ArticleAmerican journal of translational research2026
Prolactin-induced platelet activation and endothelial dysfunction in coronary artery disease: insights into PKC and TXA2 pathways.
Article in American journal of translational research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundElevated prolactin level is associated with an increased risk of coronary artery disease (CAD), probably through promoting vascular inflammation and thrombosis. This study investigated whether prolactin exacerbates atherothrombosis by regulating endothelial dysfunction and platelet activation and further explored the underlying mechanisms.
methodsA co-culture model of human umbilical vein endothelial cells (HUVECs) and platelets was employed to simulate the vascular interface. The effects of prolactin, alone or in combination with a protein kinase C (PKC) inhibitor or aspirin (a thromboxane A2 [TXA2] pathway inhibitor) were assessed. Endothelial activation was assessed by measuring proliferation, the expression of adhesion molecules vascular cell adhesion molecule 1 (VCAM-1) and intercellular cell adhesion molecule 1 (ICAM-1), and the production of inflammatory cytokines interleukin (IL)-6 and IL-1β in HUVECs. Platelet function was analyzed by measuring CD61 expression, surface levels of P-selectin and CD40L, and the release of platelet microparticles (PMPs).
resultsProlactin significantly enhanced endothelial proliferation and the expression of adhesion molecules and inflammatory cytokines. Concurrently, it enhanced platelet aggregation and increased the surface expression of activation markers (P-selectin, CD40L) and pro-thrombotic PMPs. These effects were mediated through the PKC pathway, as they were markedly reversed by PKC inhibition. Prolactin partially restored endothelial and platelet activation even in the presence of aspirin, indicating an additional role for the TXA2 pathway.
conclusionProlactin coordinately exacerbates endothelial dysfunction and platelet activation through PKC and TXA2 pathway activation. These findings identify a dual-pathway mechanism by which prolactin may promote a pro-thrombotic state, contributing to the pathogenesis of atherothrombosis in CAD.
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