The ability of bones to withstand functional loading without damage depends upon their cell populations establishing and subsequently maintaining a mass and architecture that are appropriately robust for the purpose. In women, the rapid loss of bone associated with the menopause represents a steplike decline in the effectiveness of this process with consequent increase in bone fragility. In men, loss of bone tissue and reduction in bone strength are more gradual and the increased incidence of fragility fractures occurs later. In both sexes, bone mass is associated with levels of bioavailable estrogen. This poses the major question as to how the presence or concentration of the reproductive hormone estrogen influences the relationship between bone mass and bone loading. In this paper, we briefly review evidence of the mechanism(s) by which the mechanical strains engendered by loading influence bone cells to establish and maintain structurally competent bone architecture. We highlight the finding that at least one strain-related cascade responsible for adaptive control of bone architecture is mediated through estrogen receptor (ER) alpha, the number and activity of which are regulated by estrogen. We hypothesize that a major contributor to the rapid loss of bone mass that occurs in females, and the slower age-related fall in males and females, is reduced effectiveness of ER-mediated processing of strain-related information by resident bone cells.
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L Lanyon, V Armstrong, D Ong, G Zaman, and J Price
R. W. ARMSTRONG, J. GAULDIE, and E. V. YOUNGLAI
Prepubertal (immature) and mature female rabbits were actively immunized against testosterone-3-oxime-bovine serum albumin over a period of 11 weeks. The antibody titre was significant in all animals by 5 weeks. The concentration of FSH in prepubertal animals decreased significantly (P< 0·001) between weeks 1 and 5, but no significant changes were observed in the concentration of LH at any time. After immunization for 8 weeks, there was a significant (P< 0·05) increase in the serum concentration of androgen and the percentage of bound testosterone also increased (P< 0·05). The serum concentration of oestradiol increased after immunization for 11 weeks, compared with values at 8 weeks (P<0·05) and oestradiol binding also rose by week 5 (P<0·01). Libido was not affected and significantly (P< 0·005) increased numbers of ovulations were noted in immunized animals. These results suggest that immunization of the female rabbit against testosterone may disrupt the normal regulation of follicular maturation.
P Xia, V K M Han, D Viuff, D T Armstrong, and A J Watson
We have investigated the patterns of expression and cellular localization of polypeptides and mRNAs encoding IGF-I and IGF-II in intact bovine oviduct and two bovine oviductal primary cultures (monolayers and vesicles) which are utilized for supporting development in vitro. IGF-I and IGF-II polypeptides were localized by immunocytochemistry in intact oviduct and in both primary cultures for an 8-day culture interval, but IGF-II polypeptide displayed a more restricted distribution in day 8 monolayer cultures. IGF-I and IGF-II mRNAs were localized in both oviductal cell cultures as assessed by in situ hybridization. We were unable to detect IGF-I and IGF-II mRNAs in intact oviduct by in situ hybridization; however, transcripts encoding IGF-I and IGF-II mRNAs were detected in intact oviduct cell preparations and all primary culture samples by reverse transcription-PCR methods. The origin and phenotypic stability of these cultures was assessed by immunostaining with antibodies raised against vimentin (mesenchymal cell marker) and cytokeratin (epithelial cell marker). Over the culture period, the proportion of vimentin-immunoreactive cells increased in the monolayer cultures but remained at a low level in the vesicle cultures which were predominantly composed of cytokeratin-positive cells. The results suggest that oviductal cell co-culture may facilitate early mammalian development, in part, by the establishment of paracrine growth factor circuits.
Journal of Endocrinology (1996) 149, 41–53