Hepatic Stellate Cells Contain the Functional Estrogen Receptor β but Not the Estrogen Receptor α in Male and Female Rats

2001 ◽  
Vol 286 (5) ◽  
pp. 1059-1065 ◽  
Author(s):  
Yajun Zhou ◽  
Ichiro Shimizu ◽  
Guangming Lu ◽  
Mina Itonaga ◽  
Yoshihito Okamura ◽  
...  
2001 ◽  
Vol 91 (4) ◽  
pp. 1886-1892 ◽  
Author(s):  
Shashita R. Inamdar ◽  
Kathleen M. Eyster ◽  
Evelyn H. Schlenker

We hypothesized that administration of an antisense oligodeoxynucleotide (ODN) to estrogen receptor (ER)-α mRNA decreases the ER protein in the neonatal rat brain, alters the sex-specific ventilatory responses to aspartic acid in rats, and counteracts the effects of testosterone proportionate (TP) in females. One-day-old rat pups were injected intraventricularly with vehicle, antisense ER ODN, or scrambled ODN control. Additional groups of females received TP or vehicle and one of the three treatments. Brain ER protein levels were decreased by 65% at 6 h and 35% at 24 h after antisense ODN. Aspartic acid decreased ventilation in all groups of weanling males and females except ER ODN-treated females and TP-vehicle-treated females. Aspartic acid decreased ventilation in all groups of adult females except those given TP and in males. Weanling ER ODN-treated rats were shorter and weighed less than controls. Only adult ER ODN-treated males exhibited these traits. Thus neonatal ER affects aspartic acid modulation of breathing and body growth in a sex-specific and developmental manner.


Neuroscience ◽  
2006 ◽  
Vol 141 (4) ◽  
pp. 1793-1800 ◽  
Author(s):  
C.A. Mazzucco ◽  
S.E. Lieblich ◽  
B.I. Bingham ◽  
M.A. Williamson ◽  
V. Viau ◽  
...  

2006 ◽  
Vol 290 (2) ◽  
pp. H823-H829 ◽  
Author(s):  
Maria Natalia Cruz ◽  
Gillian Douglas ◽  
Jan-Å Gustafsson ◽  
Lucilla Poston ◽  
Karolina Kublickiene

The objectives of this study were to determine whether acute dilatory responses to estrogen receptor agonists are altered in isolated arteries from estrogen receptor β-deficient mice (β-ERKO) and to gain insight into the role of nitric oxide (NO) in these responses. Femoral arteries (∼250 μm) from male and female β-ERKO mice and wild-type (WT) littermates (26 female, 13 in each group; and 24 male, 12 in each group) were mounted on a Multi-Myograph. Concentration-response curves to 17β-estradiol (17β-E2) and the selective estrogen receptor-α (ER-α) agonist propyl-[1H]-pyrazole-1,3,5-triy-trisphenol (PPT) were obtained before and after NO synthase (NOS) inhibition [ Nω-nitro-l-arginine methyl ester (l-NAME), 0.1 mM] in arteries preconstricted with U-46619 (a thromboxane analog). In WT mice, responses to the potent estrogen receptor-β (ER-β) agonist 2,3-bis(4-hydroxyphenyl)-propionitrile (DPN) and the contribution of NO were also assessed. Concentration-response curves to 17β-E2 and PPT were similar in arteries from WT and β-ERKO mice of both genders, but NO-mediated relaxation was different, since l-NAME reduced 17β-E2 mediated relaxation in arteries from male and female β-ERKO but not WT mice ( P < 0.05). NOS inhibition reduced dilation to PPT in arteries from male and female WT mice, as well as arteries from female β-ERKO mice ( P < 0.05). Responses to DPN in arteries from WT female and male mice did not differ after NOS inhibition. The acute dilatory responses to estrogenic compounds are similar in WT and β-ERKO mice but differ mechanistically. Because NO appeared to contribute to responses to 17β-E2 in arteries from β-ERKO but not WT mice, the presence of ER-β apparently inhibits ER-α-mediated NO relaxation.


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