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Prolactin does not affect human platelet aggregation or secretion.

Anne Q Reuwer¹, Rienk Nieuwland, Isabelle Fernandez

¹Department of Vascular Medicine, Academic Medical Center, Amsterdam, The Netherlands. a.q.reuwer@amc.uva.nl

Thrombosis and Haemostasis

|June 4, 2009

Summary

This study investigated the pituitary hormone prolactin

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Area of Science:

Endocrinology
Hematology
Cardiovascular Research

Background:

Platelets are crucial in atherosclerotic plaque formation and rupture, leading to atherothrombosis.
Hormonal imbalances are implicated in atherothrombotic diseases, but their precise effects on platelet function remain debated.
The role of the pituitary hormone prolactin in platelet function requires clarification.

Purpose of the Study:

To determine if prolactin directly affects platelet activation and aggregation.
To investigate the presence of prolactin receptors on platelets.

Main Methods:

Platelet function was assessed using flow cytometry and optical/whole blood aggregation assays.
Blood samples from healthy males were exposed to varying concentrations of adenosine diphosphate (ADP) and prolactin.
Western blot and flow cytometry were used to detect prolactin receptors on platelets.

Main Results:

Prolactin, at concentrations of 50 and 1,000 microg/l, did not induce platelet activation or aggregation.
Prolactin did not enhance adenosine diphosphate (ADP)-induced platelet activation or aggregation.
Prolactin receptors were not detected on the platelet surface.

Conclusions:

The findings suggest that prolactin does not directly modulate human platelet function.
This study provides evidence against a direct role for prolactin in atherothrombosis via platelet modulation.