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Impact of Pro-Inflammatory Mediators on Agonist-Induced Platelet Aggregation
Author(s):
1. Samra Fatima: Quaid-i-Azam University, Islamabad, Pakistan
2. Durre Shehwar: Quaid-i-Azam University, Islamabad, Pakistan
3. Muhammad Rizwan Alam: Quaid-i-Azam University, Islamabad, Pakistan
Abstract:
Platelets are multi-functional cells which besides playing their role in homeostasis also contribute to immunity when activated via their immune receptors. The immunological responses are associated with platelet activation which can be further enhanced by various proinflammatory mediators. In this study we investigated the role of different pro-inflammatory molecules on the priming of agonist-induced platelet aggregation responses. For this purpose, we employed several Pathogen/Damage Associated Molecular Patterns (PAMP/DAMPS) like FMLP, glucose, FMLP treated blood cell supernatant, mitochondrial DNA (mtDNA) and mitochondrial proteins (mt proteins). We isolated platelets, manually counted them and after treatment with a priming agent stimulated with adenosinediphosphate (ADP) and adrenaline (AD). Extent of aggregation was noted by using a time- lapse spectrophotometric assay. A notable aggregation of platelets in response to ADP and AD was found. Interestingly, we observed a significant difference of AD-evoked aggregation in mtDNA primed group as compared to control. We surprisingly found no significant alteration in platelet aggregation profiles after pre-treatment with other priming agents such as FMLP, Glucose, FMLP-treated blood cell lysate, mt protein). In summary, we found a so far unreported accelerated AD-dependent platelet aggregation upon priming with mtDNA. However, these findings require further experimentation to determine the exact molecular mechanism involved in this phenomenon.
Page(s): 0-0
DOI: DOI not available
Published: Journal: First International Conference on Revamped Scientific Outlook of 21st Century (Abstract Book), Volume: 0, Issue: 0, Year: 2022
Keywords:
Platelets , immunity , PAMPs , DAMPs , Proinflammatory mediators , Hemostasis
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