Acid sphingomyelinase involvement in tumor necrosis factor α-regulated vascular and steroid disruption during luteolysis in vivo
作者： L. E. Henkes , B. T. Sullivan , M. P. Lynch , R. Kolesnick , D. Arsenault
关键词:
摘要: TNF is well known for its role in inflammation, including direct effects on the vasculature. also implicated regulation of reproduction by actions to affect ovarian steroidogenic cells and induce apoptosis corpus luteum (CL)-derived endothelial vitro. We hypothesized that disruption signaling would postpone regression highly vascularized CL vivo, this effect could be replicated mutant mouse models lacking receptor (TNFRI(-/-)) and/or a critical enzyme signaling, acid sphingomyelinase (ASMase(-/-)). In current study, treatment pseudopregnant mice with luteolytic mediator prostaglandin F2-alpha (PGF) significantly increased ovaries when compared saline-treated controls. Treatment PGF reduced serum progesterone (P4) concentrations caused involution CL. However, pretreatment Etanercept (ETA), TNF-neutralizing antibody, inhibited PGF-induced decrease P4 delayed luteal regression. A similar outcome was evident TNFRI(-/-) animals. microvascular (MVECs) provoked significant increase ASMase activity corresponding Furthermore, TNF-induced MVEC death ASMase(-/-) mice. The displayed no obvious evidence 24 h after were resistant P4. Together these data provide plays an active luteolysis. Further studies are required determine deleterious anti-inflammatory agents basic processes.
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