Smoking impairs angiogenesis during maturation of human oocytes.

Objective: This study determines whether smoking influences ovarian vascularization which thus may impair follicular development.

Design: Prospective laboratory study of follicular fluids and granulosa cells from patients undergoing in vitro fertilization.

Setting: University Hospital Aachen, Germany.

Regulation of soluble vascular endothelial growth factor receptor (sFlt-1/sVEGFR-1) expression and release in endothelial cells by human follicular fluid and granulosa cells.

Background: During the female reproductive cycle, follicular development and corpus luteum formation crucially depend on the fast generation of new blood vessels. The importance of granulosa cells and follicular fluid in controlling this angiogenesis is still not completely understood. Vascular endothelial growth factor (VEGF) produced by granulosa cells and secreted into the follicular fluid plays an essential role in this process.

Melatonin receptor signaling in pregnant and nonpregnant rat uterine myocytes as probed by large conductance Ca2+-activated K+ channel activity.

The mRNAs of MT1 and MT2 melatonin receptors are present in cells from nonpregnant (NPM) and pregnant (PM) rat myometrium. To investigate the coupling of melatonin receptors to Gq- and Gi-type of heterotrimeric G proteins, we analyzed the activity of large-conductance Ca2+-activated K+ (BKCa) channels, the expression of which in the uterus is confined to smooth muscle cells. The melatonin receptor agonist 2-iodomelatonin induced a pertussis toxin (PTX)-insensitive increase in channel open probability that was blocked by the nonselective antagonist luzindole.

beta8 integrins are required for vascular morphogenesis in mouse embryos.

In order to assess the in vivo function of integrins containing the beta8 subunit, we have generated integrin beta8-deficient mice. Ablation of beta8 results in embryonic or perinatal lethality with profound defects in vascular development. Sixty-five percent of integrin beta8-deficient embryos die at midgestation, with evidence of insufficient vascularization of the placenta and yolk sac.