Martine Gaillard-Kelly

TL;DR: Only ERalpha was shown to regulate bone remodeling in males, whereas in females both receptor subtypes influenced this process and could, at least under basal knockout conditions, compensate for each other.

TL;DR: IGF-I treatment almost completely rescued all effects of the GHR(-/-) on both bone growth and remodeling, supporting a direct effect of IGF-I on both osteoblasts and chondrocytes.

TL;DR: It is concluded that ERalpha is the main effector of estradiol's protective function in bone in both male and female mice, and that, in its absence, AR is not sufficient to mediate this response.

TL;DR: In this article, the role of the PRL receptor gene in bone development was investigated in mice carrying a germline null mutation for the PRl receptor gene and showed that the absence of PRL receptors leads to a decrease in bone formation rate using double calcein labeling and a reduction of bone mineral density.

TL;DR: The PRL receptor knockout mouse model provides a new tool to investigate the involvement ofPRL in bone metabolism and suggests that an effect of PRL on osteoblasts could be required for normal bone formation and maintenance of bone mass.