Gestational hypertension plasma and human umbilical vein endothelial cells: an <i>in vitro</i> study

Cester, N.; Salvolini, Eleonora; Rabini, R. A.; Tranquilli, Andrea Luigi; Zolese, Giovanna; Mazzanti, Laura

doi:10.1046/j.1365-2362.1998.00398.x

Cited by 2 publications

(1 citation statement)

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“…At 80% confluence, cultured HAECs were incubated for 3 h at 37°C with EGM-2 alone (= HAEC), or with 20% (v/v) plasma in EGM-2 (plasma from healthy subjects = HAEC + control plasma, from MCI patients = HAEC + MCI plasma, from AD patients = HAEC + AD plasma) (20). We chose this incubation time since in vitro studies have previously shown that short-term application of Ap eptides to isolated vessels may affect vascular tone (21).…”

Section: Human Aortic Endothelial Cell Culturementioning

confidence: 99%

Effects of Plasma from Patients Affected by Mild Cognitive Impairment and Alzheimer's Disease on Cultured Endothelial Cells

et al. 2013

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There is accumulating evidence that Alzheimer's disease (AD) can have vascular contribution. In particular, endothelial dysfunction may impair nitric oxide (NO) production and cause cerebral hypoperfusion. Blood flow impairment can be provoked also by an increased production of reactive oxygen species (ROS). The present study was performed in order to investigate the effect of plasma from subjects affected by AD and mild cognitive impairment (MCI) on human aortic endothelial cells (HAECs) in vitro, since endothelial dysfunction has been suggested to be an early event in patients affected by AD. Plasma samples were obtained from 27 AD patients, 15 MCI subjects, and 19 ageand sex-matched healthy subjects. After a short incubation period the following parameters were evaluated: NO release, superoxide dismutase (SOD) and Na+fK+-ATPase activities, membrane fluidity, and thiobarbituric acid-reactive substance (TBARS) production. Exposure to MCI plasma provoked a decrease in NO release, more pronounced in the presence of AD plasma. Our data on SOD and Na+IK+-ATPase activities showed a similar trend, since the lowest values were recorded after incubation with AD plasma. Endothelial membrane fluidity was deeply affected by the exposure to MCI plasma, and even more following incubation with AD plasma. Finally, enhanced TBARS production after incubation with MCI and AD plasma was observed. In conclusion, our results showed that MCI and AD plasma affects endothelial cells, thus highlighting the need for early treatment aimed at protecting the endothelium.Alzheimer's disease (AD) represents the most common cause of dementia in the older population. It is characterized by the presence of senile plaques distributed throughout the cerebral cortex, as well as intraneuronal neurofibrillary tangles, although it is known to be a systemic disorder (1, 2).There is accumulating evidence that AD may have a vascular basis that involves impaired nitric oxide (NO) release, resulting in cerebral hypoperfusion (3). NO is a multifunctional free radical synthesized from L-arginine by NO synthases (NOS). Endothelial (eNOS) and neuronal (nNOS) isoforms are constitutively expressed and depend on intracellular calcium release, while inducible NOS (iNOS) is calcium independent and usually expressed in response to inflammatory cytokines and

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Section: Human Aortic Endothelial Cell Culturementioning

confidence: 99%