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Start Over Author "Bastelica, D" Journal thrombosis and haemostasis
5 results on '"Bastelica, D"'

1. Influence of t-pA and u-PA on adipose tissue development in a murine model of diet-induced obesity

Author

Pierre Morange, Bastelica D, Mf, Bonzi, Van Hoef B, Collen D, Juhan-Vague I, and Hr, Lijnen

Subjects
Male, Mice, Knockout, Fibrinolysis, Body Weight, Cell Count, Organ Size, Dietary Fats, Urokinase-Type Plasminogen Activator, Mice, Inbred C57BL, Mice, Adipose Tissue, Tissue Plasminogen Activator, Adipocytes, Animals, Obesity, Stromal Cells
Abstract

To investigate the potential role of tissue-type plasminogen activator (t-PA) or urokinase-type plasminogen activator (u-PA) in development of adipose tissue, we have used a nutritionally induced obesity model in t-PA (t-PA-/-) and u-PA (u-PA-/-) deficient mice. Five week old male wild-type (WT), t-PA-/- or u-PA-/- mice (n = 9 to 16) were fed a high fat diet (HFD, 42% fat). After 16 weeks of HFD, the body weight of t-PA-/- mice was significantly higher than that of WT mice (48 +/- 1.1 g vs. 39 +/- 2.2 g, p = 0.004). The total weight of the isolated subcutaneous (sc) fat deposit was higher in t-PA-/- than in WT mice (2.4 +/- 0.22 g vs. 1.2 +/- 0.29 g, p = 0.002). accompanied with higher adipocyte diameters (80 +/- 1.7 microm vs. 61 +/- 4.7 microm, p0.01). These differences were not observed in the intra-abdominal fat deposit. The number of stroma cells in both adipose tissue territories was increased in t-PA-/- as compared to WT mice (2.0 +/- 0.13 vs. 1.5 +/- 0.10, p = 0.2 and 3.0 +/- 0.17 vs 1.6 +/- 0.17, p = 0.0001, stroma cells/adipocytes in sc and intra-abdominal tissue, respectively), partly as a result of an increased number of endothelial cells (192 +/- 9 vs. 154 +/-18, p = 0.06 and 108 +/- 13 vs. 69 +/- 8, p = 0.04 CD31 stained/adipocyte area). In contrast the weight gain and adipose tissue development in u-PA-/- mice was not different from that in WT mice. These data suggest that t-PA but not u-PA plays a role in adipose tissue development.

Published
2002

3. Polymorphism A36G of the tumor necrosis factor receptor 1 gene is associated with PAI-1 levels in obese women.

Author

Mavri A, Bastelica D, Poggi M, Morange P, Peiretti F, Verdier M, Juhan-Vague I, and Alessi MC

Subjects
Case-Control Studies, Female, Gene Frequency, Humans, Obesity blood, Obesity genetics, Receptors, Tumor Necrosis Factor, Type I genetics, Solubility, Obesity etiology, Plasminogen Activator Inhibitor 1 blood, Polymorphism, Single Nucleotide physiology, Receptors, Tumor Necrosis Factor genetics
Abstract

The tumor necrosis factor (TNF) pathway may be implicated in etiopathogenesis of PAI-1 overexpression during obesity. The aim of this study was to investigate the influence of polymorphism A36G of the TNF receptor 1 (TNFRSF1A +36A/G) on plasma concentrations of PAI-1 in 163 obese (31 with the metabolic syndrome, MetS) and 150 lean, healthy women. Genotypic and allele frequencies did not significantly differ between obese and lean subjects. TNFRSF1A genotypes were significantly associated with sTNFR1 plasma levels in obese women only (p < 0.01); TNFRSF1A +36G/G obese carriers exhibited higher sTNFR1 and PAI-1 levels than A carriers (p < 0.01 and p < 0.05, respectively). In obese women, the presence of the MetS significantly potentiated the elevation of sTNFR1 and PAI-1 levels observed in the TNFRSF1A + 36G/G carriers. Our results suggest that association between TNFRSF1A +36G/G genotype and the MetS renders obese women more prone to activation of the TNF pathway reflected by high circulating sTNFR1 and PAI-1 levels.

Published
2007

5. Relationships between fibrinolytic and inflammatory parameters in human adipose tissue: strong contribution of TNFalpha receptors to PAI-1 levels.

Author

Bastelica D, Mavri A, Verdierl M, Berthet B, Juhan-Vague I, and Alessi MC

Subjects
Adult, Antigens, CD analysis, Antigens, CD blood, Biomarkers analysis, Biomarkers blood, Case-Control Studies, Female, Fibrinolysis, Humans, Inflammation, Interleukin-6 analysis, Interleukin-6 blood, Male, Middle Aged, Obesity blood, Obesity metabolism, Plasminogen Activator Inhibitor 1 blood, Receptors, Tumor Necrosis Factor analysis, Receptors, Tumor Necrosis Factor blood, Receptors, Tumor Necrosis Factor, Type I, Receptors, Tumor Necrosis Factor, Type II, Tissue Plasminogen Activator analysis, Tissue Plasminogen Activator blood, Adipose Tissue chemistry, Antigens, CD physiology, Obesity pathology, Plasminogen Activator Inhibitor 1 analysis, Receptors, Tumor Necrosis Factor physiology
Abstract

Plasminogen activator inhibitor type 1 (PAI-1), a risk marker of atherosclerosis, is highly expressed in adipose tissue from obese subjects. PAI-1 is also considered as an acute phase protein. Recently, adipose tissue has been described as a source of inflammatory cytokines. Therefore, our aim was to study the relationships between PAI-1, and IL-6, TNF, TNF receptors (TNFRSF1s) and TGFbeta1, in plasma and adipose tissue from obese (n = 60) and lean (n = 28) subjects. Study has been extended to plasminogen activators (t-PA and u-PA). Compared to lean subjects, obese subjects exhibited higher plasma levels of all the studied parameters (except for TGFbeta1) whereas in adipose tissue only PAI-1, t-PA and TGFbeta antigen levels differed. In the obese population, plasma PAI-1 levels were weakly associated with circulating TNF, and this relationship disappeared after adjustment for plasma t-PA. Adipose tissue PAI-1 levels were positively associated with TNFRSF1s and TGFbeta, the strongest relationship being observed with TNFRSF1A, which explained 82% of PAI-1 variability. TNF and IL-6 were the main contributors to t-PA variability in plasma and in adipose tissue, respectively. Our results argue on the relevance of TNFRSF1s in the regulation of PAI-1 expression by adipose tissue. Association between t-PA, which is mainly produced by endothelial cells, and IL-6 or TNF suggest that inflammation might be involved in angiogenesis in adipose tissue.

Published
2002

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