Sex-specific eNOS activity and function in human endothelial cells.

Clinical and epidemiological data show that biological sex is one of the major determinants for the development and progression of cardiovascular disease (CVD). Impaired endothelial function, characterized by an imbalance in endothelial Nitric Oxide Synthase (eNOS) activity, precedes and accelerates the development of CVD. However, whether there is any sexual dimorphism in eNOS activity and function in endothelial cells (ECs) is still unknown.

Chronic nitric oxide deprivation induces an adaptive antioxidant status in human endothelial cells.

In a previous work, we showed an increased cell motility due to the accumulation and transcriptional activation of the Hypoxia Inducible Factor-1α (HIF-1α) and a reduced mitochondrial energy production in an in vitro model of endothelial dysfunction (ED) represented by human endothelial cells (ECs) chronically deprived of nitric oxide (NO) by L-NAME treatment. In the present study, in the attempt to unravel the pathway(s) linking NO deficiency to HIF-1α accumulation and activation, we focused our attention on Reactive Oxygen Species (ROS). We found that ROS were partially involved in HIF-1α stabilization, but not in the pro-migratory phenotype.

Endometrial stromal cells from women with endometriosis reveal peculiar migratory behavior in response to ovarian steroids.

Objective: To evaluate differences in endometrial stromal cell (ESC) migration between patients with and without endometriosis.

Design: Differences in ESC migration, cellular morphology, and cytoskeletal-actin dynamics were evaluated in response to platelet-derived growth factor-BB (PDGF-BB) and steroid hormones (17beta-estradiol and progesterone).

Setting: Medical school research laboratory.

Deregulated human glioma cell motility: inhibitory effect of somatostatin.

Malignant gliomas are highly invasive tumors which are lethal despite aggressive therapy. The motility behavior of two human glioma cell lines i.e.

Human endostatin-derived synthetic peptides possess potent antiangiogenic properties in vitro and in vivo.

Pharmacological control of the angiogenic process (i.e., the neovascularization necessary for the growth and progression of tumors and metastases) is considered to be one of the most promising approaches to antineoplastic therapy.

Alprostadil suppresses angiogenesis in vitro and in vivo in the murine Matrigel plug assay.

1. Prostaglandin E(1) (PGE(1), alprostadil) is used as a vasodilator for the treatment of peripheral vascular diseases. 2.

Invasive behaviour of glioblastoma cell lines is associated with altered organisation of the cadherin-catenin adhesion system.

As little is known about the role of cadherin-mediated cell-cell adhesion in astrocytes and its alteration in migrating and invasive glioblastomas, we investigated its molecular composition and organisation in primary cultured astrocytes and the T98G and U373MG glioblastoma cell lines. Biochemical and morphological analysis indicated that all three cell types express all of the structural components of the adhesion system, including the LIN-7 PDZ protein, a novel component involved in the organisation of the junctional domain in epithelia and neurons. However, only the astrocytes and T98G cells generated and maintained mature adhesive junctional domains to which LIN-7 was recruited.