The mechanism of the endothelial supporting function of intact platelets

Johnson, Shirley A.; Balboa, Ronaldo S.; Dessel, B. H.; Monto, Raymond W.; Siegesmund, Kenneth A.; Greenwalt, Tibor J.

doi:10.1016/0014-4800(64)90045-0

Cited by 60 publications

(29 citation statements)

References 15 publications

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“…In fact, there were many polysomes around the degranulated platelets within the hepatocytes, suggesting an enhanced protein synthesis [11]. Such an entry of platelets into cells has also been observed in endothelial cells [34]. These behaviors of platelets may be related to their putative protective roles [11].…”

Section: Discussionmentioning

confidence: 91%

Hepatic platelet accumulation in Fas-mediated hepatitis in mice

Ohtaki

Yamaguchi

et al. 2009

International Immunopharmacology

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Section: Discussionmentioning

confidence: 91%

Hepatic platelet accumulation in Fas-mediated hepatitis in mice

Ohtaki

Yamaguchi

et al. 2009

International Immunopharmacology

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“…This finding was consistent with a previous report in which the phosphorylation of Akt was markedly enhanced when platelet microparticles were incorporated into endothelial cells. 25 Because activation of Akt contributes to cell proliferation and survival, we proposed that Akt signaling is involved in platelet phagocytosis to promote endothelial survival and proliferation. In this study, platelet incubation induced a moderate activation of ERK1/2 at 72 h. In contrast, Ranzato et al reported that endothelial proliferation was predominantly under the control of ERK1/2 signaling when the cells were stimulated by platelet lysates.…”

Section: Discussionmentioning

confidence: 99%

Phagocytosis of platelets enhances endothelial cell survival under serum deprivation

Ping

Ren

Lan

et al. 2015

Exp Biol Med (Maywood)

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Platelets are key players in fundamental processes of vascular biology, such as angiogenesis, tissue regeneration, and tumor metastasis. However, the underlying mechanisms remain unclear. In this study, some tumor vascular endothelial cells were positively stained by antiplatelet antibodies. Further investigation revealed that platelets were taken up by endothelial cells in vitro and in vivo. Human umbilical vascular endothelial cells were rendered apoptotic under conditions of serum deprivation. However, endothelial apoptosis was suppressed and cell viability was enhanced when platelets were added to the cultures. Endothelial survival was paralleled by an upregulation of phosphorylated Akt and p70 S6K. In conclusion, this study demonstrated that platelets can be phagocytosed by endothelial cells, and the phagocytosed platelets could suppress endothelial apoptosis and promote cell viability level. The mechanism underlying this process involves the activation of Akt signaling.

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“…Although platelets exert a trophic role on endothelium in physiological conditions [33], it has been proposed that an amplification of this phenomenon, particularly when endothelial cells are prestimulated by TNF, can lead to endothelial injury [16]. A possible role of platelets in microvascular pathology is supported by data in an experimental CM model in vivo and by the numerous mechanisms by which platelets can alter endothelial functions [27]; these mechanisms include an induction of the adhesiveness of endothelial cells for leukocytes, an enhancement of TNF-induced killing, and the modulation of leukocyte functions, notably the induction of their chemokine synthesis.…”

Section: Discussionmentioning

confidence: 99%

Platelet Accumulation in Brain Microvessels in Fatal Pediatric Cerebral Malaria

Mackenzie²,

et al. 2003

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The pathogenesis of fatal cerebral malaria (CM) is not well understood, in part because data from patients in whom a clinical diagnosis was established prior to death are rare. In a murine CM model, platelets accumulate in brain microvasculature, and antiplatelet therapy can improve outcome. We determined whether platelets are also found in cerebral vessels in human CM, and we performed immunohistopathology for platelet-specific glycoprotein, GPIIb-IIIa, on tissue from multiple brain sites in Malawian children whose fatal illness was severe malarial anemia, CM, or nonmalarial encephalopathy. Platelets were observed in 3 locations within microvessels: between malaria pigment and leukocytes, associated with malaria pigment, or alone. The mean surface area of platelet staining and the proportion of vessels showing platelet accumulation were significantly higher in patients with CM than in those without it. Platelet accumulation occurs in the microvasculature of patients with CM and may play a role in the pathogenesis of the disease.

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The mechanism of the endothelial supporting function of intact platelets

Cited by 60 publications

References 15 publications

Hepatic platelet accumulation in Fas-mediated hepatitis in mice

Hepatic platelet accumulation in Fas-mediated hepatitis in mice

Phagocytosis of platelets enhances endothelial cell survival under serum deprivation

Platelet Accumulation in Brain Microvessels in Fatal Pediatric Cerebral Malaria

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