phosphatidylserineexposed

Phosphatidylserine-exposed, or exposure of phosphatidylserine, refers to the presentation of the phospholipid phosphatidylserine on the outer leaflet of the cell’s plasma membrane. In healthy cells, PS is predominantly located on the cytosolic side due to the activity of flippases that maintain membrane asymmetry. Externalization describes a loss of this asymmetry and is observed under various physiological and pathological conditions.

Mechanisms of PS exposure involve scramblases and changes in enzyme activity. During apoptosis, caspase activation leads to inactivation of flippases and activation of caspase-dependent scramblases, resulting in PS translocation to the outer membrane. Two major pathways include caspase-activated scramblases such as Xkr8 and calcium-activated scramblases such as TMEM16F. In platelets, PS exposure occurs upon activation and contributes to the formation of a procoagulant surface that supports coagulation reactions.

Functional significance includes signaling for clearance and immune regulation as well as involvement in coagulation. PS exposure acts as an “eat-me” signal for phagocytes, promoting the removal of dying cells and helping maintain self-tolerance. It also provides a negatively charged surface that catalyzes the assembly of coagulation factor complexes, accelerating thrombin generation. The duration and extent of PS exposure vary by cell type and stimulus, influencing downstream outcomes.

Detection and relevance: PS exposure is commonly detected by annexin V or lactadherin binding assays in flow cytometry or microscopy. Clinically and experimentally, PS exposure is used as a biomarker for apoptosis or cell activation and is explored in contexts such as cancer, autoimmune disease, infections, and therapies that target PS for drug delivery or immunomodulation.