G Bricca

Claude Bernard University Lyon 1, Villeurbanne, Rhône-Alpes, France

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Publications (13)43.31 Total impact

  • Diabetes & Metabolism 03/2015; 41:A77. DOI:10.1016/S1262-3636(15)30289-5 · 2.85 Impact Factor
  • Journal des Maladies Vasculaires 09/2010; 35(5):317-317. DOI:10.1016/j.jmv.2010.07.070 · 0.24 Impact Factor
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    ABSTRACT: Lipogenesis is expressed in vascular smooth muscle cells (VSMCs), and such in situ lipogenesis could be providing the fatty acids for triglyceride synthesis and cholesterol esterification, and contributing to lipid accumulation in the arterial wall. This study investigated both the expression and regulation of lipogenesis in VSMCs to determine if they are modified in Psammomys obesus gerbils fed a high-fat diet as a model of insulin resistance and diabetes. Aortas were collected from diabetic and non-diabetic P. obesus for histological examination, measurement of lipogenic gene expression and VSMC culture. The aortas of diabetic animals exhibited lipid deposits and foam cells as well as disorganization of elastic fibres. However, lipogenic gene expression was not modified. VSMCs in vitro from the aortas of diabetic animals had, compared with cells from non-diabetic animals, lower mRNA levels of SREBP-1c and ChREBP. An adipogenic medium stimulated moderate FAS and ACC1 expression in cells from both diabetic and non-diabetic animals, but glucose and insulin on their own had no such stimulatory action. Also, triiodothyronine (T3) had a clear stimulatory action, while angiotensin II had a moderate effect, in cells from non-diabetic P. obesus, but not from diabetic animals, whereas LXR agonists stimulated lipogenesis in cells from both animal groups. Lipogenesis is expressed in the arterial walls and VSMCs of P. obesus. However, its expression was not increased in diabetes, and did not respond to either T3 or angiotensin II. Therefore, lipogenesis in situ is unlikely to contribute to the accumulation of lipids in the arterial walls of diabetic P. obesus gerbils.
    Diabetes & Metabolism 03/2010; 36(3):221-8. DOI:10.1016/j.diabet.2010.01.003 · 2.85 Impact Factor
  • Journal of Hypertension 01/2010; 28. DOI:10.1097/01.hjh.0000378280.44189.0d · 4.22 Impact Factor
  • Journal of Hypertension 01/2010; 28. DOI:10.1097/01.hjh.0000378292.05179.25 · 4.22 Impact Factor
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    ABSTRACT: Arterial stiffness is a strong predictor of cardiovascular events and particularly of stroke. A likely explanation is the development of atherosclerotic lesions at the carotid level, favored by increased local stiffness. Another possibility involves cardiac consequences of aortic stiffness and particularly left atrial dilatation with its subsequent risk of atrial fibrillation (AF) and cerebral embolism. The present study investigated the link between arterial stiffness, pulse pressure and left atrial size, a determinant of AF risk. Arterial stiffness was determined from pulse wave velocity (PWV) and pulse pressure (PP). Left atrial size was also measured. Several potential confounders were taken into account including indices of ventricular remodeling and diastolic function (estimated by NT-Pro brain natriuretic peptide (NT-proBNP) levels). Three-hundred and ten hypertensive patients, aged 53 +/- 13 years, were included. Mean 24-h blood pressure (BP) was 154 +/- 20 over 93 +/- 13 mmHg. Significant relationships were found between left atrial diameter (LAD) and PWV (r=0.27, P<0.001) and between LAD and 24-h PP (r=0.32, P<0.001). LAD was also correlated significantly, although not always tightly, with left ventricular dimensions, geometry and NT-proBNP. In two different multivariate models, LAD remained significantly correlated with PWV or with 24-h PP, independently of classical determinants like age, gender, body mass index, ventricular remodeling (i.e. dimensions and geometry) and filling pressure. These results led us to propose AF as a new possible pathophysiological link between arterial stiffness and stroke. These results also emphasize the cardiac consequences of arterial stiffness which can fuel a new approach to AF prevention.
    Archives of Cardiovascular Diseases 01/2008; 101(1):35-40. DOI:10.1016/S1875-2136(08)70253-5 · 1.66 Impact Factor
  • Atherosclerosis Supplements 06/2006; 7(3):355-355. DOI:10.1016/S1567-5688(06)81400-5 · 9.67 Impact Factor
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    ABSTRACT: Accumulation of cholesterol in foam cells of atheroma plaques depends on the balance between uptake and efflux of cholesterol. It may also depend on proteins surrounding lipid droplets, adipophilin, and perilipins. They favor triglyceride storage in adipocytes and could play a similar role for cholesterol in atheroma. We measured in human atheroma and nearby macroscopically intact tissue (MIT) the expression of perilipin, adipophilin, and regulatory factors of cholesterol metabolism. We identified perilipin A in human arterial wall. Its expression was largely increased in atheroma compared with MIT, and perilipin was present in macrophages and vascular smooth muscle cells. Adipophilin, ACAT1, and CD36 were also overexpressed in atheroma. mRNA levels of low-density lipoprotein receptor, 3-hydroxy-3-methylglutaryl coenzyme A reductase, and SREBP-2 were unchanged. With respect to efflux of cholesterol, the mRNA levels of NCEH and ABCA-1 were unchanged, whereas CLA-1 mRNA was slightly higher in atheroma. Importantly, immunoblotting of ABCA-1 showed a dramatic decrease of ABCA1 protein, the key molecule of cholesterol efflux, in atheroma compared with MIT. We show the presence and induction of perilipin in atheroma. This overexpression and the coordinated modifications of expression of key regulatory factors for cholesterol metabolism could favor cholesterol accumulation.
    Arteriosclerosis Thrombosis and Vascular Biology 09/2005; 25(8):1711-7. DOI:10.1161/01.ATV.0000174123.19103.52 · 5.53 Impact Factor
  • European Journal of Clinical Investigation 10/2004; 34(9):643-4. DOI:10.1111/j.1365-2362.2004.01397.x · 2.83 Impact Factor
  • Journal of Hypertension 01/2004; 22(Suppl. 2):S43. DOI:10.1097/00004872-200406002-00141 · 4.22 Impact Factor
  • Journal of Hypertension 01/2004; 22(Suppl. 2):S18. DOI:10.1097/00004872-200406002-00052 · 4.22 Impact Factor
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    ABSTRACT: Our goal was to study the relative influence of systolic blood pressure (SBP) and plasmatic markers of sympathetic and renin-aldosterone systems (RAS) activities to left atrial diameter (LAD), left ventricular posterior wall thickness (LVPWT) and pulse wave velocity (PWV), which reflect cardiovascular remodeling in hypertension. In 227 consecutive patients with hypertension (mean age +/- SD: 53.3 years +/- 13.4, 126 men), we measured: PWV, LAD, LVPWT, mean 24-hours SBP, plasma renin activity, and plasma aldosterone and catecholamine levels. Multiples linear regression analyses were performed to test statistical associations between hemodynamic and neurohumoral factors, and cardiovascular remodeling parameters, after adjustment for age, gender and body mass index. LVPWT was positively correlated to SBP as well as to plasma aldosterone and meta-noradrenaline (p < 0.001). LAD and PWV were related to SBP but not to any of the biological variables. Moreover, LAD correlated to PWV independently of SBP (p < 0.05), whereas after SBP inclusion in the model, there was not significant correlation between LAD and LVPWT nor between LVPWT and PWV. In hypertension, the development of cardiac hypertrophy depends on SBP and the sympathetic and renin-aldosterone systems activities. The RAS is not involved in the PWV nor LAD modifications. Strong association between LAD and PWV suggest that left atrial enlargement, that may be considered as a marker of diastolic function, may results more from arterial stiffness than from ventricular hypertrophy.
    Archives des maladies du coeur et des vaisseaux 01/2003; 96(7-8):729-33. · 0.40 Impact Factor
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    ABSTRACT: Variations in the expression of cytokines from the interleukin-6 (IL-6) family: ciliary neurotrophic factor (CNTF), leukaemia inhibitory factor (LIF), and cardiotrophin 1 (CT-1) were studied during cardiac remodelling leading to left ventricular hypertrophy (LVH) in TGR(mRen2)27 rats at the age of 8 and 20 weeks. The cytokines mRNA levels within the free wall of the left ventricle were measured by semi-quantitative RT-PCR standardised with 18S. They were compared between heterozygous rats for the mRen2 transgene (TG+/-) and control rats (TG-/-). No significant difference was observed between results obtained at 8 and 20 weeks of age. At 20 weeks of age, TGR(mRen2)27 rats showed higher levels of mRNA LIF and IL-6 respectively by 52 and 55% compared to the control rats [LIF TG+/-: 3.17 +/- 0.21, TG-/-: 2.09 +/- 0.03; p < 0.001; n = 5; and IL-6 TG+/-: 1.53 +/- 0.13; TG-/-: 0.99 +/- 0.17; p < 0.05; n = 5]. By contrast, no variation of mRNAs levels of CT-1 and gp 130 genes was observed between control and transgenic rats. Concerning the cytokine receptors, the levels of mRNA for IL-6R did not vary while those of receptor subunits LIFR and CNTFR were decreased respectively by 48 and 42% in transgenic rats vs controls [LIFR TG+/-: 0.48 +/- 0.01; TG-/-: 0.92 +/- 0.08 p < 0.001; n = 5; and CNTFR TG+/-: 1.07 +/- 0.08; TG-/-: 1.85 +/- 0.18; p < 0.01; n = 5]. Therefore, these results show a specific pattern of activation of the cytokines pathway in the LVH of the TGR(mRen2)27 rat.
    Archives des maladies du coeur et des vaisseaux 01/2003; 96(7-8):811-4. · 0.40 Impact Factor