Key result
Advanced Huntington disease is associated with a progressive impairment of NO-mediated vasorelaxation, eNOS phosphorylation, and NO release in platelets compared to healthy controls.
Case-Control (n=83)
No
Platelet NO dysregulation worsens with Huntington Disease progression, suggesting peripheral eNOS/NO pathway changes could serve as a biomarker for advanced disease stages.
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May track Huntington disease progression via platelet NO impairment; hypothesis-generating and requires prospective validation before biomarker adoption.
Nitric oxide (NO) is a biologically active inorganic molecule involved in the regulation of many physiological processes, such as control of blood flow, platelet adhesion, endocrine function, neurotransmission and neuromodulation. In the present study, for the first time, we investigated the modulation of NO signaling in platelets of HD patients. We recruited 55 patients with manifest HD and 28 gender- and age-matched healthy controls. Our data demonstrated that NO-mediated vasorelaxation, when evoked by supernatant from insulin-stimulated HD platelets, gradually worsens along disease course. The defective vasorelaxation seems to stem from a faulty release of NO from platelets of HD patients and, it is associated with impairment of eNOS phosphorylation (Ser(1177)) and activity. This study provides important insights about NO metabolism in HD and raises the hypothesis that the decrease of NO in platelets of HD individuals could be a good tool for monitoring advanced stages of the disease.
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Carrizzo et al. (2014) conducted a case-control in Huntington Disease (n=83). Advanced Huntington Disease vs. Healthy controls and early-stage Huntington Disease was evaluated on NO-mediated vasorelaxation evoked by supernatant from insulin-stimulated platelets (p=<0.05). Advanced Huntington disease is associated with a progressive impairment of NO-mediated vasorelaxation, eNOS phosphorylation, and NO release in platelets compared to healthy controls.
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