{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,29]],"date-time":"2026-07-29T06:36:36Z","timestamp":1785306996780,"version":"3.55.0"},"reference-count":42,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Endocrinology and Metabolism"],"published-print":{"date-parts":[[2000,2,1]]},"abstract":"<jats:p>Estradiol (E<jats:sub>2<\/jats:sub>) 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 \u226410 nmol of other steroids produced limited inhibition. Topical treatment with the estrogen receptor (ER) antagonist ICI-182780 reversed the effects of E<jats:sub>2<\/jats:sub>, and when applied alone, ICI-182780 caused a telogen-to-anagen transition. Both E<jats:sub>2<\/jats:sub>and 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-\u03b1 immunoreactive dermal protein, and Northern analysis revealed the presence of a 6.7-kb ER-\u03b1 mRNA. A ribonuclease protection assay confirmed the presence of ER-\u03b1 transcripts but failed to detect ER-\u03b2 transcripts. 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