@article{porter_chanda_wang_gaido_smart_robinette_2002, title={17 beta-estradiol is a hormonal regulator of mirex tumor promotion sensitivity in mice}, volume={69}, ISSN={["1096-6080"]}, DOI={10.1093/toxsci/69.1.42}, abstractNote={Mirex, an organochlorine pesticide, is a potent non-phorbol ester tumor promoter in mouse skin. Previous studies have shown that female mice are 3 times more sensitive to mirex tumor promotion than male mice and that ovariectomized (OVX) female mice are resistant to mirex promotion, suggesting a role for ovarian hormones in mirex promotion. To determine whether the ovarian hormone 17-beta estradiol (E2) is responsible for the sensitivity of female mice to mirex promotion, female mice were initiated with DMBA; 2 weeks later groups of mice were OVX and implants, with or without E2, were surgically implanted subcutaneously. These mice were treated topically twice weekly with mirex for 26 weeks. E2 implanted OVX mice demonstrated high normal physiologic levels of serum E2 throughout the tumor promotion experiment. E2 implants restored by 80% the intact mirex-sensitive phenotype to the OVX mice. Consistent with a role for E2 and ERalpha and ERbeta, treatment of DMBA-initiated female mice with topical ICI 182,780, an estrogen-receptor antagonist, reduced mirex tumor multiplicity by 30%. However, in cells co-transfected with ERalpha or ERbeta and estrogen-responsive promoter reporter, mirex did not stimulate promoter reporter activity, suggesting that the promotion effect of mirex is downstream of ERalpha/beta. Finally, a tumor promotion study was conducted to determine whether E2 implants could increase the sensitivity of male mice to mirex promotion. E2 implants in male mice did increase sensitivity to mirex promotion; however, the implants did not produce the full female sensitivity to mirex tumor promotion. Collectively, these studies indicate that E2 is a major ovarian hormone responsible for mirex tumor promotion sensitivity in female mice.}, number={1}, journal={TOXICOLOGICAL SCIENCES}, author={Porter, KL and Chanda, S and Wang, HQ and Gaido, KW and Smart, RC and Robinette, CL}, year={2002}, month={Sep}, pages={42–48} }
 @article{chanda_robinette_couse_smart_2000, title={17 beta-Estradiol and ICI-182780 regulate the hair follicle cycle in mice through an estrogen receptor-alpha pathway}, volume={278}, ISSN={["1522-1555"]}, DOI={10.1152/ajpendo.2000.278.2.e202}, abstractNote={Estradiol (E2) applied topically twice weekly to mouse skin at doses as low as 1 nmol inhibited hair growth by blocking the transition of the hair follicle from the resting phase (telogen) to the growth phase (anagen). In contrast, application of ≤10 nmol of other steroids produced limited inhibition. Topical treatment with the estrogen receptor (ER) antagonist ICI-182780 reversed the effects of E2, and when applied alone, ICI-182780 caused a telogen-to-anagen transition. Both E2and ICI-182780 were highly effective at their site of application but not at distant sites, indicating the direct rather than secondary systemic nature of their effects. Western analysis detected a 65-kDa ER-α immunoreactive dermal protein, and Northern analysis revealed the presence of a 6.7-kb ER-α mRNA. A ribonuclease protection assay confirmed the presence of ER-α transcripts but failed to detect ER-β transcripts. These findings implicate a skin-specific ER-α pathway in the regulation of the hair follicle cycle.}, number={2}, journal={AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM}, author={Chanda, S and Robinette, CL and Couse, JF and Smart, RC}, year={2000}, month={Feb}, pages={E202–E210} }
 @article{smart_oh_chanda_robinette_1999, title={Effects of 17-beta-estradiol and ICI 182 780 on hair growth in various strains of mice}, volume={4}, ISSN={["1529-1774"]}, DOI={10.1038/sj.jidsp.5640231}, abstractNote={17-beta-Estradiol (10 nmol per 200 microl acetone) applied topically twice weekly to the clipped dorsal surface of C57BL/6 or C3H female mouse skin prevented hair growth, as previously described in the CD-1 mouse strain. Twice weekly topical application of the estrogen receptor antagonist, ICI 182 780 (10nmol per 200microl acetone), induced the telogenanagen transition and produced early pigmentation appearance in skin and hair growth in C57BL/6 and C3H female mice. Whereas twice weekly topical application of 10nmol 17-beta-estradiol blocked hair growth, the intraperitoneal administration of this dose twice weekly did not block hair growth, suggesting a direct cutaneous effect of 17-beta-estradiol. We also evaluated the effect of 17-alpha-estradiol, 17-beta-estradiol, and ICI 182 780 on hair growth in male mice. As observed in female mice, 17-beta-estradiol was a potent inhibitor of hair growth and ICI 182 780 stimulated hair growth; however, unlike the results previously observed in female mice, 17-alpha-estradiol was a potent inhibitor of hair growth in male mice. These results demonstrate that (i) the route of administration of 17-beta-estradiol is critical for its ability to block hair growth; (ii) C57BL/6 and C3H mice, two commonly employed mouse strains for hair growth studies, responded to 17-beta-estradiol and ICI 182 780 in a manner similar to that described in CD-1 mice; and (iii) the hair follicles of male and female mice respond similarly to 17-beta-estradiol and ICI 182 780, but display striking sex differences in the response to 17-alpha-estradiol on hair growth.}, number={3}, journal={JOURNAL OF INVESTIGATIVE DERMATOLOGY SYMPOSIUM PROCEEDINGS}, author={Smart, RC and Oh, HS and Chanda, S and Robinette, CL}, year={1999}, month={Dec}, pages={285–289} }