Elucidation of estrogen receptor function in bone with the use of mouse models.
Since the discovery that estrogen receptors (ERs) are present in bone cells, there has been intense research into the action of estrogen in bone. During the past decade, humans with disturbed estrogen signaling, either as a result of ER alpha or aromatase deficiency, have been reported. Furthermore, mouse models have been established with a deficiency of ER alpha, ER beta or both, in addition to deficiency of aromatase. This review focuses on data accumulated during the past three years from studies of knockout mice with impaired estrogen signaling resulting from ER or aromatase deficiency.
Windahl
Sara H
SH
Dept Biosciences, Karolinska Institutet, Novum, Huddinge, SE-14157, Sweden.
Andersson
Göran
G
Gustafsson
Jan-Ake
JA
D000818:Animals; D001141:Aromatase / Q000172:deficiency / Q000378:metabolism / Q000502:physiology; D016723:Bone Remodeling / Q000502:physiology; D001842:Bone and Bones / Q000378:metabolism / Q000502:physiology*; D047628:Estrogen Receptor alpha; D047629:Estrogen Receptor beta; D005260:Female; D006801:Humans; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D011960:Receptors, Estrogen / Q000172:deficiency / Q000378:metabolism / Q000502:physiology*
D047628:Estrogen Receptor alpha; D047629:Estrogen Receptor beta; D011960:Receptors, Estrogen; D001141:Aromatase