Abstract
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.
| Original language | English |
|---|---|
| Article number | e89745 |
| Journal | PLoS One |
| Volume | 9 |
| Issue number | 2 |
| DOIs | |
| Publication status | Published - Feb 25 2014 |
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ASJC Scopus subject areas
- Agricultural and Biological Sciences(all)
- Biochemistry, Genetics and Molecular Biology(all)
- Medicine(all)
Cite this
Nitric oxide dysregulation in platelets from patients with advanced Huntington disease. / Carrizzo, Albino; Di Pardo, Alba; Maglione, Vittorio; Damato, Antonio; Amico, Enrico; Formisano, Luigi; Vecchione, Carmine; Squitieri, Ferdinando.
In: PLoS One, Vol. 9, No. 2, e89745, 25.02.2014.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Nitric oxide dysregulation in platelets from patients with advanced Huntington disease
AU - Carrizzo, Albino
AU - Di Pardo, Alba
AU - Maglione, Vittorio
AU - Damato, Antonio
AU - Amico, Enrico
AU - Formisano, Luigi
AU - Vecchione, Carmine
AU - Squitieri, Ferdinando
PY - 2014/2/25
Y1 - 2014/2/25
N2 - 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.
AB - 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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U2 - 10.1371/journal.pone.0089745
DO - 10.1371/journal.pone.0089745
M3 - Article
VL - 9
JO - PLoS One
JF - PLoS One
SN - 1932-6203
IS - 2
M1 - e89745
ER -