School Of Basic And Applied Sciences

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Author: search.filters.author.Yadav, PoojaSubject: search.filters.subject.Platelets

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    Platelet-derived microvesicles activate human platelets via intracellular calcium mediated reactive oxygen species release
    (Academic Press Inc., 2022-08-28T00:00:00) Yadav, Pooja; Beura, Samir Kumar; Panigrahi, Abhishek Ramachandra; Bhardwaj, Taniya; Giri, Rajanish; Singh, Sunil Kumar
    Platelet-derived microvesicles (PMVs) are the most abundant microvesicles in circulation, originating from blood platelets via membrane blebbing. PMVs act as biological cargo carrying key molecules from platelets, including immunomodulatory molecules, growth factors, clotting molecules, and miRNAs that can regulate recipient cellular functions. Formation and release of PMVs play an essential role in the pathophysiology of vascular diseases such as hemostasis, inflammation, and thrombosis. Platelet activation is considered the critical event in thrombosis, and a growing number of evidence suggests that oxidative stress-mediated signaling plays a significant role in platelet activation. Ca2+ is a notable player in the generation of ROS in platelets. Reports have established that microvesicles exhibit dual nature in redox mechanisms as they possess both pro-oxidant and antioxidant machinery. However, the impact of PMVs and their ROS machinery on platelets is still a limited explored area. Here, we have demonstrated that PMVs mediate platelet activation via intracellular ROS generation. PMVs interacted with platelets and induced calcium-mediated intracellular ROS production via NADPH oxidase (NOX), leading to platelet activation. Our findings will open up new insights into the tangible relationship of PMVs with platelets and will further contribute to the therapeutic aspects of PMVs in vascular injury and tissue remodeling. � 2022
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    Role of Neurons and Glia Cells in Wound Healing as a Novel Perspective Considering Platelet as a Conventional Player
    (Springer, 2021-10-11T00:00:00) Beura, Samir K.; Panigrahi, Abhishek R.; Yadav, Pooja; Agrawal, Siwani; Singh, Sunil K.
    Wound healing is a complex physiological process in which the damaged or injured tissue is replaced or regenerated by new cells or existing cells respectively in their synthesized and secreted matrices. Several cells modulate the process of wound healing including macrophages, fibroblasts, and keratinocytes. Apart from these cells, platelet has been considered as a major cellular fragment to be involved in wound healing at several stages by secreting its granular contents including growth factors, thus resulting in coagulation, inflammation, and angiogenesis. A distant cell, which is gaining significant attention nowadays due to its resemblance with platelet in several aspects, is the neuron. Not only neurons but also glia cells are also confirmed to regulate wound healing at different stages in an orchestrated manner. Furthermore, these neurons and glia cells mediate wound healing inducing tissue repair and regeneration apart from hemostasis, angiogenesis, and inflammation by secreting various growth factors, coagulation molecules, immunomodulatory molecules as well as neurohormones, neuropeptides, and neurotrophins. Therefore, in wound healing platelets, neurons and glia cells not only contribute to tissue repair but are also responsible for establishing the wound microenvironment, thus affecting the proliferation of immune cells, fibroblast, and keratinocytes. Here in this review, we will enlighten the physiological roles of neurons and glia cells in coordination with platelets to understand various cellular and molecular mechanism in brain injury and associated neurocognitive impairments. � 2021, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.