programme | ||
|abstract= | |abstract=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. | ||
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. | |||
|keywords=Platelets, Amyloid beta (AΞ²25-35) | |keywords=Platelets, Amyloid beta (AΞ²25-35) | ||
|mipnetlab=IN Varanasi Dash D | |mipnetlab=IN Varanasi Dash D | ||
| Line 21: | Line 20: | ||
|additional=MiP2013 | |additional=MiP2013 | ||
}} | }} | ||
== Affiliations and author contributions == | == Affiliations and author contributions == | ||
Department of Biochemistry, Institute of Medical Sciences, Banaras Hindu University, Varanasi, India. Β | Department of Biochemistry, Institute of Medical Sciences, Banaras Hindu University, Varanasi, India. Β | ||
| Line 34: | Line 30: | ||
#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: 5719β5729. | #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: 5719β5729. | ||
#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 | #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 | ||
__TOC__ | |||
Revision as of 09:40, 15 September 2013
| Sonkar VK, Dash D, Kulkarn PP (2013) Platelets, amyloid beta and mitochondrial respiration. Mitochondr Physiol Network 18.08. |
Link:
MiP2013, Book of Abstracts Open Access
Sonkar VK, Dash D, Kulkarn PP (2013)
Event: MiP2013 Programme
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)
β’ 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
HRR: Oxygraph-2k
MiP2013
Affiliations and author contributions
Department of Biochemistry, Institute of Medical Sciences, Banaras Hindu University, Varanasi, India.
Email: [email protected]
- Corresponding author: [email protected]
References
- Smith CCT (1997) Stimulated release of the b-amyloid protein of Alzheimerβs disease by normal human platelets. Neurosci Lett 235: 157β159.
- 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: 5719β5729.
- 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
