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S Barduagni

Publications and source records attributed to S Barduagni.

3 recordsLinked to original sources
PubMed1999

Expression of Bcl-2, p53, c-jun and c-fos protooncogenes in keloids and hypertrophic scars.

Keloids and hypertrophic scars represent a model of altered wound healing characterized by overproduction of extracellular matrix and dermal fibroblasts with high mitotic rate. Alteration of apoptosis and cell proliferation has been implicated in the etiology of keloids. The bcl-2 protooncogene encodes a protein that protects cells from programmed cell death while p53 protein functions as negative regulator of cell proliferation. Both protooncogenes have been shown to play a role in tissue homeostasis as apoptotic regulatory genes. The c-jun and c-fos protooncogenes are transactivating factors also involved in fibroblast proliferation. In our study we investigated, by immunohistochemistry, skin specimens from three clinically active hypertrophic scars and keloids, two resting keloids and two early phase morphea to detect both bcl-2 and p53 protein expression, in order to evaluate these apoptotic regulatory genes in different fibrotic conditions. The c-jun and c-fos, at protein and mRNA level, and Ki67 nuclear antigen expression were also investigated. In hypertrophic scars and active keloids we could detect intense Bcl-2 staining in basal keratinocytes and in scattered fibroblast-like and perivascular spindle-shaped cells, while no p53 expression could be demonstrated. The c-jun and c-fos mRNA and protein expression was mainly found in dermal fibroblast-like cells and elongated perivascular cells in all skin biopsies, and similar immunostaining pattern was observed for Ki67 antigen. No protooncogene expression in morphea patients and normal skin, unless Bcl-2 staining in the basal layer of normal epidermis, was documented. Our results suggest that Bcl-2, c-jun and c-fos protein expression and lack of p53 detection in fibroblast-like and perivascular spindle cells are related to increased fibroblast proliferation, confirmed by Ki67 positivity, probably due to alteration of these regulatory apoptotic genes resulting in pathological scarring.

Apoptosis↗
PubMed1998

In situ labelling of fragmented DNA in cutaneous necrotizing vasculitis.

Apoptosis is a biochemically and morphologically gene-regulated distinctive form of cell death playing a pivotal role in tissue homeostatic, viral infections and clearance of damaged cells. The process is initiated by a cascade of intercellular and intracellular signals through an intrinsic cell suicide program resulting in early DNA fragmentation characterized by nuclear and cytoplasmic condensation. Recently some authors have reported apoptosis to occur in several inflammatory skin diseases, such as lichenoid reactions and cutaneous lymphomas. The aim of our study is to investigate the apoptotic phenomenon in two different forms of cutaneous necrotizing vasculitis (CNV) affecting the postcapillary venules such as leukocytoclastic and lymphocytic cutaneous vasculitis. For this purpose, the in situ nick end labelling of fragmented DNA technique has been performed on lesional skin biopsies from patients with acute phase of the disease. In both leukocytoclastic and lymphocytic forms apoptotic bodies were detected, evidencing two different characteristic patterns of distribution, probably related to the different nature of cellular inflammatory infiltrate. Our results seem to account for the involvement of apoptotic phenomena in cutaneous vasculitis; furthermore, the evaluation of in situ DNA fragmentation could be a useful tool to discriminate different forms of the disease.

Adult↗