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The Effects of Deletions of the Mouse Y Chromosome Long Arm on Sperm Function—Intracytoplasmic Sperm Injection-Based Analysis.
Monika A. Ward and Paul S. Burgoyne. Biol Reprod 2006; 74:652–658. Published online ahead of print 14 December 2005; 10.1095/biolreprod.105.048090
ICSI to the rescue. The development of intracytoplasmic sperm injection, commonly known as ICSI, immediately provided a major tool for treatment of human male infertility. However, its application to resource maintenance and research in model organisms has been slower in realization, partly because it is a more difficult technique with rodent gametes than with human sperm. In a paper in this issue (pp. 652), Ward and Burgoyne beautifully illustrate how ICSI can be used both to facilitate maintenance of infertile mouse mutants and to answer specific questions about sperm function. Mutant mice with deletions of Y chromosome genes that affect sperm formation and function have been particularly difficult to use as research tools simply because it is expensive and time-consuming to produce the mice. Here they show that ICSI is highly efficient for production of Y-chromosome mutant mice that would otherwise take much longer to produce. Furthermore, a research question about function of sperm from males with deleted Y chromosomes was resolved. Comparison of offspring produced from natural mating or IVF versus those produced by ICSI led to the conclusion that all genetic types of sperm are produced, but that sperm bearing an abnormal Y chromosome can be impaired in functions required in mating or IVF. Thus ICSI is proven to be a robust tool for resource management and for research on sperm function.
Nerve Growth Factor (NGFB) Translates Stress Response and Subsequent Murine Abortion via Adhesion Molecule-Dependent Pathways.
Mareike Tometten, Sandra Blois, Arne Kuhlmei, Anna Stretz, Burghard F. Klapp, and Petra C. Arck. Biol Reprod 2006; 74:674–683. Published online ahead of print 21 December 2005; 10.1095/biolreprod.105.044651
Uterine stress responses. Spontaneous abortion affects 10–25% of human pregnancies and psychosocial stress appears to be a common factor that results in adverse effects on the nervous, endocrine and immune systems. In an article in this issue (pp. 674), Tometten and colleagues report the use of the CBA/J x DBA/2J mouse model of abortion to demonstrate that stress-mediated abortion is associated with increased expression of nerve growth factor, beta (NGFB), which up-regulates intercellular adhesion molecule 1 (ICAM1) and selectin, platelet (SELP) and their ligands, integrin alpha L (ITGAL) and SELPL, which induce expression of decidual pro-inflammatory cytokines and an abortogenic uterine environment. Also, stress in these mice decreased expression of CD8 alpha+ decidual cells considered beneficial to pregnancy. These uterine stress responses were abrogated by NGFB neutralization, suggesting that NGFB is the proximal mediator of events in the hierarchical network of neurogenic inflammation and immune rejection leading to abortion in mice.
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