Hemostasis vs. Homeostasis: Platelets Are Essential for Preserving Vascular Barrier Function in the Absence of Injury

 

Platelets have a well-defined role, related to their primary function as regulators of hemostasis and thrombosis. Platelets are produced by megakaryocytes in the bone marrow and circulate for about 5–7 days in mice. Following a vascular injury, platelets become activated in the blood, resulting in adhesion to the exposed extracellular matrix, formation of a platelet plug, and finally formation and consolidation of a thrombus. On Sunday, Shuchi Gupta, Ph.D., of the University of Pennsylvania in Philadelphia, PA, presented her results on the role of platelets, their secretion machinery, and platelet signaling pathways in maintaining homeostasis vascular barrier function by studying changes in vascular permeability in thrombocytopenic and transgenic mice. This was assessed by measuring the extravasation of fluorescent dextran and albumin from capillaries and postcapillary venules in the murine skin microvasculature and meninges using multiphoton microscopy in vivo.

Gupta revealed that thrombocytopenia induced by immunodepletion or administration of busulfan caused a reduction in basal vascular barrier function. This was detectable through an increased extravasation of 40 kDa dextran, but not albumin, from dermal microcirculation. This reduction in barrier function required more than four hours to emerge and was reversed with partial recovery of circulating platelet counts. She further remarked that this finding, plus others as reported in the video, highlights the underappreciated role of platelets in maintaining vascular barrier function, which requires GPVI signaling and dense granule secretion. This homeostatic role is distinct from the platelet response to injury and inflammation.

Read the full abstract here.

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