Activation of leukocytes with complement C5a is associated with prostanoid-dependent constriction of large arteries in atherosclerotic monkeys in vivo

Lessons learned from the porcine CARPA model: constant and variable responses to different nanomedicines and administration protocols

“…Accordingly, there is a great number of reports in the literature on C activation and its consequences in various animals, Brought to you by | University of Michigan Authenticated Download Date | 6/16/15 10:59 PM including rats (9,(29)(30)(31)(32)(33), mice (33), dogs (34)(35)(36)(37), rabbits (38,39) nonhuman primates (40)(41)(42)(43)(44)(45)(46)(47)(48)(49) and pigs (50)(51)(52)(53)(54)(55). Among these experimental systems, it is the pigs' response to C activator liposomes that best mimics the human infusion reactions to liposomes in terms of kinetics and spectrum of symptoms and the conditions of reaction induction (Table 1).…”

Linking the Pathobiology of Hypercholesterolemia with the Neutrophil Mechanotransduction

“…Although the increased activity of neutrophils is not associated with increased adhesion to microvascular endothelium [78], their increased numbers raise peripheral vascular resistance [110]. One possible explanation is that circulating activated neutrophils in SHRs release vasoactive substances that constrict the small arteries and arterioles; this has been documented for atherosclerosis [114][115][116]. Extensive evidence, however, points to a hemorheological effect of leukocyte activation on microvascular resistance [1,34,36].…”

Thrombin and Vascular Smooth Muscle Cell Proliferation: Implications for Atherosclerosis and Restenosis

“…Thrombin induces multiple events that are known to participate in the vascular response to injury such as activating platelets to aggregate and release serotonin, 10,11 releasing PDGF-BB from endothelial cells, 46 increasing vascular endothelial permeability, 7 inducing endothelial cell hyperadhesivity and neutrophil adhesion to endo thelial cell monolayers, 8 stimulating SMC contraction 9 and proliferation, 13 and inducing monocyte chemotaxis and proliferation. 12 The recruitment of these various cells to the site of injury can result in the generation of a host of cytokines (such as FGF, PDGF, TGF-β, and interleukin-1), [46][47][48][49][50] vasoactive substances (such as endothelin, serotonin, and prostaglandins), [51][52][53] and chemoattractants (such as MCP-1 and interleukin-6). 54 This in turn can result in further cell proliferation, migration, and recruit ment.…”