Nitric-oxide synthases consequence

Ghosh S, Gachhui R, Crooks C, Wu C, Lisanti MP, Stuehr DJ. 1998. Interaction between caveolin-1 and the reductase domain of endothelial nitric-oxide synthase. Consequences for catalysis. J Biol Chem 273 22267-22271. 

In addition to direct effects on genes regulating inflammation, glucocorticoids also inhibit the transcription factors that initiate synthesis of pro-inflammatory cytokines (e.g., interleukin-1, tumor necrosis factor), enzymes (e.g., COX-2, nitric oxide synthase), and receptor proteins (e.g., natural killer receptors).17,87,89 Glucocorticoids may also exert some of their effects via a membrane-bound receptor that regulates activity of macrophages, eosinophils, T lymphocytes, and several other types of cells involved in the inflammatory response.89 Consequently, glucocorticoids affect many aspects of inflammation, and their powerful anti-inflammatory effects in rheumatoid arthritis result from their ability to blunt various cellular and chemical components of the inflammatory response. 

Modification of human serum albumin by o-glucose impaired its antiapoptotic activity for endothelial cells a 50% loss of activity corresponded to about four fiuctosamine residues per protein molecule. In another study, D-fiuctose-albumin enhanced nitric oxide synthase activity and a consequent NO-dependent apoptosis in vascular endothelial cells. " This effect was also attributed to a possible mechanism of hyperglycemia-induced vasculopathy in diabetic patients. In proximal tubular epithelial cells, however, the effect of co-incubated D-fiuctose-albumin was the... 

The inducible isoforms of the enzymes cyclooxygenase (COX 2), nitric oxide synthase (iNOS) and heme oxygenase 1 (HO-1) have generated great interest as possible therapeutic targets in inflammation. This book is the first publication to address the importance of all three enzymes and the consequences of their interactions to the inflammatory process. 

A schematic representation of the consequence of activation of nitric oxide synthase (NOS) and resulting cascade activation of a number of molecules leads to stabilization of HIF-la increases levels of angiogenic activity under conditions of innate alter treatment-induced hypoxia, such as chemo/radiotherapy (Fig. 25.1). Based on data generated in our laboratory (Yin et al. 2006), treatment of human squamous cell carcinoma of the head and neck (FaDu) xenografts with a defined... 

NO is also a likely candidate for the NANC messenger of the myenteric plexus of neurons in the gastrointestinal tract, which mediate peristaltic movements. These neurons are rich in NO synthase and inhibitors of this enzyme prevent the nerve-evoked relaxation of the gut [12]. Nitric oxide released from nitroprusside also stimulates ADP ribosylation of glyceradehyde 3-phosphate dehydrogenase [56]. Consequently, there may be a number of enzymes, which are probably Fe-centered, that may be activated by NO. 

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