Nitric oxide dysregulation in platelets from patients with advanced Huntington disease

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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 languageEnglish
Article numbere89745
JournalPLoS One
Volume9
Issue number2
DOIs
Publication statusPublished - Feb 25 2014

Fingerprint

Huntington Disease
Platelets
nitric oxide
Nitric Oxide
Blood Platelets
vasodilation
Vasodilation
Physiological Phenomena
Phosphorylation
disease course
Metabolism
Synaptic Transmission
blood flow
adhesion
phosphorylation
Blood
insulin
Adhesion
Modulation
Insulin

ASJC Scopus subject areas

  • Agricultural and Biological Sciences(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Medicine(all)

Cite this

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title = "Nitric oxide dysregulation in platelets from patients with advanced Huntington disease",
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.",
author = "Albino Carrizzo and {Di Pardo}, Alba and Vittorio Maglione and Antonio Damato and Enrico Amico and Luigi Formisano and Carmine Vecchione and Ferdinando Squitieri",
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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

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