PubMed · 10426748
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A Samanta, J Beardsley. 1999-07-31. Sciatica: which intervention?. https://doi.org/10.1136/bmj.319.7205.302
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Sodium-potassium ATPase (Na/K ATPase) is a major target of mineralocorticoids. Both aldosterone and glucocorticoids activate the human Na/K ATPase alpha1 and beta1 genes transcriptionally. The mineralocorticoid receptor (MR) and the glucocorticoid receptor (GR) have been shown to bind the glucocorticoid response element (GRE); however, a specific element responsible for the activation of the MR is not known. Sequence analysis of the putative regulatory region of the Na/K ATPase alpha1 gene revealed the presence of a hormone response element that allows the MR to interact with it, at least as well as if not better than the GR. This response element is designated MRE/GRE. In this investigation, we demonstrated the MR and GR induced gene expression in COS-1 cells by cotransfecting with respective expression plasmids (RshMR and RshGR) along with a luciferase reporter. The synthetic MRE/GRE linked to a neutral promoter was activated by MR (6-fold); however, the GR induced a lower level of expression (3.8-fold), suggesting that the element may be preferably MR responsive. Mutations in the synthetic MRE/GRE could not induce the expression with MR, whereas GR had a small effect. Electrophoretic mobility shift analyses demonstrated a direct interaction of MR and GR with the MRE/GRE that was supershifted by an antiMR antibody and the complex was partially cleared by an antiGR antibody, respectively, whereas nonimmune serum had no effect. Footprinting analyses of the promoter region showed that a portion of the DNA containing this element is protected by recombinant MR and GR. Thus these data confirm that this MRE/GRE interacts with both MR and GR but interaction with receptors may be more MR-responsive than response elements previously described.
This is the case of a 41-year-old renal transplant recipient taking tacrolimus immunosuppressive therapy, who had a large pleural effusion, found on a chest radiograph during the work-up of digital clubbing. The patient had undergone a renal transplant 17 months earlier for end-stage renal disease secondary to immunoglobulin A nephropathy. Analysis of the effusion fluid demonstrated a lymphocytic exudate. Biopsy specimens of pleural and lung tissues showed noncaseating granulomas. Fluid and tissue cultures were negative for viral, fungal, and bacterial pathogens. Diagnosis of sarcoidosis was established by identification of noncaseating granulomas in pleural and lung tissue, the exclusion of other conditions, and rapid resolution of the effusion after the institution of corticosteroid therapy. The patient has remained free of pulmonary symptoms and had normal chest radiographs during the 20-month follow-up period.
There is extensive evidence indicating that the noradrenergic system of the amygdala, particularly the basolateral nucleus of the amygdala (BLA), is involved in memory consolidation. Infusions of norepinephrine or beta-adrenoceptor agonists into the BLA enhance memory for inhibitory avoidance as well as water maze training. Other findings show that alpha 1-adrenoceptor activation also enhances memory for inhibitory avoidance training through an interaction with beta-adrenergic mechanisms. The central hypothesis guiding the research reviewed in this chapter is that stress hormones released during emotionally arousing experiences activate noradrenergic mechanisms in the BLA, resulting in enhanced memory for those events. Findings from experiments using rats have shown that the memory-modulatory effects of the adrenocortical stress hormones epinephrine and glucocorticoids are mediated by influences involving activation of beta-adrenoceptors in the BLA. In addition, both behavioral and microdialysis studies have shown that the noradrenergic system of the BLA also mediates the influences of other neuromodulatory systems such as opioid peptidergic and GABAergic systems on memory storage. Other findings indicate that this stress hormone-induced activation of noradrenergic mechanisms in the BLA regulates explicit/declarative memory storage in other brain regions.