PubMed · 9801208
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L Rangaswamy. 1998. Conversations with a cab driver.. https://doi.org/10.2106/00004623-199810000-00001
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BACKGROUND: Our previous study demonstrated that temperature-related microwave ablation (MWA) can safely modulate growth plates of piglets' vertebrae. Therefore, this study is designed to investigate the effects of different temperatures on chondrocyte viability and the underlying molecular mechanisms in vitro. METHODS: Following a 10-minute treatment at different temperatures (37 °C, 40 °C, 42 °C, 44 °C, 46 °C, 48 °C, and 50 °C), CCK-8 assay was used to examine the viability of ATDC5 cells at 12 h. Differentially expressed genes (DEGs) and the hub genes in ATDC5 cells treated at 37 °C, 40 °C and 44 °C were identified using RNA-seq. The expression of hub genes in ATDC5 cells was validated using RT-qPCR. RESULTS: Compared with 37 °C, exposure to 40 °C significantly increased the viability of ATDC5 cells, while 42 °C had no significant effect. Additionally, exposure to 44 °C, 46 °C, 48 °C, and 50 °C exhibited the opposite pattern, with ATDC5 cells being particularly less than 50% active after treatment at 46 °C, 48 °C, and 50 °C. Differential expression analysis identified 179, 374 and 221 DEGs in the comparisons of 40 °C vs. 37 °C, 44 °C vs. 37 °C, and 44 °C vs. 40 °C, respectively. These DEGs predominantly regulated proliferation, differentiation, necrosis, inflammatory and immune responses, and ECM synthesis/degradation. Furthermore, they were associated with the Ras, PI3K/AKT, mTOR, cAMP, and MAPK pathways. Agt, Hspa1a, Hspb1, and Nlrc4 were identified as hub genes in DEGs, and RT-qPCR confirmed that the mRNA expression patterns of these hub genes in ATDC5 cells were largely consistent with the RNA-seq results. CONCLUSION: The regulation of chondrocyte viability by temperature is associated with Ras, PI3K/AKT, mTOR, cAMP, and MAPK pathways. Additionally, Agt, Hspa1a, Hspb1, and Nlrc4 may be the key regulatory genes in this process.
OBJECTIVE: To evaluate the feasibility of in vitro fabrication of tissue-engineered cartilage from human nasoseptal chondrocytes for autologous reconstruction. DESIGN: Hyaline cartilage was reconstituted from chondrocyte-polyglycolic acid scaffolding constructs in a 3-dimensional mammalian cell culture cascade. This included monolayer cellular amplification, cell seeding in the spinner flask, and tissue growth in simulated microgravity. RESULTS: The quality of the fabricated cartilage analogue was found to depend on the initial cell density, duration of incubation, and bioreactor type. Dynamic seeding was nearly completed within the first 10 hours of inoculation regardless of the cell source (cryogenically preserved vs fresh chondrocytes) or presence of serum. A duration of incubation in excess of 4 weeks was required for complete matrix biosynthesis at low seeding densities in the spinner flasks. Seeding densities greater than 2.3x10(6) chondrocytes per scaffold were required for early hyaline cartilage formation as well as longer-time mature matrix regeneration. In addition, maintaining the structural integrity of the unreinforced scaffold, which is necessary for continued mature matrix regeneration, was achievable through postseeding tissue growth in simulated microgravity. CONCLUSION: Once combined with polyglycolic acid scaffolds in the bioreactor cascades that allow efficient seeding and quiescent tissue growth, human septal chondrocytes become a valuable source of reproducible ex vivo cartilage regeneration in the laboratory.
OBJECTIVE: To examine the mechanism of interleukin-1 (IL-1)-induced collagenase 3 (matrix metalloproteinase 13 [MMP-13]) gene expression in cultured chondrocytes for the purpose of better understanding how the gene is induced in these cells, and how it contributes to cartilage degradation in osteoarthritis. METHODS: The transcriptional and posttranscriptional responses of the MMP-13 gene to IL-1 were assessed first. Then, direct inhibitors of mitogen-activated protein kinase (MAPK) signaling pathways and a constitutive repressor of nuclear factor kappaB (NF-kappaB) were used to assess the role of each pathway in IL-1-mediated induction of MMP-13. RESULTS: We found that IL-1 induction of MMP-13 requires p38 activity, c-Jun N-terminal kinase (JNK) activity and NF-kappaB translocation. These results suggest that both NF-kappaB and activator protein 1 transcription factors are necessary for IL-1 induction of MMP-13. We also compared the signaling pathways necessary for IL-1 to stimulate collagenase 1 (MMP-1) in articular chondrocytes and chondrosarcoma cells and found that IL-1 induction of MMP-1 requires different pathways from those required by MMP-13. In chondrosarcoma cells, MMP-1 induction depends on p38 and MEK (an MAPK kinase of the extracellular signal-regulated kinase pathway) and does not require JNK or NF-kappaB. In articular chondrocytes, inhibition of MEK had no effect, while inhibition of p38 gave variable results. CONCLUSION: These studies demonstrate, for the first time, that p38, JNK, and NF-kappaB are required for IL-1 induction of MMP-13. The results also highlight the differential requirements for signaling pathways in the induction of MMP-1 and MMP-13. Additionally, they demonstrate that induction of MMP-1 by IL-1 in chondrocytic cells depends on unique combinations of signaling pathways that are cell type-specific.