Evidence for contribution of vascular NAD P H oxidase to increased oxidative stress in animal models of diabetes and obesity. Internalization of endothelin by cultured human vascular smooth muscle: Role of Tissue Kallikrein in response to flow in mice resistance arteries. Risk factors for ipsilateral reamputation in patients with diabetic foot lesions. Interleukin-2 causes endothelium-dependent contractions to arachidonic acid in rat aorta. Intraluminal pressure increases vascular neuronal NOS expression. Tissue destruction by neutrophils.

Furthermore, the downregulation of the anti-inflammatory cytokine IL in DFUs environments represents the collapse of an important inflammatory restrainer [77]. Hyperglycemia appears as the proximal detonator of toxic effectors including pro-inflammation, spillover of reactive oxygen and nitrogen species. INS-1 cells undergoing caspase-dependent apoptosis in response to mutant HNF1A enhance the regenerative capacity of neighbouring cells. The emerging roles of microparticles in liver diseases. Sci Aging Knowledge Environ. Furthermore, insulin has a dramatic impact on the endothelial homeostasis by its ability to stimulate NO release via a cascade that involves activation of the phosphatidylinositol 3-kinase PI3K -A kt signaling and eNOS phosphorylation. Another factor to be considered is that diabetes per se is a metabolic disease in which fuels metabolism is perturbed given the rupture of one of the most important anabolic axis of the organism:

Microvesicles in cell-cell communication in cardiovascular diseases. Boulanger october porcine coronary arteries: Bone marrow stromal cells, preadipocytes, and dermal fibroblasts promote epidermal regeneration in their distinctive fashions.

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Insulin as an anti-inflammatory and currlculum modulator. Multiple evidences indicate that the number of circulating EPCs is decreased under both clinical forms of diabetes, which is likely to be ailliam in the pathogenesis of vascular complications [70]. Vasc Biol,23 Keratinocyte migration, proliferation, and differentiation in chronic ulcers from patients with diabetes and normal wounds. In contrast to acute wounds in non-diabetic subjects, the inflammatory reaction in diabetics appears prolonged [93] and sharply delays granulation tissue formation and maturation [94].


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C Boulanger coordonator; P. Heart Lung Transplantation, 35 6: An extraordinary background has accumulated about the role of NO in vascular biology in diverse horizons as ischemia, inflammation and neovascularization.

Studies with human fibroblasts have confirmed the pro-degradative phenotype by the increased MMP-2 and MMP-3 production and reduced collagens gene expression [31].

For subjects with macrovascular disease, the defective angiogenesis prolongs and disturbs the healing process. A potential predictor for the individual capacity to develop collaterals. Chronic treatment with the Calcium channel inhibitor RO potentiates endothelium-dependent relaxations in the aorta of the hypertensive salt sensitive dahl rat.

Chantal Boulanger | Inserm –

Boulanger october Pharmacol, Lower extremities ulcerations and the potential for amputation are currently acknowledged as members of the list of diabetes complications [4]. Res4: Endothelial cells and fibroblasts, in particular senescent fibroblasts, are a prominent source for oxygen radicals, but at the same time they turn into these radicals targets which, by converging mechanisms, arrest cell proliferation and induce apoptosis [].

Boulanger october D. Cells harvested and cultured from hypoperfused granulation tissues orchestrate a molecular program of arrest and senescence Jorge Berlanga, manuscript in preparation. This poor-healing condition appears to be a multifactorial process which includes the amalgamation of systemic and local factors that ensure a perpetual forward loop up to chronification.


Circulating microparticles from patients with myocardial infarction cause endothelial dysfunction. Effects of glucose and its modulation by insulin and estradiol on BMSC differentiation into osteoblastic lineages. Anabolic action of insulin on skin wound protein is augmented by exogenous amino acids.

william benessiano curriculum vitae

Cyclooxygenase-1 and – 2 contribution to endothelial dysfunction in ageing. Vascular renin angiotensin system and endothelial function: Under this ambient, the expression of the proapoptotic Bax protein increases, cytochrome c is released, subsequently conjugating to the apoptotic protease activating factor-1 and triggering a caspase cascade-induced death [55]. Oxygen-free radicals mediate endothelium-dependent contractions to acetylcholine in aortas from spontaneously hypertensive rats.

Glutathione enhances fibroblast collagen contraction and protects keratinocytes from apoptosis in hyperglycaemic culture. Interactions between endothelium- derived relaxing and contracting factors in health and cardiovascular disease. Evidence for contribution of vascular NAD P H oxidase to increased oxidative stress in animal models of diabetes and obesity.

Int J Low Extrem Wounds. Abnormal angiogenesis in diabetes mellitus. Nichols; Gower Medical Currriculum, London, Furthermore, high glucose levels selectively trigger apoptosis in cultured endothelial cells as has been demonstrated by different laboratories [53].