Dr hab. Anna Gromotowicz-Popławska from the Department of Biopharmacy MUB in cooperation with scientists from Harvard Medical School in Boston, published in the Journal of the American Heart Association the results of a study on the protective effect of striatins in the haemostatic system – “Enhanced Thrombotic Responses Are Associated With Striatin Deficiency and Aldosterone”
Striatins play an important role as signaling proteins in the non-genomic effects of aldosterone on homeostasis and blood pressure. Experimental studies have shown that a mouse model lacking one functional copy of striatin (Strn+/-) shows elevated blood aldosterone levels, salt sensitivity of blood pressure, enhanced vasoconstriction and decreased vascular relaxation. Moreover, clinical studies confirm that individuals who carry rs2540923, a single nucleotide polymorphic gene variant of striatin, exhibit salt sensitivity of blood pressure. Previous study from the Department of Biopharmacy showed that aldosterone enhances the experimental thrombotic process in a mechanism dependent on non-genomic signaling. Research conducted in Boston by dr hab. Anna Gromotowicz-Popławska was to determine the role of striatins in the prothrombotic effect of aldosterone.
The studies were performed in a model of laser-induced thrombosis in cremaster arterioles in Strn+/- mice, the control group was the 'wild type' strain (WT). Thrombus formation was observed intravitaly with confocal microscopy. Additionally, the animals received a single intravenous dose of aldosterone. The dynamics of thrombus formation, platelet involvement and fibrin deposition within the thrombus formation were measured.
The studies showed an increased thrombotic process in Strn+/- mice, compared to WT, in a mechanism dependent on increased platelet activation and fibrin accumulation within the thrombus. Additionally, it was observed that the prothrombotic effect of aldosterone is definitely more pronounced in Strn+/- than in WT mice. These results indicate that striatins, the main mediators of the non-genomic effects of aldosterone, have a protective effect in the cardiovascular system and haemostasis, since striatin deficiency enhances the thrombotic process and the prothrombotic effect of aldosterone as well.
The results of the experiment are translational in nature, as they suggest that patients with hypertension and the striatin gene polymorphism may present a prothrombotic phenotype leading to increased risk of thrombotic events e.g. strokes and myocardial infarction. Currently, the team is preparing a grant application to the National Institutes of Health (USA) to finance a research project with further experimental research and clinical study on the role of striatins in thrombotic complications in patients with hypertension and the striatin gene polymorphism.
