Accumulation and binding of 3H-estradiol-17.BETA. by lymphoid tissues of castrated mice.

Seiki, Kanji; Imanishi, Yoshio; Haruki, Yasuo

doi:10.1507/endocrj1954.25.289

Cited by 7 publications

(1 citation statement)

References 4 publications

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“…ER mRNA and protein expression (Price & O'Brien 1993, Mizutani et al 1994 and ER mRNA expression (Crandall et al 1998, Pedersen et al 2001 have been detected in human adipose tissue. In mouse and rat adipose tissue, estrogen receptors have been detected by estradiol-binding (Seiki et al 1978, Wade & Gray 1978, Haslam & Shyamala 1981. However, to our knowledge, the relative levels of ER and have not been reported.…”

Section: Introductionmentioning

confidence: 99%

Gene expression profiling identifies liver X receptor alpha as an estrogen-regulated gene in mouse adipose tissue

Lundholm¹,

Movérare²,

Steffensen³

et al. 2004

Journal of Molecular Endocrinology

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Estrogens reduce adipose tissue mass in both humans and animals. The molecular mechanisms for this effect are, however, not well characterized. We took a gene expression profiling approach to study the direct effects of estrogen on mouse white adipose tissue (WAT). Female ovariectomized mice were treated for 10, 24 and 48 h with 17 -estradiol or vehicle. RNA was extracted from gonadal fat and hybridized to Affymetrix MG-U74Av2 arrays. 17 -Estradiol was shown to decrease mRNA expression of liver X receptor (LXR) after 10 h of treatment compared with the vehicle control. The expression of several LXR target genes, such as sterol regulatory element-binding protein 1c, apolipoprotein E, phospholipid transfer protein, ATP-binding cassette A1 and ATP-binding cassette G1, was similarly decreased. We furthermore identified a 1·5 kb LXR promoter fragment that is negatively regulated by estrogen. Several genes involved in lipogenesis and lipolysis were identified as novel targets that could mediate estrogenic effects on adipose tissue. Finally, we show that ER is the main estrogen receptor expressed in mouse white adipose tissue (WAT) with mRNA levels several hundred times higher than those of ER mRNA.

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Section: Introductionmentioning

confidence: 99%

Gene expression profiling identifies liver X receptor alpha as an estrogen-regulated gene in mouse adipose tissue

Lundholm¹,

Movérare²,

Steffensen³

et al. 2004

Journal of Molecular Endocrinology

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Short-term and long-term effects of estrogen on lymphoid tissues and lymphoid cells with some remarks on the significance for carcinogenesis

Forsberg

1984

Arch Toxicol

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Estrogens have long been thought to play a role in regulating the immune system. The difference in some types of immune responses between males and females is well-known, as is the pronounced thymic involution induced by exogenous estrogens. Estrogens stimulate some aspects of macrophage activity and, depending on dose and mitogen, inhibit or stimulate lymphocyte proliferative response in vitro. Another example is the estrogen effect on the delayed type hypersensitivity response. A broad review is given of such estrogen effects on lymphoid tissue and immune response. Most of the studies published so far are phenomenological. However, the recent description of estrogen receptors in the thymus and in some lymphocyte subpopulations, as well as a deeper understanding of regulating factors in the immune system, open the possibility of a more detailed understanding of the estrogen mechanism of interference. Estrogen effects in adults are reversible. After treating neonatal mice with the synthetic estrogen diethylstilbestrol (DES), disturbances are induced in lymphocyte populations and lymphocyte functions which are permanent and irreversible. Lymphocytes from adult, neonatally DES-treated female mice have a reduced mitogen response to ConA and LPS (T and B cell mitogen) and the delayed type hypersensitivity response is depressed. A detailed analysis demonstrated a decreased T helper cell population. The activity of Natural Killer cells is permanently reduced and this functional impairment is related to a decreased number of these cells, in turn determined at the bone marrow level. The same animals have an increased sensitivity to chemical carcinogens (methylcholanthrene) and they spontaneously develop epithelial changes in the uterine cervix which morphologically are similar to adenocarcinoma. The association between estrogen-associated malignancy and estrogen effects in lymphocyte functions deserves further study.

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Glucocorticoid receptors and their functions in lymphocytes

Homo

Picard

Durant

et al. 1980

Journal of Steroid Biochemistry

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Accumulation and binding of 3H-estradiol-17.BETA. by lymphoid tissues of castrated mice.

Cited by 7 publications

References 4 publications

Gene expression profiling identifies liver X receptor alpha as an estrogen-regulated gene in mouse adipose tissue

Gene expression profiling identifies liver X receptor alpha as an estrogen-regulated gene in mouse adipose tissue

Short-term and long-term effects of estrogen on lymphoid tissues and lymphoid cells with some remarks on the significance for carcinogenesis

Glucocorticoid receptors and their functions in lymphocytes

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