PubMed · 5642263
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M Linquette. 1968-03-16. [Does a natriuretic hormone exist?].. https://pubmed.ncbi.nlm.nih.gov/5642263/
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The potential antioxidant activity of 17-beta estradiol and other steroid hormones in neuronal cells was investigated by studying oxidative stress-induced cell death caused by the neurotoxins amyloid beta protein, hydrogen peroxide and glutamate in the clonal mouse hippocampal cell line HT22. Preincubation of the cells with 10(-5) M 17-beta estradiol prior to addition of the neurotoxins prevented oxidative stress-induced cell damage and ultimately cell death, as detected with cell viability (MTT) and cell lysis (trypan blue exclusion/cell counting; propidium iodide staining) assays. At the DNA level, 17-beta estradiol blocked the DNA degradation caused by glutamate. Other steroid hormones, such as progesterone, aldosterone, corticosterone and the steroid precursor cholesterol, did not protect the cells. The neuronal protection afforded by 17-beta estradiol was estrogen receptor-independent. These data demonstrate a potent neuroprotective activity of the antioxidant 17-beta estradiol, which may have implications for the prevention and treatment of Alzheimer's disease.
Recent studies have confirmed that the 90 kDa heat-shock protein (hsp90) interacts both in vitro and in vivo with steroid receptors, encouraging further detailed physicochemical and functional analysis of its chaperone role. Thus, to explore the relationship between hsp90 and receptors, the baculovirus system was used to overexpress the chick hsp90 alpha (chsp90) along with the chick oestradiol receptor (cER) or the human mineralocorticosteroid receptor (hMR). These receptors were able to form 9 S complexes with chsp90, demonstrating the association of the co-expressed recombinant proteins. Three mutants of chsp90 (delta A, delta B and delta Z) have been created by deletion of the A (residues 221-290) and B (530-581) regions, rich in charged amino acids, and the Z (392-419) region, a putative leucine zipper. After co-expression, anti-receptor antibodies immunoprecipitated the cER or hMR complexed with the wild-type chsp90, the delta B or the delta Z mutant, but not with the delta A chsp90, indicating that deletion of the A region of chsp90 leads to a lack of interaction with these receptors. The hormone binding capacity of the cER was unaffected after its co-expression with each of the three mutants. In contrast, the hMR co-expressed with the delta B mutant failed to bind aldosterone, a finding confirmed in vivo by the absence of hormone-induced hMR nuclear translocation. Thus the B region is required for high-affinity ligand binding by the hMR. Our results suggest that the A region (but not the B or Z regions) is involved in binding of chsp90 to the cER and hMR, while the B region is essential for hormone binding by the hMR, consistent with a chaperone function for hsp90.
Our better understanding of the terminal steps of aldosterone production based on enzyme cloning has led to new clinical approaches to three aldosterone-related types of hypertension: mineralocorticoid excess, Liddle's disease and glucocorticoid-sensitive hyperaldosteronism. In all three cases, hypertension results from volume expansion due to increased reabsorption of sodium in the distal renal tube with decreased plasma renin activity and hypokaliaemia. Genetic testing now allows early diagnosis of these severe familial diseases and specific treatment. Although both glucocorticoid-sensitive hypertension and Liddle's disease are dominantly inherited diseases, other genes can also modulate the degree of volume expansion, hypokaliaemia and blood pressure levels within a given family. The degree of hypertension observed in a given individual results from the interactions between the expression of "hypertenser" and "hypotenser" genes. Recent progress raises the possibility that other similar genetic mechanisms exist in more common forms of primary hypertension. Systematic exploration of the renin-angiotensin-aldosterone system based on measurement of the renin/aldosterone ratio as proposed in the diagnosis of primary hyperaldosteronism will make it possible to determine whether there exists a relationship between these genes and the hypertension observed.