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Mouse models to evaluate the role of estrogen receptor α in skeletal maintenance and adaptation
Author(s) -
Rooney Amanda M.,
der Meulen Marjolein C.H.
Publication year - 2017
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/nyas.13523
Subject(s) - osteoblast , estrogen receptor , cancellous bone , knockout mouse , estrogen , progenitor cell , endocrinology , periosteum , biology , medicine , bone cell , estrogen receptor alpha , gene knockout , conditional gene knockout , microbiology and biotechnology , phenotype , receptor , stem cell , in vitro , anatomy , gene , genetics , cancer , breast cancer
Estrogen signaling and mechanical loading have individual and combined effects on skeletal maintenance and adaptation. Previous work investigating estrogen signaling both in vitro and in vivo using global estrogen receptor α (ERα) gene knockout mouse models has provided information regarding the role of ERα in regulating bone mass and adaptation to mechanical stimulation. However, these models have inherent limitations that confound interpretation of the data. Therefore, recent studies have focused on mice with targeted deletion of ERα from specific bone cells and their precursors. Cell stage, tissue type, and mouse sex all influence the effects of ERα gene deletion. Lack of ERα in osteoblast progenitor and precursor cells generally affects the periosteum of female and male mice. The absence of ERα in differentiated osteoblasts, osteocytes, and osteoclasts in mice generally resulted in reduced cancellous bone mass, with differing reports of the effect by animal sex and greater deficiencies in bone mass typically occurring in cancellous bone in female mice. Limited data exist for the role of bone cell–specific ERα in skeletal adaptation in vivo . Cell‐specific ERα gene knockout mice provide an excellent platform for investigating the function of ERα in regulating skeletal phenotype and response to mechanical loading by sex and age.