Gene expression profiling reveals that ERα controls the mitochondrial biogenesis in LysM-Cre targeted cells

Estrogens decrease osteoclast numbers via direct and indirect effects. In trabecular bone, the anti-osteoporotic efficacy of estrogens is mediated via the estrogen receptor α (ERα) present in myeloid lineage cells, but the molecular mechanism mediating these effects remain controversial. In contrast to published findings by others, FasLgld/gld mice which lack functional FasL lost cortical and cancellous bone following OVX indistinguishably from FasL-intact controls. Microarray analysis of osteoclast progenitors isolated from the bone marrow of ERαf/f;LysM-Cre mice and ERαf/f controls indicated that ERα deleted macrophages exhibited significant enrichment for the term “oxidative phosphorylation”, suggesting that estrogen signaling via ERα inhibits this process Erα knock out is compare with control in osteoclast progenitors, pre-osteoclasts and mature osteoclasts