Figure 7. Model of the mechanism of estrogen induces hair cycle arrest.
The intrinsic or extrinsic estrogen activates ER α on DP cells. Then the expression of TGF β2 is up-regulated and the precortex cells undergo apoptosis, which triggers premature onset of catagen. Immediately after the catagen, the anagen chalone BMP4 increases its expression in DP and hair matrix. As the result, telogen is sustained. Although estrogen plays a suppressive role on hair growth, the HFSCs are kept from damage. After estrogen treatment withdrawal, the reserved HFSCs were reactivated and the hairs could regenerate. ER: estrogen receptor; DP: dermal papilla; HFSC: hair follicle stem cell.