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

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.

• 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
• Journal: Bioscience, biotechnology, and biochemistry (Biosci Biotechnol Biochem) Vol. 86 Issue 2 Pg. 185-198 (Jan 24 2022) ISSN: 1347-6947 [Electronic] England
• PMID: 34849571 (Publication Type: Journal Article)
• Copyright: © The Author(s) 2021. Published by Oxford University Press on behalf of Japan Society for Bioscience, Biotechnology, and Agrochemistry.

Chemical References

• Amyloid beta-Peptides

Topics

• Amyloid beta-Peptides