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On page 163, Daimon and Wada present information on a role for neutrophils in matrix metalloproteinase activity in the preimplantation mouse uterus, indicating that mating and introduction of a component of fluid from seminal vesicles induces infiltration of neutrophils containing pro-matrix metalloprotein 9 (MMP9) into the uterine lumen. The neutrophils then release MMP9 to affect implantation and decidualization in uteri of mice. These results along with previous reports of reduced fertility in MMP9-deficient female mice, led the authors to conclude that seminal plasma acts as a chemoattractant to recruit neutrophils containing proMMP9 into the uterine lumen and that activation of MMP9 induces modifications of the extracellular matrix required for the establishment of pregnancy.
Selenoprotein P Is Required for Mouse Sperm Development. Gary E. Olson, Virginia P. Winfrey, Subir K. NagDas, Kristina E. Hill, and Raymond F. Burk. Biol Reprod 2005; 73:201–208. Published online 2 March 2005; 10.1095/biolreprod.105.040360
On page 201, Olson and colleagues offer evidence that selenoprotein P (SEPP1) in blood protein delivers the dietary micronutrient selenium to germ cells and that selenium is required for the germ cells to form normal sperm. Dietary selenium is essential for normal sperm development and male fertility. Olson et al. created Sepp1-knockout mice; the males have levels of selenium that are less than 10 percent of those in control mice, are generally infertile, and produce sperm with defective tails, similar to the sperm produced by normal mice fed a low-selenium diet. Knockout mice did not recover normal sperm production after prolonged feeding on a high-selenium diet. Thus SEPP1 is the likely carrier of the selenium needed for development of normal sperm and for male mice to maintain their fertility.
Weaning Initiates a Rapid and Powerful Anabolic Phase in the Rat Maternal Skeleton. Scott C. Miller, Brian L. Anderson, and Beth M. Bowman. Biol Reprod 2005; 73:156–162. Published online 23 March 2005; 10.1095/biolreprod.105.039610
On p. 156 of this issue, novel results from Miller and colleagues document the origin of the active osteoblasts responsible for forming new bone after lactation. It is known that maternal skeletal mineral lost during lactation is rapidly restored after weaning. Thus study of the early post-lactation period is advantageous for understanding the basis for rapid physiological stimulation of bone formation. BrdU labeling allowed the authors to find that many, if not most, of the newly formed osteoblasts were derived from proliferating progenitors. This suggests that the endocrine milieu of lactation expands and/or primes the osteoprogenitor pool, leading to the rapid anabolic phase. This insight, taking advantage of a reproductive event, reflects on wider biological mechanisms of stem cell proliferation and differentiation.
Related articles in Biol Reprod:
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