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- Title
Amyloid β protein negatively regulates human platelet activation induced by thrombin receptor-activating protein.
- Authors
Daisuke Mizutani; Haruhiko Tokuda; Takashi Onuma; Kodai Uematsu; Daiki Nakashima; Kyohei Ueda; Tomoaki Doi; Yukiko Enomoto; Rie Matsushima-Nishiwaki; Shinji Ogura; Hiroki Iida; Osamu Kozawa; Toru Iwama
- Abstract
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.
- Subjects
THROMBIN receptors; BLOOD platelet activation; THROMBIN; AMYLOID; HEAT shock proteins; MITOGEN-activated protein kinases
- Publication
Bioscience, Biotechnology & Biochemistry, 2022, Vol 86, Issue 2, p185
- ISSN
0916-8451
- Publication type
Article
- DOI
10.1093/bbb/zbab201