Expression and regulation of the tumor suppressor, SEF, during folliculogenesis in humans and mice.

Similar expression to FGF (Sef or IL17-RD), is a tumor suppressor and an inhibitor of growth factors as well as of pro-inflammatory cytokine signaling. In this study, we examined the regulation of Sef expression by gonadotropins during ovarian folliculogenesis. In sexually immature mice, in situ hybridization (ISH) localized Sef gene expression to early developing oocytes and granulosa cells (GC) but not to theca cells.

Novel and unique diagnostic biomarkers for Bacillus anthracis infection.

A search for bacterium-specific biomarkers in peripheral blood following infection with Bacillus anthracis was carried out with rabbits, using a battery of specific antibodies generated by DNA vaccination against 10 preselected highly immunogenic bacterial antigens which were identified previously by a genomic/proteomic/serologic screen of the B. anthracis secretome. Detection of infection biomarkers in the circulation of infected rabbits could be achieved only after removal of highly abundant serum proteins by chromatography using a random-ligand affinity column.

Inhibition of rat oocyte maturation and ovulation by nitric oxide: mechanism of action.

Established gap junctional communication (GJC) in the ovarian follicle is essential for maintaining the oocytes in meiotic arrest. Alternatively, LH-induced reinitiation of meiosis is subsequent to breakdown of GJC. It was recently reported that nitric oxide (NO) inhibits maturation in rat follicle-enclosed oocytes and elevates GJC in cultured mesangial cells.

Oocyte-directed depletion of connexin43 using the Cre-LoxP system leads to subfertility in female mice.

Gap junctions, predominantly comprising connexin43 (Cx43), mediate cell-to-cell communication within the ovarian follicle. However, the partaking of Cx43 in the formation of the gap junction channels, between the oocyte and the somatic cells, is controversial. We addressed this dispute by crossing females that carry a Cx43 coding region, flanked by loxP recognition sites, with males expressing the Cre recombinase under the control of Zp3 promoter.

Meiotic arrest of oocytes depends on cell-to-cell communication in the ovarian follicle.

The source of the inhibitory levels of cAMP that maintain oocytes meiotically arrested is under controversy. A model for regulation of the meiotic division that suggests the transfer of a somatic follicular cells-derived cAMP into the oocyte via gap junctions was first proposed by us in 1978. Later studies provide strong evidence that established gap-junctional communication within the ovarian follicle is indispensable for maintenance of meiotic arrest.

Disruption of gap junctional communication within the ovarian follicle induces oocyte maturation.

Meiotically arrested mammalian oocytes are stimulated to resume meiosis by LH. This response, which can be reversed by elevation of intraoocyte cAMP levels, is associated with interruption of gap junctional communication (GJC) within the ovarian follicle. In the present study, we examined the hypothesis that disruption of GJC within the ovarian follicle is sufficient for induction of oocyte maturation.

Mitogen-activated protein kinase mediates luteinizing hormone-induced breakdown of communication and oocyte maturation in rat ovarian follicles.

Resumption of meiosis, induced by LH, is preceded by the breakdown of gap junctional communication, which terminates the supply of cAMP from the somatic cells of the ovarian follicle to the oocyte. It has recently been shown that LH-induced reinitiation of meiosis is mediated by MAPK; however, the underlying molecular mechanism involved in the action of this enzyme remains unknown. We hypothesized that activation of MAPK interrupts junctional communication within the ovarian follicle, leading, in turn, to oocyte maturation.