Chondrogenic differentiation by mesenchymal progenitor cells (MPCs) is associated with cytokines such as transforming growth factor-beta 1 (TGF-PI) and dexamethasone. Extracellular matrix (ECM) also regulates the differentiation by MPCs. To define whether ECM plays a functional role in regulation of the chondrogenic differentiation by MPCs, an in vitro model was used. That model exposed to dexamethasone, recombinant human TGF-@l(rhTGF-@I) and collagens. The results showed that MPCs incorporated with dexamethasone and rhTGF-01 increased proliferation and expression of glycosaminoglycan (GAG) after 14 days. Type 11 collagen enhanced the GAG synthesis, but did not increase alkaline phosphatase (ALP) activity. When adding dexamethasone and rhTGF-PI MPCs increased mRNA expression of sox9. Incorporation with type I1 collagen, dexamethasone and rhTGF-Pl, MPCs induced mRNA expression of aggrecan and enhanced levels of type I1 collagen, and sox9 mRNA. In contrast, incorporation with type I collagen, dexamethasone and rhTGF-PI MPCs reduced levels of aggrecan, and sox9 mRNA, and showed no type I1 collagen mRNA. Altogether, these results indicate that type I and I1 collagen, in addition to the cytokine effect, may play a functional role in regulating of chondrogenic differentiation by MPCs.
Adipose-derived stem cells (ADSCs) are multipotent cells that have attracted much recent attention. Here, we show that ADSCs enhance sphere formation and in vivo tumor initiation of breast and colon cancer cells. In co-culture, ADSCs induced several stem cell markers in cancer cells. ADSCs also accelerated tumor growth. Interaction of ADSCs and cancer cells stimulated secretion of interlukin-6 in ADSCs, which in turn acted in a paracrine manner on cancer cells to enhance their malignant properties. Interleukin-6 regulated stem cell-related genes and activated JAK2/STAT3 in cancer cells. We suggest that ADSCs may enhance tumor initiation and promotion.
The limited source of healthy primary chondrocytes restricts the clinical application of tissue engineering for cartilage repair. Therefore, method to maintain or restore the chondrocyte phenotype during in vitro expansion is essential. The objective of this study is to establish the beneficial effect of ECM molecules on restoring the re-expression of cartilaginous markers in primary human chondrocytes after extensive monolayer expansion. During the course of chondrocyte serial expansion, COL2A1, SOX9, and AGN mRNA expression levels, and GAG accumulation level were reduced significantly in serially passaged cells. Exogenous type II collagen dose-dependently elevated GAG level and induced the re-expression of cartilaginous marker mRNAs in P7 chondrocytes. Chondroitin sulfate did not show significant effect on P7 chondrocytes, while hyaluronic acid inhibited the expression of SOX9 and AGN mRNAs. Upon treatment with type II collagen, FAK, ERK1/2, and JNK were activated via phosphorylation in P7 chondrocytes within 15 min. Furthermore, GFOGER integrin blocking peptide, MEK inhibitor and JNK inhibitor, not p38 inhibitor, significantly reduced the type II collagen-induced GAG deposition level. Finally, in the presence of TGF-β1 and IGF-I, P7 chondrocytes cultured in 3D type II collagen matrix exhibited better cartilaginous features than those cells cultured in the type I collagen matrix. In conclusion, type II collagen alone can effectively restore cartilaginous features of expanded P7 human chondrocytes. It is probably mediated via the activation of FAK-ERK1/2 and FAK-JNK signaling pathways. The potential application of type II collagen in expanding a scarcity of healthy chondrocytes in vitro for further tissue engineering is implicated.
Short-term treatment using the cFIR neck device partly reduced muscle stiffness. Although the differences in the VAS and PPT scores for the experimental and control groups were not statistically significant, the improvement in muscle stiffness in the experimental group warrants further investigation of the long-term effects of cFIR treatment for pain management.
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