Most authors have concluded that early wide surgical excision of the tumor is the treatment of choice. The efficiency of adjuvant therapy generally has not established.

For cartilage reconstruction, it is still difficult to obtain a sufficient volume of cartilage and to maintain its functional phenotype for a long period. Utilizing tissue stem cells is one approach to overcome such difficulties. We show here the presence of cartilage progenitor cells in the ear perichondrium of adult rabbits by 5-bromo-2 0 -deoxyuridine labeling, clonogenicity, and differentiation analyses. Long-term label-retaining cells were demonstrated in the perichondrium. Cells from the perichondrium, that is, perichondrocytes were mechanically isolated using a raspatory and maintained in D-MEM/F-12 medium with 10% FCS. They proliferated more vigorously than chondrocytes from the cartilage. Perichondrocytes could differentiate into adipocytes as well as osteocytes in differentiation induction medium. For cartilage reconstruction in vivo, perichondrocytes were seeded on collagen sponge scaffolds and implanted in nude mice. After 4 weeks, the composites with perichondrocytes generated the same weight of cartilaginous tissue as those with chondrocytes. They produced glycosaminoglycan and type II collagen as shown by RT-PCR and immunohistochemical examination. On the contrary, rabbit bone marrow mesenchymal stem cells used as control could regenerate significantly smaller cartilage than perichondrocytes in the implant study. Based on these findings, we propose that the perichondrium containing tissue progenitor cells is one of the potential candidates for use in reconstructing cartilage and new therapeutic modalities.

Syndecans function as receptors for extracellular matrix (ECM) with integrins in cell spreading. However, the molecular mechanism of their specific involvement in cell migration or in wound healing has not been elucidated yet. Here, we report that a synthetic peptide, PEP75, which contains the syndecan-binding sequence of the laminin alpha 3LG4 module, induces keratinocyte migration in in vitro and in vivo. Soluble PEP75 induced the clustering of syndecan-4 and conformation-modified integrin beta1 colocalized with syndecan-4 in soluble PEP75-induced clusters. Treatment of cells in solution with PEP75 resulted in the exposure of the P4G11 antibody epitope of integrin beta1 in immunostaining as well as in flow cytometry and augmented integrin beta1-dependent cell adhesion to ECM. Pulldown assays demonstrated that PEP75 bound to syndecan-4, but not to integrin beta1. A siRNA study revealed a role for syndecan-4 in PEP75-induced up-regulation of P4G11 antibody binding and migration of HaCaT cells. We conclude that binding of soluble PEP75 to syndecan-4 induces the coupling of integrin beta1, which is associated with integrin beta1-conformational changes and activation, and leads to keratinocyte migration. To activate integrin function through syndecans could be a novel therapeutic approach for chronic wound.

No abstract

Soft-tissue reconstruction of the feet in diabetic patients with angiopathy, sensorial neuropathy, and immunopathy is a complicated problem. Until the mid-1980s, chronic foot ulcers in diabetic patients were treated conservatively, because flap surgery was regarded as too risky. However, in recent years, early debridement and flap coverage have become popular reconstructive methods for diabetic foot wounds. Several flap donor sites are available, depending on the nature of the defect. The deep inferior epigastric artery perforator (DIEP) flap is a relatively new flap that developed as a modification of the transverse rectus abdominis muscle (TRAM) flap. It provides a large amount of skin and subcutaneous tissue, without the donor-site morbidity of the ordinary TRAM flap. Furthermore, using the DIEP flap avoids the loss of major vessels. In this study, we report on the successful use of the DIEP flap in four cases of diabetic foot ulceration.