PubMed · 4886360
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C Toussaint, A Verniory, J P Naets, J Corvilain, P P Lambert. 1968. [Anephric man].. https://pubmed.ncbi.nlm.nih.gov/4886360/
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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.
Several published reports describe an abnormal circadian blood pressure profile in chronic renal failure subjects. Factors other than renal failure, including age, diagnosis of diabetes mellitus, autonomic dysfunction, and race, also may affect circadian blood pressure profiles. To further elucidate the relationship between renal function and circadian blood pressure variation, we compared day/night circadian blood pressure changes in three groups of male veteran hypertensive patients: group A, creatinine clearance (CC) > 80 mL/min, n = 20; group B, CC 20 to 80 mL/min, n = 19; and group C, CC < 20 mL/min, n = 14. We use postural changes in catecholamines, renin, and aldosterone as a measure of autonomic function. No significant difference in day/night percent change in systolic, diastolic, mean arterial pressure (MAP), or heart rate was seen by renal function group. Regression analysis using age, diagnosis of diabetes mellitus, postural hormonal changes, and creatinine clearance found race to be the only significant predictor of the day/night percent change in MAP (P < 0.05). Compared with whites, black subjects had higher nocturnal heart rates (P = 0.01); smaller day/night heart rate changes (P = 0.03); significantly higher diastolic blood pressure (P = 0.01); and a trend toward smaller day/night change in diastolic blood pressure (P = 0.06). In conclusion, renal function level does not influence day/night blood pressure changes. The blunting or reversal of the normal circadian blood pressure pattern seen in some chronic renal failure hypertensive subjects may be attributable to the association between chronic renal failure and cofactors associated with abnormal circadian blood pressure, including black race and possibly severity of atherosclerosis.