Plump endothelial cells integrated into pre-existing venules contribute to the formation of 'mother' and 'daughter' vessels in pyogenic granuloma: possible role of galectin-1, -3 and -8.

Introduction: Pyogenic granuloma (PG) is a reactive inflammatory vascular lesion of the skin and mucous membranes, characterised by the presence of enlarged venules and seamed and seamless capillaries with plump endothelial cells (EC), and numerous macrophages. EC activation upregulates the synthesis of galectins and induces their translocation to the EC surface promoting angiogenesis and lymphangiogenesis, particularly galectin-1 (Gal-1), Gal-3 and Gal-8. However, the presence and distribution of Gal-1, -3 and -8, as well as their implications in the pathogenesis of PG, has not been considered.

Galectin-1 and Galectin-3 and Their Potential Binding Partners in the Dermal Thickening of Keloid Tissues.

Keloids are defined histopathologically as an inflammatory disorder characterized by exhibiting numerous fibroblasts, abnormal vascularization, increased number of proinflammatory immune cells as well as uncontrolled cell proliferation, and exacerbated and disorganized deposition of extracellular matrix (ECM) molecules. Importantly, many of these ECM molecules display N- and O-linked glycan residues and are considered as potential targets for galectin-1 (Gal-1) and galectin-3 (Gal-3). Nevertheless, the presence and localization of Gal-1 and Gal-3 as well as the interactions with some of their binding partners in keloid tissues have not been considered.

Mucin1 expression in focal epidermal dysplasia of actinic keratosis.

Background: Actinic keratoses (AKs) are generally considered as premalignant skin lesions that can progress into squamous cell carcinoma (SCC) in situ and invasive SCC. However, its progression to SCC is still matter of debate. A transmembrane glycoprotein that contributes to the progression of certain premalignant and malignant lesions is mucin1 (MUC1).

Presence of MUC1 in the epidermal thickening of psoriatic plaques.

Mucin 1 (MUC1) is a transmembrane glycoprotein that protects epithelial cells from injury caused by external stimuli. In addition to this role, MUC1 is involved in cell-cell adhesion, proliferation, motility, invasion and survival. In epithelial cells, MUC1 expression is regulated by binding of TNFα to TNFR1 and activation of the NFκB pathway.

Possible role of NFkappaB in the embryonic vascular remodeling and the endothelial mesenchymal transition process.

The NFkappaB family of transcription factors, particularly the activated p50/p65 heterodimer, is expressed in vascular cells during intimal thickening formation when hemodynamic conditions are altered. Here, we report that p50, p65, IkappaBalpha and IKKalpha display different spatial and temporal patterns of expression and distribution during both chicken embryo aortic wall remodeling and intimal thickening development. Additionally, we show that both p50 and p65 were located in the nucleus of some mesenchymal cells expressing alpha-smooth muscle actin which are present in the spontaneous intimal thickening observed at embryonic days 12-14 of development.

Perspectives on endothelial-to-mesenchymal transition: potential contribution to vascular remodeling in chronic pulmonary hypertension.

All forms of pulmonary hypertension are characterized by structural changes in pulmonary arteries. Increased numbers of cells expressing alpha-smooth muscle (alpha-SM) actin is a nearly universal finding in the remodeled artery. Traditionally, it was assumed that resident smooth muscle cells were the exclusive source of these newly appearing alpha-SM actin-expressing cells.

Potential role for insulin-like growth factor II and vitronectin in the endothelial-mesenchymal transition process.

Endothelial-to-mesenchymal transition (EndoMT) is a process through which certain subsets of endothelial cells lose endothelial characteristics and transform into mesenchymal or smooth muscle-like cells. Emerging evidence suggests that this process plays an important role during vascular development and in many vascular pathologies. As in epithelial-mesenchymal transition, EndoMT seems to progress through a series of important steps whose interdependence and order are not clear, and that some of them are regulated by soluble growth factors.

Endothelial-mesenchymal transition occurs during embryonic pulmonary artery development.

Pulmonary vascular remodeling is a process generally associated with pulmonary hypertension that involves intimal thickening, medial hyperthrophy, and plexiform lesions. Morphological studies during pulmonary hypertension have indicated that intimal thickening consists of immature smooth muscle cells (SMCs) associated with determined extracellular matrix components, suggesting an important role for these cells in vascular lesions. Controversy exists regarding the nature and origin of the cells conforming the intimal thickenings.

Differential versican isoforms and aggrecan expression in the chicken embryo aorta.

Members of the family of large chondroitin sulfate proteoglycans (CSPGs), such as versican and aggrecan, are involved in early heart development, and in the development and progression of atherosclerosis and restenosis. Given the important roles played by versican and aggrecan in such processes, we sought to determine whether these molecules are present in the aortic wall during the advanced stages of chicken embryo development and the endothelial-mesenchymal transformation (EMT). Immunolabeling of serial cryosections revealed versican immunoreactivity around the cells within the intimal thickening, and the cells organized in lamellar and interlamellar cell layers.

Transforming growth factor-beta2 and beta3 expression in carcinoma of the prostate.

Objectives: The present study reports the clinical and histological features of 14 cases of prostate adenocarcinoma coupled with their expression of the TGF isoforms beta2 and beta3, as well as their receptor endogline (CD105).

Methods: Fourteen (14) cases of adenocarcinoma (ADC) of the prostate were examined. Relevant clinical data were gathered From the histological point of view, the tumor's grade and the evidence of perineural, vascular and/or lymphatic invasion were the key elements taken into account.

Lipoprotein lipase protects bovine endothelial cells from human NK cytotoxic activity.

Human lipoprotein lipase (LPL), in a dose dependent fashion, significantly inhibited spontaneous human natural killer (NK) cells, but not lymphokine-activated killer (LAK) cytotoxic activity against bovine pulmonary endothelial cells. The effect was dependent on endothelial heparan sulfate (HS) sites, since heparitinase reverted it. When HS is added before LPL, NK and LAK cytotoxicity are markedly reduced.

CD40 and CD40L expression in the chicken embryo aorta: possible role in the endothelial-mesenchymal transdifferentiation process.

Endothelial-mesenchymal transdifferentiation (EMT) is believed to play a crucial role in embryonic vascular development and intimal thickening, which contributes to the pathogenesis of atherosclerotic lesions. However, the mechanisms by which it occurs, as well as the signals that control it, have not yet been elucidated. Given the important role played by the CD40-CD40 ligand (CD40L) system during the initiation and progress of atherosclerosis, we investigated whether both CD40 and CD40L were present in the aortic wall during EMT and the advanced stages of chicken embryo development.

Mechanically altered embryonic chicken endothelial cells change their phenotype to an epithelioid phenotype.

Monolayers of retracted endothelial cells exhibiting wounds or zones denuded of cells were obtained from aortic explants from 10- to 12-day-old chicken embryos. Using time-lapse videomicroscopy, we investigated the sequence of events that occurred both during and after closure of the monolayer wounds. Such wound closure (re-endothelialization process) occurred 4-12 hr after removing the explants, depending on wound width and presence of serum.