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Negative effects of late maternal age in women on offspring aneuploidy and its associated defects are well known. However, other potential negative effects on offspring from delayed motherhood have been only anecdotal. In what is sure to be a controversial topic of discussion, on page 1336 of this issue, Tarín et al., presents data that delayed motherhood in mice results in decreased life expectancy and reduced body weight of their adult male offspring. Several other aspects of reproductive fitness of offspring were assessed, but none showed significant deleterious effects. This report identifying effects of delayed motherhood on life expectancy and body weight of male offspring will surely stimulate inquiries into mechanisms resulting in these disturbing consequences, as well as epidemiological studies in humans.
Local Delivery of Angiopoietin-2 into the Preovulatory Follicle Terminates the Menstrual Cycle in Rhesus Monkeys. Fuhua Xu and Richard L. Stouffer. Biol Reprod 2005; 72:1352–1358. Published online 9 February 2005; 10.1095/biolreprod.104.037143
Angiogenesis is an important part of tissue remodeling during developmental processes in normal tissue and in cancers. For over 30 years, investigators have worked toward elucidating the factors and processes controlling angiogenesis during development of the corpus luteum. The family of vascular endothelial growth factors (VEGF) has received much attention based on their ability to promote angiogenesis and ovarian function at the time of ovulation. Angiopoietins (ANGPT) are other factors that have been recently described to modulate blood vessel growth and regression. On page 1352 of this issue, Xu and Stouffer describe experiments using female rhesus monkeys to examine effects of injection of the agonist ANGPT1 or the antagonist ANGPT2 into the preovulatory follicle on subsequent ovarian function. Intrafollicular injection of ANGPT1 did not disrupt normal ovarian function; however, injection of ANGPT2 into the preovulatory follicle resulted in dose-dependent inhibition of ovulation and prevention of the development of the corpus luteum and the expected rise in circulating progesterone levels. These data extend the concept that angiogenesis is important for ovulation by demonstrating that a balance between ANGPT agonists (ANGPT1) and antagonists (ANGPT2) in the preovulatory follicle may be critical for ovulation and corpus luteum function. Further studies to characterize the cellular and molecular responses to angiopoietins will likely lead to new concepts regarding the role of the vasculature in corpus luteum development and regression.
Cell-Cycle Inhibitors p27Kip1 and p21Cip1 Regulate Murine Sertoli Cell Proliferation. Denise R. Holsberger, Gregory M. Buchold, Marcelo Castro Leal, Sarah E. Kiesewetter, Deborah A. O'Brien, Rex A. Hess, Luiz R. Franca, Hiroaki Kiyokawa, and Paul S. Cooke. Biol Reprod 2005; 72:1429–1436. Published online 23 February 2005; 10.1095/biolreprod.105.040386
Nearly twenty years ago, elegant studies by Orth established that the numbers of spermatids produced by adults depend on the numbers of Sertoli cells formed during perinatal testis development. Consequently, much effort has been devoted to discovering factors regulating Sertoli cell proliferation. Thyroid hormone is a known inhibitor of Sertoli cell proliferation, and neonatal hypothyroidism results in larger than normal testis size in rodents. On page 1429 of this issue, Holsberger et al. report results of a study designed to test the hypothesis that the effect of thyroid hormone is mediated by cyclin-dependent kinase inhibitors. They studied mice with null mutations in the genes encoding CDKN1B (commonly known as p27) and CDKN1A (also known as p21). Testis weights, Sertoli cell numbers, and daily sperm production were increased in adult single-knockout and double-knockout mice. However, the length of the perinatal period of Sertoli cell proliferation was not extended. Thus, both CDKN1B (p27) and CDKN1A (p21) play inhibitory roles in regulating adult Sertoli cell number, but also there must be other factors that regulate the cessation of Sertoli cell proliferation. The latter point is of interest with respect to a paper published last month in Biology of Reproduction, wherein Chaudhary et al. (Biol Reprod 2005; 72:1205–1217) found the helix-loop-helix inhibitor of differentiation proteins can induce post-mitotic terminally differentiated Sertoli cells to re-enter a proliferative phase.
Related articles in Biol Reprod:
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