Nonirradiated human fibroblasts and irradiated 3T3-J2 murine fibroblasts as a feeder layer for keratinocyte growth and differentiation in vitro on a fibrin substrate.

The standard method for producing graftable epithelia relies on the presence of a feeder layer of lethally irradiated 3T3-J2 murine fibroblasts (Rheinwald and Green technique). Here, we studied a new keratinocyte culture system, which envisages the utilization of nonirradiated human fibroblasts embedded into a fibrin substrate, in cultures destined for a future clinical application. We tested this culture system using keratinocytes grown on a fibrin gel precoated with 3T3-J2 murine fibroblasts as a control.

Tissue engineering for damaged surface and lining epithelia: stem cells, current clinical applications, and available engineered tissues.

Tissue engineering is an important tool for the treatment of damaged surface and lining epithelia. A source of cells and biocompatible substrates upon which cells can grow and differentiate are key components of this technology. Cultured normal human epithelial cells reconstitute sheets of stratified epithelia that retain biochemical and histological characteristics as well as specific differentiation features of the original donor site.

High-mobility group box 1 protein in human and murine skin: involvement in wound healing.

High-mobility group box 1 (HMGB1) protein is a multifunctional cytokine involved in inflammatory responses and tissue repair. In this study, it was examined whether HMGB1 plays a role in skin wound repair both in normoglycemic and diabetic mice. HMGB1 was detected in the nucleus of skin cells, and accumulated in the cytoplasm of epidermal cells in the wounded skin.

3,3',5-Triiodo-L-thyronine inhibits ductal pancreatic adenocarcinoma proliferation improving the cytotoxic effect of chemotherapy.

The pancreatic adenocarcinoma is an aggressive and devastating disease, which is characterized by invasiveness, rapid progression, and profound resistance to actual treatments, including chemotherapy and radiotherapy. At the moment, surgical resection provides the best possibility for long-term survival, but is feasible only in the minority of patients, when advanced disease chemotherapy is considered, although the effects are modest. Several studies have shown that thyroid hormone, 3,3',5-triiodo-l-thyronine (T(3)) is able to promote or inhibit cell proliferation in a cell type-dependent manner.

3,5,3'-triiodothyronine (T3) is a survival factor for pancreatic beta-cells undergoing apoptosis.

3,5,3'-triiodothyronine (T3) is essential for the growth and the regulation of metabolic functions, moreover, the growth-stimulatory effect of T3 has largely been demonstrated and the pathways via which T3 promotes cell growth have been recently investigated. Type 1 diabetes (T1D) is due to the destruction of beta-cells, which occurs even through apoptosis. Aim of our study was to analyze whether T3 could have an antiapoptotic effect on cultured beta-cells undergoing apoptosis.

3,5,3'-Triiodo-L-thyronine enhances the differentiation of a human pancreatic duct cell line (hPANC-1) towards a beta-cell-Like phenotype.

The thyroid hormone, 3,5,3'-Triiodo-L-thyronine (T3), is essential for growth, differentiation, and regulation of metabolic functions in multicellular organisms, although the specific mechanisms of this control are still unknown. In this study, treatment of a human pancreatic duct cell line (hPANC-1) with T3 blocks cell growth by an increase of cells in G(0)/G(1) cell cycle phase and enhances morphological and functional changes as indicated by the marked increase in the synthesis of insulin and the parallel decrease of the ductal differentiation marker cytokeratin19. Expression analysis of some of the genes regulating pancreatic beta-cell differentiation revealed a time-dependent increase in insulin and glut2 mRNA levels in response to T3.

Omomyc, a potential Myc dominant negative, enhances Myc-induced apoptosis.

The Myc basic helix-loop-helix zipper domain determines dimerization with Max and binding to the DNA E-box, both of which play a critical role in Myc regulation of growth, proliferation, tumorigenesis, and apoptosis. The mutant basic helix-loop-helix zipper domain, Omomyc, dimerizes with Myc, sequestering it in complexes unable to bind the E-box, and so acting as a potential dominant negative. Consistent with this, Omomyc reverses Myc-induced cytoskeletal disorganization in C2C12 myoblasts.