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M T Pieraggi

Publications and source records attributed to M T Pieraggi.

105 records · Page 6Linked to original sources
PubMedDate not supplied

The mitogenic effect of 17beta-estradiol on in vitro endothelial cell proliferation and on in vivo reendothelialization are both dependent on vascular endothelial growth factor.

In addition to their actions on reproductive function, estrogens have important effects on endothelial cells. The present study was designed to evaluate the mechanism(s) by which 17beta-estradiol (E2) promotes endothelial cell proliferation. The potential involvement of vascular endothelial growth factor (VEGF) was investigated by the coadministration of polyclonal anti-VEGF antibody. First, the effect of E2 on the proliferation of cultured foetal bovine aortic endothelial cells (FBAEC) was studied. E2 stimulated this proliferation with an EC50 between 10(-11) and 10(-10) M and this effect was inhibited by the anti-VEGF antibody. The effect of a physiological dose of E2 was then studied in the rat model of carotid injury. After deendothelializing balloon injury, reendothelialization of the denuded surface may influence the growth of the underlying smooth muscle cells. Male Sprague-Dawley rats were castrated and then received E2 from subcutaneously implanted pellets that released 3.2 microg/kg/day. Endothelial regrowth (Evans blue staining) and neointimal thickening were evaluated 2 weeks after the carotid injury. In comparison to the placebo group, E2 increased the extent of reendothelialization (p = 0.0002) and reduced neointimal thickening (p = 0.0007). Anti-VEGF antibody abolished the effect of E2 on reendothelialization as well as on neointimal thickening. Thoracic aorta VEGF content was increased in E2-treated rats compared to control rats. In conclusion, the present study demonstrates that E2 increases endothelial cell proliferation in vitro and reendothelialization in vivo by means of a mechanism dependent on endogenous VEGF. This effect could contribute to the antiatherogenic effect of a physiological dose of E2.

Animals↗
PubMedDate not supplied

[Dermal aging. Immunofluorescence study of collagens I and III and fibronectin].

In this study the authors have studied 10 young subjects and 10 old subjects. The biopsies are examined by light microscopy, and by immunofluorescence techniques with specific antibodies against collagen I, III and fibronectin. In this last case the authors used also immunoelectron microscopy with peroxidase labeling and immunofluorescence techniques in fibroblasts cultures. The results showed that there was no difference in collagen localization in young and old subjects. But the fibronectin was found decreased in papillary dermis of old subjects. These results are confirmed in culture, where the fibrillar extracellular fibronectin was abundant in culture of young subjects and very poor in old subjects. The role of fibronectin will be very important in ageing, its decrease will explain the morphological modifications of dermal connective tissue with age.

Adult↗
PubMedDate not supplied

[Communicating acute aortic dissection (pathogenetic study)].

Thirty-five dissecting aneurisms of the aorta (D.A.). have been microscopically and ultramicroscopically examined. These data have been compared to those obtained from personal experiences on human aorta aging, as well as from Beta Aminopropionitrile treated rats. The authors conceive D.A. as a non-obligatory complication of a precocious and intense medianecrosis of the aortic wall, particularly characterized by a mucous imbibition and a loss elastic laminae. This medianecrosis is identical in dysplasic D.A. (Martan's syndrome for example) and in acquired D.A. (rapid aging or arteriosclerosis). The simultaneous occurence of a medianecrosis and conditions triggering tunica intima rupture, with blood afflux in the necrotic zone are undoubtedly rare. This explains the small number of observed D.A. in comparison to the large number of aortas with accentuated medial lesions.

Aged↗