Browsing by Author "Ayusman Dash"

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Aspirin delimits platelet life span by proteasomal inhibition
(Public Library of Science, 2014) Manasa K. Nayak; Ayusman Dash; Nitesh Singh; Debabrata Dash
Aspirin is widely used in clinical settings as an anti-inflammatory and anti-platelet drug due its inhibitory effect on cyclooxygenase activity. Although the drug has long been considered to be an effective and safe therapeutic regime against inflammatory and cardiovascular disorders, consequences of its cyclooxygenase-independent attributes on platelets, the key players in thrombogenesis, beg serious investigation. In this report we explored the effect of aspirin on platelet lifespan in murine model and its possible cytotoxicity against human platelets in vitro. Aspirin administration in mice led to significant reduction in half-life of circulating platelets, indicative of enhanced rate of platelet clearance. Aspirin-treated human platelets were found to be phagocytosed more efficiently by macrophages, associated with attenuation in platelet proteasomal activity and upregulation of conformationally active Bax, which were consistent with enhanced platelet apoptosis. Although the dosage of aspirin administered in mice was higher than the therapeutic regimen against cardiovascular events, it is comparable with the recommended anti-inflammatory prescription. Thus, above observations provide cautionary framework to critically re-evaluate prophylactic and therapeutic dosage regime of aspirin in systemic inflammatory as well as cardiovascular ailments. © 2014 Nayak et al.
Correction to: Plasma fibrinogen is a natural deterrent to amyloid β-induced platelet activation and neuronal toxicity (Molecular Medicine (2016) 22 (224-232) DOI: 10.2119/molmed.2016.00003)
(BioMed Central Ltd., 2019) Vijay K. Sonkar; Paresh P. Kulkarni; Susheel N. Chaurasia; Ayusman Dash; Abhishek Jauhari; Devendra Parmar; Sanjay Yadav; Debabrata Dash
Following publication of the original article [1], the author reported an error in Figure 1. The correct version of Figure 1 is as follows: (Figure Presented). © 2019 The Author(s).
Plasma fibrinogen is a natural deterrent to amyloid β–induced platelet activation and neuronal toxicity
(Uninversity of Michigan, 2016) Vijay K. Sonkar; Paresh P. Kulkarni; Susheel N. Chaurasia; Ayusman Dash; Abhishek Jauhari; Devendra Parmar; Sanjay Yadav; Debabrata Dash
Alzheimer’s disease (AD) is a devastating neurodegenerative disorder, characterized by extensive loss of neurons and deposition of amyloid β (Aβ) in the form of extracellular plaques. Aβ is considered to have a critical role in synaptic loss and neuronal death underlying cognitive decline. Platelets contribute to 95% of circulating amyloid precursor protein that releases Aβ into circulation. We have recently demonstrated that the Aβ active fragment containing amino acid sequence 25–35 (Aβ25–35) is highly thrombogenic in nature and elicits strong aggregation of washed human platelets in a RhoA-dependent manner. In this study, we evaluated the influence of fibrinogen on Aβ-induced platelet activation. Intriguingly, Aβ failed to induce aggregation of platelets suspended in plasma but not in buffer. Fibrinogen brought about dose-dependent decline in aggregatory response of washed human platelets elicited by Aβ25–35, which could be reversed by increasing doses of Aβ. Fibrinogen also attenuated Aβ-induced platelet responses such as secretion, clot retraction, rise in cytosolic Ca+2 and reactive oxygen species. Fibrinogen prevented intracellular accumulation of full-length Aβ peptide (Aβ42) in platelets as well as neuronal cells. We conclude that fibrinogen serves as a physiological check against the adverse effects of Aβ by preventing its interaction with cells. © 2016, Uninversity of Michigan. All rights reserved.