Abstract:
:The PI3K/Akt signaling pathway has been implicated in playing an important role in platelet activation during hemostasis and thrombosis involving platelet-matrix interaction and platelet aggregation. Its role in non-physiological shear stress (NPSS)-induced platelet activation relevant to high-shear blood contacting medical devices (BCMDs) is unclear. In the context of blood cells flowing in BCMDs, platelets are subjected to NPSS (>100 Pa) with very short exposure time (<1 s). In this study, we investigated whether NPSS with short exposure time induces platelet activation through the PI3K/Akt signaling pathway. Healthy donor blood treated with or without PI3K inhibitor was subjected to NPSS (150 Pa) with short exposure time (0.5 s). Platelet activation indicated by the surface P-selectin expression and activated glycoprotein (GP) IIb/IIIa was quantified using flow cytometry. The phosphorylation of Akt, activation of the PI3K signaling, was characterized by western blotting. Changes in adhesion behavior of NPSS-sheared platelets on fibrinogen, collagen, and von Willebrand factor (vWF) were quantified with fluorescent microscopy by perfusing the NPSS-sheared and PI3K inhibitor-treated blood through fibrinogen, collagen, and vWF-coated microcapillary tubes. The results showed that the PI3K/Akt signaling was involved with both NPSS-induced platelet activation and platelet-matrix interaction. NPSS-sheared platelets exhibited exacerbated platelet adhesion on fibrinogen, but had diminished platelet adhesion on collagen and vWF. The inhibition of PI3K signaling reduced P-selectin expression and GPIIb/IIIa activation with suppressed Akt phosphorylation and abolished NPSS-enhanced platelet adhesion on fibrinogen in NPSS-sheared blood. The inhibition of PI3K signaling can attenuate the adhesion of unsheared platelets (baseline) on collagen and vWF, while had no impact on adhesion of NPSS-sheared platelets on collagen and vWF. This study confirmed the important role of PI3K/Akt signaling pathway in NPSS-induced platelet activation. The finding of this study suggests that blocking PI3K/Akt signaling pathway could be a potential method to treat thrombosis in patients implanted with BCMDs.
journal_name
Artif Organsjournal_title
Artificial organsauthors
Chen Z,Li T,Kareem K,Tran D,Griffith BP,Wu ZJdoi
10.1111/aor.13465subject
Has Abstractpub_date
2019-09-01 00:00:00pages
897-908issue
9eissn
0160-564Xissn
1525-1594journal_volume
43pub_type
杂志文章abstract::A 68-year-old woman with fulminant hepatic failure of unknown etiology was treated with a bioartificial liver assist device. Prior to treatment, she had a number of clinical and laboratory features that suggested a hopeless outcome. Treatment was associated with a dramatic change in her mental status, and her clinical...
journal_title:Artificial organs
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doi:10.1111/j.1525-1594.1993.tb00381.x
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journal_title:Artificial organs
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journal_title:Artificial organs
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journal_title:Artificial organs
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pub_type: 杂志文章,随机对照试验
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journal_title:Artificial organs
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journal_title:Artificial organs
pub_type: 杂志文章
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pub_type: 杂志文章
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journal_title:Artificial organs
pub_type: 杂志文章
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journal_title:Artificial organs
pub_type: 杂志文章
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journal_title:Artificial organs
pub_type: 杂志文章,评审
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journal_title:Artificial organs
pub_type: 杂志文章
doi:10.1111/j.1525-1594.1995.tb02371.x
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journal_title:Artificial organs
pub_type: 杂志文章
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journal_title:Artificial organs
pub_type: 杂志文章
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pub_type: 杂志文章
doi:10.1111/aor.12294
更新日期:2014-12-01 00:00:00
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pub_type: 杂志文章
doi:10.1111/j.1525-1594.1997.tb00344.x
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journal_title:Artificial organs
pub_type: 杂志文章
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journal_title:Artificial organs
pub_type: 杂志文章
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