Both ER subtypes are expressed in RPE and regulated in a dose-dependent fashion by E(2). Estrogens similarly regulate MMP-2. This estrogen-induced effect is, at least in part, mediated through NF-kappaB. These data support the hypothesis that estrogens may exert biological function in RPE through ERs and that estrogen deficiency or excess may cause dysregulation of molecules that influence the turnover of ECM in Bruch's membrane associated with ARMD.
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