Advisor: Mihaela Pavličev
Master's Defensio - Thursday, March 19th 2026, 13:15
Seminarroom 1.3, UBB, Djerassiplatz 1, 1030 Vienna
Abstract
Decidualization is a vital process for successful eutherian mammal embryo implantation, as itis a hormonally initiated transformation of endometrial stromal cells into specialized secretorycells. Impaired decidualization is associated with infertility and pregnancy loss in multiplespecies. However, the mechanisms by which decidualization enables pregnancy remaininsufficiently understood. Even though previous studies have characterized gene expressionchanges during decidualization, changes within the metabolome remain largely unexplored.
This master’s thesis aims to investigate the metabolic changes occurring duringdecidualization in a conventional laboratory inbred mouse strain (C57BL/6) as well as atransgenic mouse line carrying a human allele associated with pregnancy-related changeslinked to decidual disorders. Using a standardized in- vitro model, decidualization is inducedin primary cell culture using 8-bromoadenosine 3’,5’-cyclic monophosphate (8-Br-cAMP)and progesterone. Through GC-MS (Gas chromatography - Mass spectrometry) a total of 33metabolites were detected, out of which 7 showed statistical significance, suggestingsignificant changes during decidualization in central metabolic pathways.
Increased fructose-1,6-bisphosphate and pyruvic acid levels in WT cells suggest enhancedglycolysis and a Warburg-like effect, with pyruvic acid accumulation and partial decouplingfrom the TCA cycle. Decreasing glutamic acid levels indicate its potential use to compensatefor a potential downregulation of the TCA cycle activity. Downregulated levels of thepolyamine putrescine might indicate efficient turnover for downstream polyamine synthesisas they are considered crucial for cell proliferation and differentiation. In the transgenic line,no increase in fructose-1,6-bisphosphate was detected, possibly affecting the fructose-1,6-bisphosphate-IL-27 axis. Parallel decreasing glutamic acid as well as 2-oxoglutaric acid levelssuggest insufficient compensation via glutaminolysis and a potential decrease in TCA cycleactivity. In general, our findings support the hypothesis of metabolic reprogramming duringdecidualization, particularly involving glycolysis and the TCA cycle.
