Is expression of TGF-betas and their receptors differentially modulated by reactive oxygen species and nitric oxide in human articular chondrocytes?
The modulation of TGF-beta system was found to be differentially controlled by NO and ROS productions. Indeed, the control exerted on TGF-beta expression varied according to the isoform: TGF-beta1 mRNA level depends on NO whereas that of TGF-beta2 is regulated by ROS and TGF-beta3 seems to be unaffected by both of them. The expression of TGF-beta receptors appeared to be modulated by NO and ROS levels. The relevance of the present findings to osteoarthritis (OA) physiopathology and the potential use of antioxidant therapy to treat this disease are discussed.
The induction of the glycation reaction, which is known to occur in pancreatic beta cells in chronic hyperglycaemia, suppresses the glucokinase gene transcription and its enzymatic activity. Thus, hyperglycaemia-dependent inhibition of glucokinase activity could in part explain beta-cell glucose toxicity.