Biological Effects of ERα-and ERβ-Selective Estrogens

Fritzemeier, Karl Heinrich; Hillisch, Alexander; Elger, W.; Kaufmann, Ulrike; Kollenkirchen, U.; Kosemund, Dirk; Lindenthal, B.; Müller, G; Muhn, Peter; Nubbemeyer, Reinhard; Peters, Olaf; Siebel, Philip; Hegele‐Hartung, Christa

doi:10.1007/978-3-662-05386-7_9

Cited by 12 publications

(14 citation statements)

References 32 publications

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“…In fact, the vaginal smears that were characteristic of pseudopregnancy suggest a progesterone-rich environment in DPN-treated mice. This agrees with the fact that the administration of estrogens to ERKO mice, or an ERb agonist to a wild type animal, induces high levels of LH [57], which might be associated with increased progesterone. The systemic effects induced by these agonists are currently being studied in this strain of mice.…”

Section: Discussionsupporting

confidence: 83%

Inhibition of mammary tumor growth by estrogens: is there a specific role for estrogen receptors alpha and beta?

Soldati

Wargon

Cerliani

et al. 2009

Breast Cancer Res Treat

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To evaluate the extent to which each estrogen receptor (ER) subtype contributes to the stimulation or to the inhibition of mammary tumor growth, we evaluated the effects of specific agonists in MC4-L2 cells, which are stimulated by 17β-estradiol (E(2)), and in mammary carcinomas of the MPA mouse breast cancer model, which are inhibited by E(2). Both express ERα and ERβ. In MC4-L2 cells, 4,4',4"-(4-propyl-(1H)-pyrazole-1,3,5-triyl)trisphenol (PPT; ERα agonist) and (4-hydroxy-phenyl)-propionitrile (DPN; ERβ agonist) stimulated cell proliferation, whereas the opposite occurred in C4-HI primary cultures. The inhibitory effect was associated with a decrease in ERα and cyclin D1 expression and an increase in progesterone receptor (PR) expression as well as in the Bax/Bcl-xl ratio. In vivo, mice carrying C4-HI or 32-2-HI tumors were treated with E(2), PPT or DPN (3 mg/kg/day) or with vehicle. PPT and DPN inhibited tumor size, as did E(2), during the first 72 h. After a few days, DPN-treated tumors started to grow again, while PPT-treated tumors remained quiescent for a longer period of time. A pronounced decrease in the mitotic index and an increase in the apoptotic index was associated with tumor regression. All treated tumors showed: (a) an increase in integrin α6 and Bax expression, (b) an increased stromal laminin redistribution, and (c) a decrease in ERα, Bcl-xl and Bcl-2 expression (P < 0.001). Apoptosis-inducing factor (Aif) expression was increased in DPN-treated tumors, while active caspase 9 was up-regulated in PPT-treated mice, demonstrating the involvement of the intrinsic apoptotic pathway in estrogen-induced regression in this model. In conclusion, our data indicate that although there may be some preferences for activation pathways by the different agonists, the stimulatory or inhibitory effects triggered by estrogens are cell-context dependent rather than ER isoform dependent.

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Section: Discussionsupporting

confidence: 83%

Inhibition of mammary tumor growth by estrogens: is there a specific role for estrogen receptors alpha and beta?

Soldati

Wargon

Cerliani

et al. 2009

Breast Cancer Res Treat

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show abstract

“…Using the ER selective agonists 16alpha-LE2 and 8beta-VE2 [29], we were able to show that the E2 and Gen effects on Gastrocnemius MHC-IIb and Soleus MHC-I are both predominantly mediated via the ER␤ (Figs. 3 and 5).…”

Section: Discussionmentioning

confidence: 97%

“…For these doses activation and subsequent signaling through either ER␣ or ER␤, respectively can be anticipated [29,30].…”

Section: Animals and Study Designmentioning

confidence: 99%

“…Because the ER␣ and ER␤ agonists activate both receptors at higher concentrations [29,30], doses of 10 g kg −1 b.wt d −1 (16␣-LE2) and 100 g kg −1 b.wt d −1 (8␤-VE2) were chosen, respectively. For these doses activation and subsequent signaling through either ER␣ or ER␤, respectively can be anticipated [29,30].…”

Section: Animals and Study Designmentioning

confidence: 99%

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Estradiol and genistein antagonize the ovariectomy effects on skeletal muscle myosin heavy chain expression via ER-β mediated pathways

Velders

Solzbacher

Schleipen

et al. 2010

The Journal of Steroid Biochemistry and Molecular Biology

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“…While they are most studied for transcriptional activation of genes, estrogens also act post-transcriptionally to regulate splicing, stability and translation of specific mRNAs [1,2]. In the mammalian uterus, estrogens primarily act through the estrogen receptor alpha (ER) protein [3][4][5]. Our investigations of estrogen regulation of ER gene expression have determined that in vivo estradiol (E2) treatment strongly up-regulates ER mRNA and protein concentrations in the uteri of ovariectomized sheep by stabilizing ER mRNA [6,7].…”

Section: Introductionmentioning

confidence: 97%

Estradiol up-regulates expression of the A+U-rich binding factor 1 (AUF1) gene in the sheep uterus

Ing

2010

The Journal of Steroid Biochemistry and Molecular Biology

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Biological Effects of ERα-and ERβ-Selective Estrogens

Cited by 12 publications

References 32 publications

Inhibition of mammary tumor growth by estrogens: is there a specific role for estrogen receptors alpha and beta?

Inhibition of mammary tumor growth by estrogens: is there a specific role for estrogen receptors alpha and beta?

Estradiol and genistein antagonize the ovariectomy effects on skeletal muscle myosin heavy chain expression via ER-β mediated pathways

Estradiol up-regulates expression of the A+U-rich binding factor 1 (AUF1) gene in the sheep uterus

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