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It has been reported that for cancer cells in order to form metastases, the cells proliferate locally, detach from the primary environment and migrate through the tissue and survive in the circulation, adhere and proliferate at a distant organ [ 62].
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Here EMT plays a major role in aiding the tumor cells to migrate out from the primary site, enter into the circulation and adhere to endothelial cells of target organs.
These findings are consistent with recent reports that NLRP3 activation and IL-1β in experimental liver injury can direct neutrophil trafficking by drawing neutrophils out of the circulation to adhere to the vascular endothelium at inflammation sites (McDonald et al, 2010).
This accumulation was reported to result from the circulating neutrophils that had marginated into the pulmonary circulation and adhered to endothelial cells in the alveolar wall before infiltrating into the alveolar space [ 36, 37].
sFlt-1 is secreted by the placenta into the maternal circulation and adheres to the receptor-binding domains of placental growth factor and vascular endothelial growth factor (VEGF), preventing interaction with endothelial receptors, blocking VEGF-mediated vasodilation and inducing endothelial dysfunction [ 8], considered to be key to the pathogenesis of preeclampsia [ 6].
Hematogenous metastasis of cancer consists of several steps enabling cancer cells to intravasate, to survive in the blood circulation and to adhere to the vessels, eventually extravasating and establishing new metastatic lesions.
In fact, in mouse models it has been shown that circulation-derived platelets adhere to the peritoneum surface [ 17].
After arterial circulation, some MSC adhered in tumour capillaries and later also in tumour venules and veins (vessel diameter 45 μm, centerline blood flow velocity of 800 μm/s with a resulting wall shear rate of 700 s−1).
Although many circulating tumour cells fail to survive this phase of the metastatic cascade, the establishment of metastases depends upon the arrest of surviving cells and their exit from the circulation, which involves adhering to and crossing the barriers imposed by the microvascular endothelium and extracellular matrix (Weiss, 1985; Fosse et al, 1987).
As the infected monocytes travel through the circulation, they may exhibit a greater propensity to adhere to endothelial cells and extravasate.
It has been known for many years that platelets localize and adhere to sites of bacterial lesions in the circulation, for example in endocarditis [80].
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