Angela Tesse - Academia.edu (original) (raw)

Papers by Angela Tesse

PLoS One, 2009

Background: Obesity is associated with increased risks for development of cardiovascular diseases... more Background: Obesity is associated with increased risks for development of cardiovascular diseases. Epidemiological studies report an inverse association between dietary flavonoid consumption and mortality from cardiovascular diseases. We studied the potential beneficial effects of dietary supplementation of red wine polyphenol extract, Provinols TM , on obesityassociated alterations with respect to metabolic disturbances and cardiovascular functions in Zucker fatty (ZF) rats.

American Journal of Hypertension, 2016

Pharmacological reports: PR

Both inflammation and thrombosis can be orchestrated by the interactions between circulating cell... more Both inflammation and thrombosis can be orchestrated by the interactions between circulating cells, such as leukocytes and platelets, with vascular, endothelial and smooth muscle cells, which, during activation or apoptosis, can release circulating microparticles (MPs). Indeed, MPs are membrane vesicles with procoagulant and proinflammatory properties. MPs are present in blood from healthy individuals and in patients under several pathological states, for instance sepsis, preeclampsia, Crohn's disease and diabetes, strengthening the notion that MPs may play a role in these diseases. Circulating MPs or those generated in vitro from apoptotic T cells display deleterious effects on endothelial and/or vasomotor function. In contrast, MPs might be protective to endothelial cells. We have shown that MPs harboring the morphogen sonic hedgehog may represent a new therapeutic approach against endothelial dysfunction during acute severe endothelial injury. Indeed, these types of MPs induc...

Fundamental & clinical pharmacology, Jan 25, 2015

Elevated plasmatic levels of lympho-monocyte and platelet microparticles have been reported in pr... more Elevated plasmatic levels of lympho-monocyte and platelet microparticles have been reported in preeclampsia. Previous studies suggest that microparticles could participate in preeclampsia vascular impairment. In the present study, we investigated the ex vivo vascular effects of microparticles from preeclamptic women on arteries from normotensive pregnant women. Omental arteries were collected from normal pregnant women undergoing caesarean section and incubated during 24 hrs with microparticles from normal pregnant or preeclamptic women. Vascular contraction to serotonin and phenylephrine was studied on a wire myograph with or without pharmacological selective inhibitors of iNOS and/or COX-2. Expression of iNOS, COX-2 and NF-κB, production of superoxide anion and 8-isoprostane were also assessed by immunohistological or biochemical staining and/or Western Blot or ELISA assay, respectively. Microparticles from preeclamptic women, but not those from normal pregnant women, induced hypo...

Ethnopharmacological relevance: Different parts of Mimosa pigra (MPG) are used in traditional med... more Ethnopharmacological relevance: Different parts of Mimosa pigra (MPG) are used in traditional medicine in Madagascar, tropical Africa, South America and Indonesia for various troubles including cardiovascular disorders. Aim of the study: To investigate the mechanisms underlying the vascular effects of MPG by assessing in vitro its antioxidant and anti-inflammatory properties, and its vascular relaxing effects, and in vivo, its action on hypoxic pulmonary hypertension (PAH) in rats. Material and methods: The antioxidant activity of MPG leaf hydromethanolic extract was determined by using both the 1,1-diphenyl-2-picrylhydrazyl radical scavenging and the oxygen radical absorbance capacity in vitro assays. Anti-inflammatory properties were assayed on TNFα-induced VCAM-1 expression in endothelial cells. The vasorelaxant effect of MPG extract was studied on rat arterial rings precontracted with phenylephrine (1 μM) in the presence or absence of the endothelium. In vivo MPG extract effects were analyzed in chronic hypoxic PAH, obtained by housing male Wistar rats, orally treated or not with MPG extract (400 mg/kg/d), in a hypobaric chamber for 21 days. Results: MPG leaf extract had antioxidant and anti-inflammatory properties. It induced endotheliumdependent, NO-mediated relaxation of rat aorta and pulmonary artery. In vivo, chronic MPG treatment reduced hypoxic PAH in rat by decreasing by 22.3% the pulmonary arterial pressure and by 20.0% and 23.9% the pulmonary artery and cardiac remodelling, respectively. This effect was associated with a restoration of endothelium function and a 2.3-fold increase in endothelial NO synthase phosphorylation. MPG leaf hydromethanolic extract contained tryptophan and flavonoids, including quercetin glycosides. Both compounds also efficiently limit hypoxia-induced PAH. Conclusions: Our results show endothelial protective action of MPG leaf hydromethanolic extract which is likely to be due to its antioxidant action. MPG successfully attenuated the development of PAH, thus demonstrating the protective effect of MPG on cardiovascular diseases.

PLoS ONE, 2009

Archives of Cardiovascular Diseases Supplements, 2014

PLoS ONE, 2014

Red wine polyphenol compounds (RWPC) exert paradoxical effects depending on the dose on post-isch... more Red wine polyphenol compounds (RWPC) exert paradoxical effects depending on the dose on post-ischemic neovascularisation. Low dose RWPC (0.2 mg/kg/day) is pro-angiogenic, whereas high dose (20 mg/kg/day) is antiangiogenic. We recently reported that the endothelial effect of RWPC is mediated through the activation of a redoxsensitive pathway, mitochondrial biogenesis and the activation of a isoform of the estrogen receptor (ERa). Here, we investigated the implication of ERa on angiogenic properties of RWPC. Using ovariectomized mice lacking ERa treated with high dose of RWPC after hindlimb ischemia, we examined blood flow reperfusion, vascular density, nitric oxide (NO) production, expression and activation of proteins involved in angiogenic process and muscle energy sensing network. As expected, high dose of RWPC treatment reduced both blood flow and vascular density in muscles of mice expressing ERa. These effects were associated with reduced NO production resulting from diminished activity of eNOS. In the absence of RWPC, ERa deficient mice showed a reduced neo-vascularisation associated with a decreased NO production. Surprisingly in mice lacking ERa, high dose of RWPC increased blood flow and capillary density in conjunction with increased NO pathway and production as well as VEGF expression. Of particular interest is the activation of Sirt-1, AMPKa and PGC-1a/b axis in ischemic hindlimb from both strains. Altogether, the results highlight a pro-angiogenic property of RWPC via an ERaindependent mechanism that is associated with an up-regulation of energy sensing network. This study brings a corner stone of a novel pathway for RWPC to correct cardiovascular diseases associated with failed neovascularisation.

Endocrine‚ Metabolic & Immune Disorders-Drug Targets, 2006

Cardiovascular Toxicology, 2011

Cardiovascular dysfunction characterizes septic shock, inducing multiple organ failure and a high... more Cardiovascular dysfunction characterizes septic shock, inducing multiple organ failure and a high mortality rate. In the heart, it has been shown an up-regulation of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expressions with subsequent overproduction of nitric oxide (NO) and eicosanoids. This study is focused on the links between these products of inflammation and cell loss of mouse cardiomyocytes during treatment by the Salmonella typhimurium lipopolysaccharide (LPS) in presence or in absence of NOS or COX inhibitors. LPS induced RelA/NF-jB p65 activation, iNOS and COX-2 up-regulations, resulting in NO and prostacyclin releases. These effects were reversed by the NO-synthase inhibitor and increased by the specific COX-2 inhibitor. Immunostainings with FITC-conjugated anti-Annexin-V and propidium iodide and caspase 3/7 activity assay showed that cardiomyocyte necrosis was inhibited by L-NA during LPS treatment challenge, while apoptosis was induced in presence of both LPS and NS-398. No effect on LPS cellular injury was observed using the specific cyclooxygenase-1 (COX-1) inhibitor, SC-560. These findings strongly support the hypothesis of a link between iNOS-dependent NO overproduction and LPS-induced cell loss with a selective protective role allotted to COX-2 and deriving prostacyclins.

Réanimation, 2007

Preeclampsia consists in a pathological disorder of pregnancy that is potentially harmful and lif... more Preeclampsia consists in a pathological disorder of pregnancy that is potentially harmful and life-threatening. It is the major cause of maternal-fetal morbidity and mortality. Clinical symptoms are now better documented, yet its physiopathology remains controversial. A generalized vascular injury, mainly at the endothelial level, is considered to be responsible for the persistence of cardiovascular manifestations such as arterial hypertension. This disease does not develop without the placenta, which represents the first organ that serves as a medium for exchange between the mother and the embryo, later the foetus. Inflammatory and immune reactions, along with gene expression that take place during normal pregnancy, are usually harmonious and limited, but an imbalance, probably from multifunctional origin, could lead to an insufficient development of helical arteries, which is necessary for the foetal growth. It appears plausible that a local hypoxia and oxidative stress will generate an increased inflammation, initially local and later generalized at the maternal systemic level. Then activated cells, such as leucocytes, platelets as well as the reactive oxygen species, induce the endothelial dysfunction. The vascular injury is also the consequence of the enhanced anti-angiogenic placental proteins, which primarily inhibit placental development. The general cell activation enters a vicious circle, originating microparticles of various phenotypes, which contribute to enhance a pathological systemic reaction, and vascular inflammation, which lead to complications such as eclampsia. It seems that the anti-angiogenic factors and microparticles may currently serve as a basis for research and development of therapeutics research. © 2007 Société de réanimation de langue française. Publié par Elsevier Masson SAS. Tous droits réservés.

PLoS ONE, 2013

Background: Microparticles (MPs) are small vesicles released during cell activation or apoptosis.... more Background: Microparticles (MPs) are small vesicles released during cell activation or apoptosis. They are involved in coagulation, inflammation and vascular dysfunction in several diseases. We characterized circulating MPs from Crohn's Disease (CD) patients and evaluated their effects on endothelial function and vascular reactivity after in vivo injection into mice.

PPAR Research, 2009

Activation of peroxisome proliferator-activated receptors (PPARs), and particularly of PPARα and ... more Activation of peroxisome proliferator-activated receptors (PPARs), and particularly of PPARα and PPARγ, using selective agonists, is currently used in the treatment of metabolic diseases such as hypertriglyceridemia and type 2 diabetes mellitus. PPARα and PPARγ anti-inflammatory, antiproliferative and antiangiogenic properties in cardiovascular cells were extensively clarified in a variety of in vitro and in vivo models. In contrast, the role of PPARδ in cardiovascular system is poorly understood. Prostacyclin, the predominant prostanoid released by vascular cells, is a putative endogenous agonist for PPARδ, but only recently PPARδ selective synthetic agonists were found, improving studies about the physiological and pathophysiological roles of PPARδ activation. Recent reports suggest that the PPARδ activation may play a pivotal role to regulate inflammation, apoptosis, and cell proliferation, suggesting that this transcriptional factor could become an interesting pharmacological target to regulate cardiovascular cell apoptosis, proliferation, inflammation, and metabolism.

PLoS ONE, 2010

Background: A greater reduction in cardiovascular risk and vascular protection associated with di... more Background: A greater reduction in cardiovascular risk and vascular protection associated with diet rich in polyphenols are generally accepted; however, the molecular targets for polyphenols effects remain unknown. Meanwhile evidences in the literature have enlightened, not only structural similarities between estrogens and polyphenols known as phytoestrogens, but also in their vascular effects. We hypothesized that alpha isoform of estrogen receptor (ERa) could be involved in the transduction of the vascular benefits of polyphenols.

PLoS ONE, 2012

We aimed to characterize circulating microparticles in association with arterial stiffness, infla... more We aimed to characterize circulating microparticles in association with arterial stiffness, inflammation and endothelial dysfunction in aldosterone-salt-induced hypertension in rats and to investigate the preventive effects of red wine polyphenols. Uninephrectomized male Sprague-Dawley rats were treated with aldosterone-salt (1 mg.h 21 ), with or without administration of either red wine polyphenols, Provinols TM (20 mg.kg 21 .day 21 ), or spironolactone (30 mg.kg 21 .day 21 ) for 4 weeks. Microparticles, arterial stiffness, nitric oxide (NO) spin trapping, and mesenteric arterial function were measured. Aldosterone-salt rats showed increased microparticle levels, including those originating from platelets, endothelium and erythrocytes. Hypertension resulted in enhanced aortic stiffness accompanied by increased circulating and aortic NO levels and an upregulation of aortic inducible NO-synthase, NFkB, superoxide anions and nitrotyrosine. Flow-induced dilatation was reduced in mesenteric arteries. These effects were prevented by spironolactone. Provinols TM did not reduce arterial stiffness or systolic hypertension but had effects similar to those of spironolactone on endothelial function assessed by flowmediated vasodilatation, microparticle generation, aortic NO levels and oxidative stress and apoptosis in the vessel wall. Neither the contractile response nor endothelium-dependent relaxation in mesenteric arteries differed between groups. The in vivo effects of Provinols TM were not mediated by mineralocorticoid receptors or changes in shear stress. In conclusion, vascular remodelling and endothelial dysfunction in aldosterone-salt-mediated hypertension are associated with increased circulating microparticles. Polyphenols prevent the enhanced release of microparticles, macrovascular inflammation and oxidative stress, and microvascular endothelial dysfunction independently of blood pressure, shear stress and mineralocorticoid receptor activation in a model of hyperaldosteronism. Citation: Ló pez Andrés N, Tesse A, Regnault V, Louis H, Cattan V, et al. (2012) Increased Microparticle Production and Impaired Microvascular Endothelial Function in Aldosterone-Salt-Treated Rats: Protective Effects of Polyphenols. PLoS ONE 7(7): e39235.

Journal of Ethnopharmacology, 2013

Endocrinology, 2008

PTHrP is produced in vessels and acts as a local modulator of tone. We recently reported that PTH... more PTHrP is produced in vessels and acts as a local modulator of tone. We recently reported that PTHrP(1-34) is able to induce vasorelaxation in rat uterine arteries, but in pregnancy, this response is blunted and becomes strictly endothelium dependent. The present study aimed to get insights into the mechanisms involved in these changes because the adaptation of uterine blood flow is essential for fetal development. On d 20 of gestation, RT-PCR analysis of uterine arteries showed that PTH/PTHrP receptor (PTH1R) mRNA expression was decreased, whereas that of PTHrP mRNA was increased. This was associated with a redistribution of the PTHrP/PTH1R system, with both PTH1R protein and PTHrP peptide becoming concentrated in the intimal layer of arteries from pregnant rats. On the other hand, the blunted vasorelaxation in-duced by PTHrP(1-34) in uterine arteries from pregnant rats was specifically restored by indomethacin and a specific cyclooxygenase-2 inhibitor, NS 398. This was associated with an increase in cyclooxygenase-2 expression and in 8-iso-prostaglandin F 2␣ release when uterine arteries from pregnant rats were exposed to high levels of . Most interestingly, 8-iso-prostaglandin F 2␣ itself was able to increase PTHrP expression and reduce PTH1R expression in cultured rat aortic smooth muscle cells. These results suggest a local regulation of uterine artery functions by PTHrP during pregnancy resulting from PTH1R redistribution. Moreover, they shed light on a potential role of 8-iso-prostaglandin F 2␣ .