Detail of "1428-67-7"

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Identification of estrogen receptor beta expression in Chinese hamster ovary (CHO) cells and comparison of estrogen-responsive gene transcription in cells adapted to serum-free media

Identification of estrogen receptor beta expression in Chinese hamster ovary (CHO) cells and comparison of estrogen-responsive gene transcription in cells adapted to serum-free media. Thomas, Padmaja B.; Risinger, Kelly E.; Klinge, Carolyn M. ( Department of Biochemistry and Molecular Biology, University of Louisville School of Medicine, Louisville, KY 40292, USA). Journal of Steroid Biochemistry and Molecular Biology, 86(1), 41-55 (English) 2003 : Elsevier Science Ltd. CODEN: JSBBEZ. ISSN: 0960-0760. DOCUMENT TYPE: Journal CA Section: 2 (Mammalian Hormones) Section cross-reference(s): 9 Most cultured cell lines require addn. of serum to the medium to maintain their proliferative capacity. For studies examg. the cellular effects of estrogens serum is charcoal-stripped to remove steroids. Nonetheless, addn. of the selective estrogen receptor modulator (SERM) 4-hydroxytamoxifen (4-OHT) inhibits the basal transcriptional activity of estrogen receptors alpha or beta (ERa or ERb) in transfected cells. The authors tested the hypothesis that elimination of serum from the culture medium will block 4-OHT's repression of basal activity. Chinese hamster ovary (CHO-K1) cells adapted to serum-free medium exhibited estrogen responsiveness that was identical with that of the cells grown in serum-contg. media. 4-OHT-suppressed basal transcription of an estrogen response element (ERE)-reporter in ERa-transfected cells even in the absence of serum, indicating that the 4-OHT suppressive activity is not mediated by blocking ER interaction with serum estrogens. The authors speculate that 4-OHT-ER recruits co-repressors to suppress basal transcription. The authors discovered that CHO-K1 cells express ERa and ERb mRNA.In this experiment, several chemicals are used like 1428-67-7 and 263717-53-9 However only ERb protein was expressed and use of ERb-selective 2,3-bis(4-hydroxy-phenyl)propionitrile (DPN) and ERa-selective 4-propyl-1,3,5-tris(4-hydroxy-phenyl)pyrazole (PPT) revealed that only ERb was transcriptionally active. In conclusion, growing CHO-K1 in serum-free medium does not impact the estrogen responsiveness and this cell line expresses functional ERb. .

Inhibition of neointima formation by local delivery of estrogen receptor alpha and beta specific agonists

All Rights Reserved. Inhibition of neointima formation by local delivery of estrogen receptor alpha and beta specific agonists. Krom, Yvonne D.; Pires, Nuno M. M.; Jukema, J. Wouter; de Vries, Margreet R.; Frants, Rune R.; Havekes, Louis M.; van Dijk, Ko Willems; Quax, Paul H. A. (Department of Human Genetics, Leiden University Medical Center, Leiden 2333 ZA, Neth.). Cardiovascular Research, 73(1), 217-226 (English) 2007 Elsevier B.V. CODEN: CVREAU. ISSN: 0008-6363. 1428-67-7 and 263717-53-9 which are cas registry numbers are also used here. DOCUMENT TYPE: Journal CA Section: 2 (Mammalian Hormones) Section cross-reference(s): 1 Neointima formation is the underlying mechanism of (in-stent) restenosis. 17b-Estradiol (E2) is known to inhibit injury-induced neointima formation and post-angioplasty restenosis. Estrogen receptor a (ERa) was demonstrated to mediate E2 anti-restenotic properties. However, the role of estrogen receptor b (ERb) is not fully elucidated. In the present study, the specific role of vascular ERa and ERb in neointima formation is assessed. Neointima formation was induced by placement of a perivascular cuff around the femoral artery of male C57BL/6J mice. E2-eluting cuffs significantly inhibited cuff-induced neointima formation. To address the specific roles of ERa and ERb on neointima formation, the ERa-selective agonist 4,4',4''-(4-propyl-[1H]-pyrazole-1,3,5-triyl)tris-phenol (PPT) and the ERb-selective agonist 2,3-bis(4-hydroxy-phenyl)-propionitrile (DPN) were applied via a drug-eluting cuff. PPT inhibited neointima formation at low but not at high concns. Conversely, DPN inhibited neointima formation dose dependently. To demonstrate the specificity of these responses, an ERa-selective antagonist, MPP, was also used in combination with E2, PPT, or DPN. While the effect of PPT on neointima formation inhibition was blocked by co-delivery of MPP, E2 and DPN could still inhibit neointima formation. Our data suggest that, in addn. to ERa, specific ERb activation inhibits neointima formation in a mouse model of restenosis. These data reveal a yet unidentified protective role of ERb on neointima formation. .