A number of tissues have been identified as non-classical targets of oestrogen action. Oestrogen can significantly influence the hair cycle and the human hair follicle provides an accessible tissue to investigate mesenchymal:epithelial interactions in vitro. Recently, oestrogen receptor alpha (ERalpha) and beta (ERbeta) have been identified in human hair follicle cells. Although human hair follicles vary significantly with body site, non-balding scalp follicles have not been recognised as a target for androgen or oestrogen action. Therefore, we have used a whole follicle organ culture system to investigate the effect of 17beta-oestradiol, 17alpha-oestradiol and tamoxifen on human hair growth in vitro.
Individual hair follicles (n=4 patients; mean age 51.25yrs) were microdissected out from scalp skin and incubated individually in phenol red-free William's E medium with L-glutamine, penicillin, streptomycin and 5mM glucose. A minimum of 6 follicles from each patient was incubated with either the vehicle control (0.0001% alcohol), 10nM 17beta-oestradiol, 10nM 17alpha-oestradiol, 100nM tamoxifen or 10nM 17beta-oestradiol plus 100nM tamoxifen for 7 days. Every 24 hours, the increase in the length of the follicles was measured sequentially with an inverted microscope fitted with an eyepiece measuring graticle.
Follicles in each group exhibited linear growth over the seven-day period and sectioning of individual follicles showed all groups to exhibit a similar morphology. Follicles incubated with 17alpha-oestradiol grew at a similar rate to the control group. However, follicles incubated with 17beta-oestradiol grew at a significantly (p=0.02) slower rate than the control group. Tamoxifen alone had no effect on hair growth, but inhibited the effect of 17beta-oestradiol.
These results show that the biologically active oestrogen, 17beta-oestradiol, can inhibit human hair growth in vitro, by reducing the rate of growth, which parallels the in vivo effects seen in rodents. Studies are in progress to determine whether these effects are mediated via ERalpha or ERbeta.
22 - 24 Mar 2004
British Endocrine Societies