Integrins represent a candidate group of cell surface receptors that may control the homing and population of the thymus by T-cell precursors and the subsequent migration of developing thymocytes through the thymic architecture. We have used multiparameter flow cytometric methods to characterize the expression of several members of the integrin family (alpha 3 beta 1, alpha 4 beta 1, alpha 5 be...

Cancer cell drug resistance develops via several mechanisms, including apoptosis evading, efflux, reprogramming, DNA repair. Recently numerous data pointed out an ability of cancer cells reversibly exit from cycle to enter in G0 phase that may favor survival. Therefore, the goal study was determine transcriptional phenotype associated with quiescent/senescent state acquisition. Melanoma were tr...

Neurotensin receptor activation augments the biosctivity of glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). JMV-449, a C-terminal neurotensin-like fragment with reduced peptide bond, represents neurotensin agonist. The present study assessed actions JMV-449 on pancreatic beta-cells alone, in combination GIP GLP-1. Further studies examined impact incretin ...

The present study evaluates the development and functional properties of beta cells differentiated in vitro. The authors have previously demonstrated that when E12.5 rat pancreatic rudiments are cultured in vitro in the absence of mesenchyme, the majority of the epithelial cells differentiate into endocrine beta cells. Thus, depletion of the mesenchyme provokes the expansion of endocrine tissue...

Introduction: Inflammation has been linked to hemichannel-mediated release of adenosine triphosphate (ATP) and downstream fibrosis in various tissue type-specific complications diabetes. In the current study we examined how inflammatory cytokines alter markers renal tubular injury ahead evaluating efficacy connexin-43 (Cx43) hemichannel blocker Tonabersat negating these effects. Methods: Human...

Insulin-producing pancreatic islet beta cells (beta-cells) are destroyed, severely depleted or functionally impaired in diabetes. Therefore, replacing functional beta-cell mass would advance clinical diabetes management. We have previously demonstrated the importance of Cdk4 in regulating beta-cell mass. Cdk4-deficient mice display beta-cell hypoplasia and develop diabetes, whereas beta-cell hy...