We are analyzing https://link.springer.com/article/10.1007/s10585-014-9660-7.

Title:
Living in shear: platelets protect cancer cells from shear induced damage | Clinical & Experimental Metastasis
Description:
Pharmacologically and genetically induced thrombocytopenia is associated with decreased metastasis, highlighting the importance of platelets in the bloodborne dissemination of cancer cells. It is frequently suggested that platelets support metastasis, in part, by protecting cancer cells from shear stress, a biomechanical force generated by blood flow. However, there is currently no evidence to support this hypothesis. To address this, we investigated the effect of shear stress on A2780 ovarian cancer cells in the presence and absence of platelets. Using a cone and plate viscometer, suspensions of A2780 cells with and without platelets were exposed to shear rates representing venous (200 s−1) and arterial (1,500 s−1) blood flow. Lactate dehydrogenase (LDH) release was used to quantify shear induced membrane damage. Both venous and arterial shear rates induced the release of LDH from A2780 cells, demonstrating their susceptibility to shear forces. In contrast, platelets released minimal levels of LDH in response to similar conditions. In the presence of platelets, there was a significant decrease in LDH release by A2780 cells under shear conditions, suggesting that platelets can confer protection against shear induced damage. The disruption of platelet–cancer cell interactions could increase the shear stress induced destruction of cancer cells in vivo.
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Keywords {🔍}

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Topics {✒️}

month download article/chapter shear-induced platelet aggregation tumor-induced platelet aggregation niamh cooke & dermot kenny shear-mediated platelet activation platelet-derived mhc class platelet–cancer cell interactions degranulation induce pro-survival platelet-secreted matrix proteins biomedical diagnostics institute shear induced damage caspase-mediated activation matrix metalloproteinase-2 contributes full article pdf biomechanical force generated related subjects natural killer cytotoxicity natural killer cells metastatic prostate cancer matrix metalloproteinase expression privacy choices/manage cookies genetically induced thrombocytopenia platelet–cancer interactions alonso-escolano circulating apoptotic cells red blood cell hemodynesamic shear stress shear stress modulates article egan cell surface sialylation increased platelet reactivity platelet aggregating material platelet adhesion platelets support metastasis platelet tumor interaction cancer cells induces pro-angiogenic signalling cellular therapeutics metastatic esophageal cancer protecting tumor cells ovarian cancer cells dermot kenny niamh cooke protecting cancer cells european economic area high frequency components protease-activated receptors syngenic mouse models virally-transformed tumors sv3t3 mouse fibroblast

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         description:Pharmacologically and genetically induced thrombocytopenia is associated with decreased metastasis, highlighting the importance of platelets in the bloodborne dissemination of cancer cells. It is frequently suggested that platelets support metastasis, in part, by protecting cancer cells from shear stress, a biomechanical force generated by blood flow. However, there is currently no evidence to support this hypothesis. To address this, we investigated the effect of shear stress on A2780 ovarian cancer cells in the presence and absence of platelets. Using a cone and plate viscometer, suspensions of A2780 cells with and without platelets were exposed to shear rates representing venous (200 s−1) and arterial (1,500 s−1) blood flow. Lactate dehydrogenase (LDH) release was used to quantify shear induced membrane damage. Both venous and arterial shear rates induced the release of LDH from A2780 cells, demonstrating their susceptibility to shear forces. In contrast, platelets released minimal levels of LDH in response to similar conditions. In the presence of platelets, there was a significant decrease in LDH release by A2780 cells under shear conditions, suggesting that platelets can confer protection against shear induced damage. The disruption of platelet–cancer cell interactions could increase the shear stress induced destruction of cancer cells in vivo.
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