Amyloid β protein negatively regulates human platelet activation induced by thrombin receptor-activating protein

Amyloid β protein deposition in cerebral vessels, a characteristic of Alzheimer's disease, is a risk factor for intracerebral hemorrhage. Amyloid β protein directly modulates human platelet function; however, the exact mechanism of action is unclear. Therefore, we investigated the effects of am...

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Published in:Bioscience, biotechnology, and biochemistry biotechnology, and biochemistry, 2022-01, Vol.86 (2), p.185-198
Main Authors: Mizutani, Daisuke, Tokuda, Haruhiko, Onuma, Takashi, Uematsu, Kodai, Nakashima, Daiki, Ueda, Kyohei, Doi, Tomoaki, Enomoto, Yukiko, Matsushima-Nishiwaki, Rie, Ogura, Shinji, Iida, Hiroki, Kozawa, Osamu, Iwama, Toru
Format: Article
Language:English
Subjects:
Amyloid beta-Peptides
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Summary:Amyloid β protein deposition in cerebral vessels, a characteristic of Alzheimer's disease, is a risk factor for intracerebral hemorrhage. Amyloid β protein directly modulates human platelet function; however, the exact mechanism of action is unclear. Therefore, we investigated the effects of amyloid β protein on human platelet activation using an aggregometer with laser scattering. Amyloid β protein decreased platelet aggregation induced by thrombin receptor-activating protein, but not by collagen and ADP. Amyloid β protein also suppressed platelet aggregation induced by SCP0237 and A3227. Platelet-derived growth factor-AB secretion and phosphorylated-heat shock protein 27 release by thrombin receptor-activating protein were inhibited by amyloid β protein. Additionally, thrombin receptor-activating protein-induced phosphorylation of JNK and p38 MAP kinase was reduced by amyloid β protein. Collectively, our results strongly suggest that amyloid β protein negatively regulates protease-activated receptor-elicited human platelet activation. These findings may indicate a cause of intracerebral hemorrhage due to amyloid β protein.
ISSN:1347-6947
1347-6947
DOI:10.1093/bbb/zbab201