Misiti, F.; Diotaiuti, P.; Lombardo, G.E.; Tellone, E. Sphingosine-1-Phosphate Decreases Erythrocyte Dysfunction Induced by Beta-Amyloid. Preprints2024, 2024031128. https://doi.org/10.20944/preprints202403.1128.v1
APA Style
Misiti, F., Diotaiuti, P., Lombardo, G.E., & Tellone, E. (2024). Sphingosine-1-Phosphate Decreases Erythrocyte Dysfunction Induced by Beta-Amyloid. Preprints. https://doi.org/10.20944/preprints202403.1128.v1
Chicago/Turabian Style
Misiti, F., Giovanni Enrico Lombardo and Ester Tellone. 2024 "Sphingosine-1-Phosphate Decreases Erythrocyte Dysfunction Induced by Beta-Amyloid" Preprints. https://doi.org/10.20944/preprints202403.1128.v1
Abstract
Background: Amyloid beta peptides (Aβ) have been identified as the main pathogenic agents in Alzheimer’s disease (AD). Soluble Aβ oligomers, rather than monomer or insoluble amyloid fibrils, show membrane-binding capacity to red blood cells (RBCs) and trigger several morphological and functional alterations in RBCs that can result in impaired oxygen transport and delivery. Since bioactive lipids have been recently proposed as potent protective agents against Aβ toxicity, we investigated the role of sphingosine-1-phosphate (S1P) in signaling pathways involved in the mechanism underlying ATP release in Aβ-treated RBCs.
Methods: In RBCs following different treatments, ATP, 2,3 DPG, cAMP levels, and caspase 3 activity were determined by spectrophotometric and immunoassay.
Results: S1P rescued the inhibition of ATP release from RBCs triggered by Aβ through a mechanism involving caspase-3 and restoring 2,3 DPG and cAMP levels within the cell.
Conclusions: These findings reveal the molecular basis of S1P protection against Aβ in RBCs and suggest new therapeutic avenues in AD.
Keywords
Sphingosine-1-phosphate; Band 3; erythrocyte; caspase-3; beta-amyloid; Alzheimer's disease
Subject
Biology and Life Sciences, Biochemistry and Molecular Biology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
