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Prolactin-induced platelet activation and endothelial dysfunction in coronary artery disease: insights into PKC and
Jingren Li1,2, Chong Wang1, Shuping Li1
1Department of Cardiology, Beijing Chest Hospital, Capital Medical University Beijing 101149, China.
Insights
Elevated prolactin levels worsen coronary artery disease (CAD) by increasing endothelial dysfunction and platelet activation via protein kinase C (PKC) and thromboxane A2 (TXA2) pathways, promoting atherothrombosis.
Area of Science:
- Cardiovascular Biology
- Endothelial Function
- Platelet Physiology
Background:
- Elevated prolactin is linked to increased coronary artery disease (CAD) risk.
- Prolactin may promote atherothrombosis via vascular inflammation and thrombosis.
Purpose of the Study:
- Investigate if prolactin exacerbates atherothrombosis.
- Determine prolactin's role in endothelial dysfunction and platelet activation.
- Explore the underlying molecular mechanisms.
Main Methods:
- Used a co-culture model of human umbilical vein endothelial cells (HUVECs) and platelets.
- Assessed prolactin's effects alone and with protein kinase C (PKC) inhibitor or aspirin (TXA2 inhibitor).
- Measured endothelial activation markers (proliferation, VCAM-1, ICAM-1, IL-6, IL-1β) and platelet function (P-selectin, CD40L, PMPs).
Main Results:
- Prolactin increased endothelial proliferation, adhesion molecules, and inflammatory cytokines.
- Prolactin enhanced platelet aggregation, activation markers (P-selectin, CD40L), and pro-thrombotic platelet microparticles (PMPs).
- Effects were mediated by PKC and partially by TXA2 pathways.
Conclusions:
- Prolactin exacerbates endothelial dysfunction and platelet activation.
- A dual-pathway mechanism involving PKC and TXA2 activation by prolactin promotes a pro-thrombotic state.
- Prolactin contributes to the pathogenesis of atherothrombosis in CAD.
Background:
Elevated 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.
Methods:
A 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).
Results:
Prolactin 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.
Conclusion:
Prolactin 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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