Amyloid beta and its naturally occurring N-terminal variants are potent activators of human and mouse formyl peptide receptor 1.

ABSTRACT: Formyl peptide receptors (FPRs) may contribute to inflammation in Alzheimer's disease through interactions with neuropathological Amyloid beta (Aβ) peptides. Previous studies reported activation of FPR2 by Aβ_1-42, but further investigation of other FPRs and Aβ variants is needed. This study provides a comprehensive overview of the interactions of mouse and human FPRs with different physiologically relevant Aβ-peptides using transiently transfected cells in combination with calcium imaging. We observed that, in addition to hFPR2, all other hFPRs also responded to Aβ_1-42, Aβ_1-40, and the naturally occurring variants Aβ_11-40 and Aβ_17-40. Notably, Aβ_11-40 and Aβ_17-40 are very potent activators of mouse and human FPR1,

SUBMITTER: Busch L 

PROVIDER: S-EPMC9694488 | biostudies-literature | 2022 Oct

REPOSITORIES: biostudies-literature