Hypoxia-Mediated Soluble Fms-Like Tyrosine Kinase 1 Increase Is Not Attenuated in Interleukin 6-Deficient Mice. (June 2015)

• Record Type: Journal Article
• Authors: Appel, Sarah; Turnwald, Eva-Maria; Ankerne, Janina; Wohlfarth, Maria; Appel, Jan; Rother, Eva; Janoschek, Ruth; Alejandre Alcazar, Miguel A.; Schnare, Markus; Meißner, Udo; Dötsch, Jörg
• Is Part Of: Reproductive sciences. Volume 22:Number 6(2015:Jun.)
• Page Start: 735
• Page End: 742
• Publication Date: 2015-06
• Subjects: hypoxia -- placenta -- sFlt-1; Reproductive health -- Periodicals; Reproduction -- Periodicals; 612.6
• DOI: 10.1177/1933719114557898
• Languages: English
• ISSNs: 1933-7191

Abstract

The soluble fms-like tyrosine kinase 1 (sFlt-1), known to be increased in the serum of preeclamptic patients, is a relevant factor in causing maternal symptoms like hypertension and proteinuria. In this study, we aimed to reveal whether hypoxia is a cause of increased sFlt-1 levels and inflammation markers in vivo and whether these symptoms can be attenuated by interleukin 6 (IL-6) depletion. For this purpose, pregnant wild-type (wt) mice or IL-6 −/− mice on embryonic day 16 were placed under either normoxic (20.9% oxygen) or hypoxic (6% oxygen) conditions for 6 hours. This led to a rise of sFlt-1 levels in maternal serum, independent of the IL-6 status of the dam. Increased maternal sFlt-1 serum levels were, however, not due to an increase in sFlt-1 messenger RNA levels in the placenta. Moreover, there was no increase in inflammatory markers in neither wt mice nor IL-6 −/− mice. This suggests that hypoxia alone does not contribute to the induction of an inflammatory placenta. Also, the hypoxia-induced rise in sFlt-1 levels seems not to be mediated by IL-6 in vivo.