Chondrogenic Potential of Pellet Culture Compared to High-Density Culture on a Bacterial Cellulose Hydrogel.

Cell-based approaches of cartilage lesions use different culture systems to obtain optimal cell quality. Pellet cultures with high cellular density (HD) are the gold standard to keep chondrocytes in a differentiated stage. Bacterial cellulose (BC) hydrogel is discussed to prevent cellular aging and dedifferentiation.

Effect of electromagnetic fields on human osteoarthritic and non-osteoarthritic chondrocytes.

Background: Studies of the effects of electromagnetic fields (EMFs) on cartilaginous cells show a broad range of outcomes. However EMFs are not yet clinically applied as standard treatment of osteoarthritis, as EMF effects are showing varying outcomes in the literature. The aim of this study was to examine effects of EMFs (5 mT or 8 mT) on osteoarthritic (OA) and non-OA chondrocytes in order to investigate whether EMF effects are related to chondrocyte and EMF quality.

Simulated microgravity affects chondrogenesis and hypertrophy of human mesenchymal stem cells.

Purpose: During in vitro chondrogenesis of human mesenchymal stem cells (hMSCs) hypertrophy is an inadvertent event associated with cell differentiation toward the osteogenic lineage. Up to now, there is no stringent experimental control mechanism to prevent hypertrophy of MSCs. Microgravity is known to have an impact on osteogenesis.

The repair of critical-sized bone defects using expedited, autologous BMP-2 gene-activated fat implants.

The repair of bone defects can be induced experimentally with bone morphogenetic protein-2 (BMP-2) producing fat-derived stem cells, but this ex vivo tissue engineering method requires the isolation and long-term culture of autologous cells. To develop an expedited bone repair strategy, we transferred BMP-2 cDNA directly to autologous fat tissue fragments that were held in culture for only 24 h before implantation. We evaluated the ability of such gene-activated fat grafts to regenerate large segmental bone defects in rats.

Healing of large segmental bone defects induced by expedited bone morphogenetic protein-2 gene-activated, syngeneic muscle grafts.

Numerous preclinical studies have shown that osseous defects can be repaired by implanting bone morphogenetic protein (BMP)-2-transduced muscle cells. However, the drawback of this treatment modality is that it requires the isolation and long-term (approximately 3 weeks) culture of transduced autologous cells, which makes this approach cumbersome, time-consuming, and expensive. Therefore, we transferred BMP-2 cDNA directly to muscle tissue fragments that were held in culture for only 24 hr before implantation.

Glycosylation is crucial for stability of tumour and cancer stem cell antigen EpCAM.

Epithelial cell adhesion molecule EpCAM is strongly over-expressed in a variety of carcinomas where it is involved in signalling events resulting in increased expression of target genes such as c-Myc, cyclins and others, eventually conferring cells an oncogenic phenotype. However, EpCAM is also expressed in a series of healthy epithelia, albeit generally to a far lesser extend. We have uncovered differential glycosylation of EpCAM as a means to discriminate normal from malignant tissues.

Evaluation of CK8-specific autoantibodies in carcinomas of distinct localisations.

Serological screening techniques, such as SEREX and AMIDA, use tumour-specific antibodies in the blood of patients to identify tumour-associated antigens. Using AMIDA, we have recently reported the identification of cytokeratin 8 (CK8) as a new tumour antigen and the presence of elevated serum levels of CK8-specific antibodies (CK8-Abs) in patients with head and neck cancer (HNC). The translation of such a biological observation into a reliable biomarker for clinical diagnosis is a major challenge across the border of biological and clinical research.

Cytokeratin 8 associates with the external leaflet of plasma membranes in tumour cells.

We reported the identification of tumour-associated antigens from head and neck carcinomas, including cytokeratin 8 (CK8). These antigens were isolated based on the humoral immune response they elicit in vivo using the antibody-mediated identification of antigens technology. Unlike healthy squamous epithelium, tumour cells displayed CK8 at the plasma membrane.

The carcinoma-associated antigen EpCAM upregulates c-myc and induces cell proliferation.

Epithelial cell adhesion molecule (EpCAM) is a membrane glycoprotein expressed on adenomatous and simple epithelia, where it is involved in homophilic adhesion at the basolateral membrane. Carcinomas strongly overexpress EpCAM through an, as yet, unknown mechanism. Interestingly, otherwise EpCAM-negative squamous epithelia are seen to express EpCAM concomitant with their transformation and de-differentiation.

Antitumour effects of a bispecific trivalent antibody in multicellular tumour spheroids.

Background: New adjuvant immunological therapies that selectively redirect effector cells towards tumour cells are currently under development. These strategies include the use of bispecific antibodies as promising tools for the elimination of disseminated tumour cells and micrometastases. At present, bispecific molecules have demonstrated their antitumour potential in investigations in vitro using monolayer cell cultures.

New Target Genes for Tumor-derived Soluble Factors in Primary Monocytes.

Background: Tumor cells have developed several strategies to escape the immune system. One of these strategies consists of the secretion of immunosuppressive factors like interleukin-10 or prostaglandin E2 (PGE), which impair the immune system. We have demonstrated recently that tumor-derived PGE down-regulates the expression of the integrin Mac-1 and the chemokine receptor CCR5 on primary monocytes, resulting in reduced adhesion and migration.

Impaired monocyte function in cancer patients: restoration with a cyclooxygenase-2 inhibitor.

Epidemiological data and animal models have provided evidence that nonsteroidal antiinflammatory drugs (NSAIDs) have an anticancer effect. However, the molecular mechanisms underlying these antineoplastic effects are not well understood. We described previously that expression levels of the chemokine receptor, CCR5, and the beta2-integrin, Mac-1, were down-regulated on primary monocytes after incubation in supernatants from human carcinoma cell lines, and that this down-regulation resulted in impaired monocyte function with respect to migration and adhesion.