PubMed · 6224913
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
G Senechal, B Senechal. 1983. [Otoplasties].. https://pubmed.ncbi.nlm.nih.gov/6224913/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
In vitro models based on primary cultured human chondrocytes could be useful to study the ROS-mediated inflammatory processes that seem to involve chondrocytes in vivo. In this work, we studied the enzymatic antioxidative capability of human chondrocytes removed from vertebral plates during micro-discectomy and cultured 18 days, measuring total superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSHPx) activities. We also evaluated in the same cells the amount of malondialdehyde (MDA) in order to verify the effect of the variation of the cellular enzymatic antioxidative capability on the degree of membrane lipid peroxidation. Total SOD activity increased, even if not significantly, between the 12th and the 18th day. A significant variation of GSHPx (P<0.01) and of catalase (P<0.001) activity was observed between the 3rd and the 6th day with no further variation until the 18th day. A significant increase (P<0.001) of lipid peroxidation from the 3rd to the 18th day was also observed. These results seem to indicate that only fresh human cultured chondrocytes are suitable to study, through in vitro models, the in vivo behavior of the antioxidative status of these cells.
Explore the source record for details and available documents.
In response to various stress stimuli, heat shock genes are induced to express heat shock proteins (Hsps). Previous studies have revealed that expression of heat shock genes is regulated both at transcriptional and posttranscriptional level, and the rapid transcriptional induction of heat shock genes involves activation of the specific transcription factor, heat shock factor 1 (HSF1). Furthermore, the transcriptional induction can vary in intensity and kinetics in a signal- and cell-type-dependent manner. In this study, we demonstrate that mechanical loading in the form of hydrostatic pressure increases heat shock gene expression in human chondrocyte-like cells. The response to continuous high hydrostatic pressure was characterized by elevated mRNA and protein levels of Hsp70, without activation of HSF1 and transcriptional induction of hsp70 gene. The increased expression of Hsp70 was mediated through stabilization of hsp70 mRNA molecules. Interestingly, in contrast to static pressurization, cyclic hydrostatic loading did not result in the induction of heat shock genes. Our findings show that hsp70 gene expression is regulated posttranscriptionally without transcriptional induction in chondrocyte-like cells upon exposure to high continuous hydrostatic pressure. We suggest that the posttranscriptional regulation in the form of hsp70 mRNA stabilization provides an additional mode of heat shock gene regulation that is likely to be of significant importance in certain forms of stress.