scholarly journals The Differential Fate of Mesonephric Tubular-Derived Efferent Ductules in Estrogen Receptor-α Knockout Versus Wild-Type Female Mice*

Endocrinology ◽  
2000 ◽  
Vol 141 (10) ◽  
pp. 3792-3798 ◽  
Author(s):  
Cheryl S. Rosenfeld ◽  
Paul S. Cooke ◽  
Thomas H. Welsh ◽  
Gretchen Simmer ◽  
Martha G. Hufford ◽  
...  

Author(s):  
Emmanuel Guivarc'h ◽  
Julie Favre ◽  
Anne‐Laure Guihot ◽  
Emilie Vessières ◽  
Linda Grimaud ◽  
...  

Background The cardiovascular protective effects of estrogens in premenopausal women depend mainly on estrogen receptor α (ERα). ERα activates nuclear gene transcription regulation and membrane‐initiated signaling. The latter plays a key role in estrogen‐dependent activation of endothelial NO synthase. The goal of the present work was to determine the respective roles of the 2 ERα activities in endothelial function and cardiac and kidney damage in young and old female mice with hypertension, which is a major risk factor in postmenopausal women. Methods and Results Five‐ and 18‐month‐old female mice lacking either ERα (ERα −/− ), the nuclear activating function AF2 of ERα (AF2°), or membrane‐located ERα (C451A) were treated with angiotensin II (0.5 mg/kg per day) for 1 month. Systolic blood pressure, left ventricle weight, vascular reactivity, and kidney function were then assessed. Angiotensin II increased systolic blood pressure, ventricle weight, and vascular contractility in ERα −/− and AF2° mice more than in wild‐type and C451A mice, independent of age. In both the aorta and mesenteric resistance arteries, angiotensin II and aging reduced endothelium‐dependent relaxation in all groups, but this effect was more pronounced in ERα −/− and AF2° than in the wild‐type and C451A mice. Kidney inflammation and oxidative stress, as well as blood urea and creatinine levels, were also more pronounced in old hypertensive ERα −/− and AF2° than in old hypertensive wild‐type and C451A mice. Conclusions The nuclear ERα‐AF2 dependent function attenuates angiotensin II–dependent hypertension and protects target organs in aging mice, whereas membrane ERα signaling does not seem to play a role.





Biochemistry ◽  
2004 ◽  
Vol 43 (21) ◽  
pp. 6698-6708 ◽  
Author(s):  
Brian J. Philips ◽  
Pete J. Ansell ◽  
Leslie G. Newton ◽  
Nobuhiro Harada ◽  
Shin-Ichiro Honda ◽  
...  


2017 ◽  
Vol 38 (5) ◽  
pp. 1061-1072 ◽  
Author(s):  
Luhong Wang ◽  
Laura L. Burger ◽  
Megan L. Greenwald-Yarnell ◽  
Martin G. Myers ◽  
Suzanne M. Moenter




2020 ◽  
pp. 101149
Author(s):  
Zhenlei Zhao ◽  
Fan Xue ◽  
Yanpei Gu ◽  
Jianxin Han ◽  
Yingxian Jia ◽  
...  


Endocrinology ◽  
2012 ◽  
Vol 153 (3) ◽  
pp. 1183-1193 ◽  
Author(s):  
Hong Guo ◽  
Yuanyuan Zhang ◽  
David A. Brockman ◽  
Wendy Hahn ◽  
David A. Bernlohr ◽  
...  

We have previously characterized lipocalin 2 (Lcn2) as a new adipokine having a critical role in energy and lipid metabolism in male mice. Previous studies by others have suggested that Lcn2 is a putative target gene of estrogens. In this study, we reported the effect of Lcn2 deficiency on estradiol biosynthesis and estrogen receptor signaling in female Lcn2-deficient (Lcn2−/−) mice. We found that Lcn2 expression in white adipose tissue is gender, depot, and age dependent. In female mice, Lcn2 is predominantly expressed in inguinal adipose tissue but at relatively very low levels in perigonadal depot and ovary. After 22 wk of high-fat diet (HFD) feeding or at old age, Lcn2−/− female mice had significantly reduced levels of serum 17β-estradiol and down-regulated expression of estrogen receptor α in multiple metabolic tissues. Consistently, the expression of estrogen-regulated genes involved in cholesterol homeostasis, such as liver X receptor β and low-density lipoprotein receptor was also down-regulated in the adipose tissue of Lcn2−/− mice. These changes were in line with the development of atherogenic dyslipidemia in response to HFD feeding; female Lcn2−/− mice had significantly elevated levels of total cholesterol and low-density lipoprotein cholesterol, whereas reduced high-density lipoprotein cholesterol levels compared with wild-type female mice. Interestingly, when compared with wild-type controls, HFD-fed female Lcn2−/− mice had significantly reduced expression levels of aromatase, a key enzyme regulating estradiol biosynthesis, in adipose tissue. Moreover, Lcn2 deficiency markedly blunted age-related increase in adipose aromatase expression but had no significant impact on age-related reduction in ovarian aromatase expression. Our findings suggest that Lcn2 has a tissue-specific role in adipose estradiol biosynthesis, which may link Lcn2 to obesity- and age-related estradiol production and metabolic complications in females.



1997 ◽  
Vol 32 (3) ◽  
pp. 176-183 ◽  
Author(s):  
Scott R Wersinger ◽  
Koen Sannen ◽  
Constanza Villalba ◽  
Dennis B Lubahn ◽  
Emilie F Rissman ◽  
...  


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