Carrizzo Albino, Di Pardo Alba, Maglione Vittorio, Damato Antonio, Amico Enrico, Formisano Luigi, Vecchione Carmine, Squitieri Ferdinando
IRCCS Neuromed, Pozzilli (IS), Italy.
Department of Science and Technology, University of Sannio, Benevento, Italy.
PLoS One. 2014 Feb 25;9(2):e89745. doi: 10.1371/journal.pone.0089745. eCollection 2014.
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.
一氧化氮（NO）是一种具有生物活性的无机分子，参与许多生理过程的调节，如血流控制、血小板黏附、内分泌功能、神经传递和神经调节。在本研究中，我们首次调查了HD患者血小板中NO信号的调节。我们招募了55名明显HD患者和28名年龄及性别匹配的健康对照。我们的数据表明，当由胰岛素刺激的HD血小板上清液诱发时，NO介导的血管舒张沿病程逐渐恶化。血管舒张缺陷似乎源于HD患者血小板中NO释放异常，并且与eNOS磷酸化（Ser(1177)）和活性受损有关。本研究为HD中NO代谢提供了重要见解，并提出假说，即HD个体血小板中NO的减少可能是监测疾病晚期的良好工具。
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