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Platelets expressing CD36 may mediate microvascular occlusion either by facilitating clumping of iRBC (Pain et al, 2001) or by bridging adhesion of iRBC to endothelial cells (Bridges et al, 2010).
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The expression of eNOS may be induced by calcium-dependent binding of calmodulin via proinflammatory cytokines or by serine phosphorylation through the Akt pathway [ 19]. eNOS may mediate the systemic microvascular leak of VILI [ 20].
Other workers in our research group have found that eNOS but not inducible nitric oxide synthase may mediate the systemic microvascular leak in a rat model of VILI [ 20].
This may be important knowledge as inflammatory mechanisms related to coagulation activation, such as hyaline membrane formation and microvascular thrombosis, may mediate lung injury [ 2, 3].
Platelet monocyte complexes may mediate adherence to the brain microvascular endothelial cells promoting extravasation of platelet-monocytes complexes in the central nervous system (CNS) of HIV-infected patients with associated encephalitis [ 43].
In summary, CFH may mediate PGD through oxidative effects on microvascular permeability, which are augmented by hyperoxia and abrogated by acetaminophen.
Microvascular platelet aggregation following SAH is another potential mechanism which may mediate DCI secondary to small vessel thrombosis and cortical and subcortical ischemia.
Alternatively, periplasmic proteases may mediate proteostasis of these amyloidogenic proteins.
EN2 secretion may mediate anti-viral changes in the stroma.
Some of these channels may mediate mechanosensory responses.
Interestingly, the V ATPase complex is localized to the plasma membrane in human lung microvascular endothelial cells (Rojas et al. 2004) and rabbit alveolar macrophages (Heming and Bidani 2003), so that "mediatophore" may mediate ACh release from these cells.
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