Analysis of cellular and molecular mechanisms appearing in blood vessels in response to elastic fibre components.
type: Dataset
description: Elastic fibres are composed of elastin and fibrillin-1 rich microfibrils, whose genetic mutations result in severe cardiovascular pathologies characterized by aortic stenosis (Williams syndrome, WS) or aneurysm (Marfan Syndrom, MS), respectively. We studied and compared the effect of elastin (kappa-elastin, kE and recombinant tropoelastin, rTE) and microfibrils (MF and PF14, fibrillin-1 fragment) on vascular cell signaling. In human umbilical vein endothelial cells (HUVEC), kE, rTE and MF activated the elastin complex receptors (ECR) and integrins, the production of intracellular messengers and, with varying efficiencies, membrane and endoplasmic reticulum calcium channels, mobilizing both intra- and extra-cellular calcium. Actin microfilaments were involved only in the case of elastin signaling. All these proteins enhanced the proliferation and adhesion of HUVECs, as well as synthesis or degradation –through matrix metalloproteinanse (MMP) activation- of several extracellular matrix components. HUVEC migration was enhanced by kE, rTE and PF14 and diminished by MF. Also, in rats, these proteins induced nitric oxide (NO) synthesis by endothelial cells, resulting in aortic vasodilatation, although PF14 had an additional constrictor effect on endothelium-free aorta, indicating that PF14 also stimulates vascular smooth muscle cells (VSMCs). To study these interactions in a cellular model, we designed a new protocol to culture VSMCs from aorta of adult, aged, and elastin or fibrillin-1 knock-out mice. Elastic fibre proteins induced an increase in VSMC intracellular calcium level, which characteristics varied with the protein, age and genotype of mice. These findings confirm the major role of elastin and fibrillin-1 in the regulation of vascular cell functions. Despite some differences, elastin and fibrillin-1 often stimulated vascular cells similarly. This suggests that the onset of the contradictory features observed in MS and WS also involve additional factors, probabl…
landing page: https://theses.hal.science/tel-00949211
identifier: NNT: 2013GRENV013
keyword: ageing
keyword: arteres
keyword: arteries
keyword: cellules-vasculaires
keyword: elastin
keyword: elastine
keyword: infoeu-reposemanticsdoctoralthesis
keyword: microfibrilles
keyword: microfibrils
keyword: sdvsalife-sciences-q-bioagricultural-sciences
keyword: signaling
keyword: signalisation
keyword: theses
keyword: vascular-cells
keyword: vieillissement
issued: 2026-05-06T07:52:48.167643
modified: 2026-05-06T07:52:48.167648
language: fr
contact point: Organization
  fn: CCSD

test_moissonnage_selune
type: Agent

Analysis of cellular and molecular mechanisms appearing in blood vessels in response to elastic fibre components.
type: Distribution
format: HTML
access URL: https://theses.hal.science/tel-00949211
issued: 2026-05-06T07:52:48.169814
modified: 2026-05-06T07:52:48.141993