University of Texas Health Science Center other research news
Research published in Nature Medicine shows that estrogen prompts the apoptosis of bone-dissolving osteoclasts, which may explain why women tend to develop osteoporosis in menopause. Using an in vitro system to study osteoclast apoptosis in a mouse bone marrow culture that generates osteoclasts, the researchers found that 17-beta-estradiol increased the proportion of apoptotic osteoclasts. The nonsteroidal, partial estrogen mimic tamoxifen also gave this effect, while an inactive isomer of 17-beta-estradiol had no effect. An antibody to transforming growth factor-beta (TGF-B) blocked the apoptosis induced by both TGF-B and by estrogen and tamoxifen.
In mice with ovaries removed, the percent of apoptotic osteoclasts was increased by two- to three-fold, after both one and three weeks of treating with 17-beta-estradiol. ...