Publications by authors named "M Dieber-Rotheneder"
Adequate anchoring of the placenta in the uterus through invasion of first trimester cytotrophoblasts (CTB) is required for a successful pregnancy. This process is mediated by matrix metalloproteinases (MMPs) and regulated by the maternal environment. Obesity is known to alter the intrauterine milieu and has been related to impaired invasion.
View Article and Find Full Text PDFStudy Question: Does endothelin-1 (ET-1) regulate matrix metalloproteinase (MMP) 14 and 15 production and invasion of human first trimester trophoblasts?
Summary Answer: ET-1 in pathophysiological concentrations down-regulates MMP14 and MMP15 expression via endothelin receptor (ETR) type B and decreases trophoblast migration and invasion.
What Is Known Already: MMP14 and MMP15 are involved in trophoblast invasion. Impairment of invasion has been linked to pregnancy complications such as pre-eclampsia (PE).
Saliva is an important physiological fluid that contains a complex mixture of analytes that may produce a characteristic individual signature. In recent years, it has been demonstrated that urine possesses a clear signature of the individual metabolic phenotype. Here NMR-based metabolomics was employed to analyze saliva from 23 healthy volunteers.
View Article and Find Full Text PDFArticle Synopsis
- Membrane-type matrix metalloproteinases (MT-MMPs) are enzymes crucial for breaking down the extracellular matrix and play significant roles in both tumor biology and pregnancy.
- Their functions in pregnancy include aiding cytotrophoblast migration, remodeling spiral arteries, and forming the syncytiotrophoblast, which are essential for successful implantation and maintenance of the pregnancy.
- Dysregulation of MT-MMP expression has been associated with various pregnancy complications, such as preeclampsia and gestational diabetes, highlighting the importance of understanding their role in placental health.
The pathogenesis of preeclampsia (PE) includes the release of placental factors into the maternal circulation, inducing an inflammatory environment in the mother. One of the factors may be the proinflammatory chemokine fractalkine, which is expressed in the syncytiotrophoblast of human placenta, from where it is released into the maternal circulation by constitutive shedding. We examined whether placental fractalkine is up-regulated in severe early-onset PE and whether the proinflammatory cytokines tumor necrosis factor (TNF)-α and IL-6 are able to increase the expression of fractalkine.
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