Lipopolysaccharide Potentiates Platelet Aggregation in Association with Apoptosis Through a Novel TLR4-Bax/Bcl-2-Mitochondrial Dysfunction Axis in Humans.

ABSTRACT: Platelets are anucleate cells whose dysregulation contributes to thrombocytopenia during sepsis. Thrombocytopenia is an early complication of Gram-negative infection, in which lipopolysaccharide (LPS) serves as a principal mediator; however, its precise contribution remains unclear. In this study, LPS, at concentration 10 µg/mL, did not induce human platelet aggregation but significantly potentiated low-dose collagen (0.5 μg/mL)-induced aggregation, ATP release, intracellular calcium levels ([Ca²⁺]i) and P-selectin expression. Scanning electron microscopy revealed that either collagen or LPS activated filopodia elongation in human platelets, whereas LPS combined with collagen further activated the phenotype of platelet activation (lamellipodia formation). Beyond these activation

SUBMITTER: Chen CC 

PROVIDER: S-EPMC12730485 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature