NAP Reduces Murine Microvascular Endothelial Cells Proliferation Induced by Hyperglycemia

Hyperglycemia has been identified as a risk factor responsible for micro- and macrovascular complications in diabetes. NAP (Davunetide) is a peptide whose neuroprotective actions are widely demonstrated, although its biological role on endothelial dysfunctions induced by hyperglycemia remains uninve...

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Bibliographic Details
Published in:Journal of molecular neuroscience 2014-11, Vol.54 (3), p.405-413
Main Authors: D’Amico, Agata Grazia, Scuderi, Soraya, Maugeri, Grazia, Cavallaro, Sebastiano, Drago, Filippo, D’Agata, Velia
Format: Article
Language:English
Subjects:
Angiogenesis
Animals
Atherosclerosis
Biomedical and Life Sciences
Biomedicine
Cell Biology
Cell cycle
Cell growth
Cell Line
Cell Proliferation
Cyclin D1 - genetics
Cyclin D1 - metabolism
Diabetes
Endothelial Cells - drug effects
Endothelial Cells - metabolism
Endothelial Cells - physiology
Endothelium
Endothelium, Vascular - cytology
Glucose
Glucose - pharmacology
Hyperglycemia
Hyperglycemia - metabolism
Investigations
Kinases
MAP Kinase Signaling System
Mice
Neurochemistry
Neurology
Neurosciences
Oligopeptides - pharmacology
Pathogenesis
Phosphatidylinositol 3-Kinases - metabolism
Polypeptides
Protein expression
Proteins
Proteomics
Proto-Oncogene Proteins c-akt - metabolism
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Summary:Hyperglycemia has been identified as a risk factor responsible for micro- and macrovascular complications in diabetes. NAP (Davunetide) is a peptide whose neuroprotective actions are widely demonstrated, although its biological role on endothelial dysfunctions induced by hyperglycemia remains uninvestigated. In the present study we hypothesized that NAP could play a protective role on hyperglycemia-induced endothelial cell proliferation. To this end we investigated the effects of NAP on an in vitro model of murine microvascular endothelial cells grown in high glucose for 7 days. The MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide) assay and cyclin D1 protein expression analysis revealed that NAP treatment significantly reduces viability and proliferation of the cells. Hyperglycemia induced the activation of mitogen-activated protein kinase/extracellular signal-regulated protein kinase and/or phosphatidylinositol-3 kinase/Akt pathways in a time-dependent manner. NAP treatment reduced the phosphorylation levels of ERK and AKT in cells grown in high glucose. These evidences suggest that NAP might be effective in the regulation of endothelial dysfunction induced by hyperglycemia.
ISSN:0895-8696
1559-1166
DOI:10.1007/s12031-014-0335-2