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Oxygen modulates the response of first-trimester trophoblasts to hyperglycemia
Institute of Cell Biology, Histology, and Embryology, Medical University of Graz, Graz, Austria; Department of Obstetrics & Gynaecology, Medical University of Graz, Graz, Austria.
Institute of Cell Biology, Histology, and Embryology, Medical University of Graz, Graz, Austria.
Institute of Cell Biology, Histology, and Embryology, Medical University of Graz, Graz, Austria.
Institute of Cell Biology, Histology, and Embryology, Medical University of Graz, Graz, Austria.ORCID-id: 0000-0003-0466-1861
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2012 (Engelska)Ingår i: American Journal of Pathology, ISSN 0002-9440, E-ISSN 1525-2191, Vol. 180, nr 1, s. 153-164Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Pregestational diabetes retards early embryonic growth. Placental and fetal growth are closely associated, suggesting that placental growth is also impaired. During the first trimester of gestation, oxygen tension rises steeply, leading to excessive production of reactive oxygen species (ROS), which is exacerbated in diabetes and may affect placental development. We hypothesized that oxygen modifies hyperglycemic effects on ROS formation, resulting in decreased first-trimester trophoblast growth. This was tested using a first trimester trophoblast-derived cell line (ACH-3P). Normoglycemia did not alter ACH-3P proliferation at 2.5%, 8%, and 21% oxygen. Hyperglycemic conditions for up to 3 days reduced cell number by 65% and resulted in cell cycle (G(1)- and S-phase) changes but only at 21% oxygen. Proliferation reduction could be partially restored by an inhibitor of mitogen-activated protein kinase (MAPK) ERK1/2 but not of Akt/PkB. Intracellular ROS elevation under hyperglycemia was oxygen independent, whereas mitochondrial superoxide levels were enhanced under hyperglycemia only at 21% oxygen. Intervention to modulate cytosolic and mitochondrial ROS, using ROS formation inducers and inhibitors, did not alter cell growth under hyperglycemia at 21% oxygen. The combination of hyperglycemia and high oxygen levels (21%) reduces proliferation of human first-trimester trophoblasts in a ROS-independent manner involving MAPK. This may account for reduced placental growth and, therefore, also for embryonic growth during the first-trimester pregestational diabetic pregnancies when the oxygen tension increases.

Ort, förlag, år, upplaga, sidor
Elsevier, 2012. Vol. 180, nr 1, s. 153-164
Nationell ämneskategori
Medicinsk bioteknologi (med inriktning mot cellbiologi (inklusive stamcellsbiologi), molekylärbiologi, mikrobiologi, biokemi eller biofarmaci)
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URN: urn:nbn:se:oru:diva-39621DOI: 10.1016/j.ajpath.2011.09.012ISI: 000298976000017PubMedID: 22056361Scopus ID: 2-s2.0-83455164916OAI: oai:DiVA.org:oru-39621DiVA, id: diva2:771221
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Sponsors:

Medical University of Graz  

Austrian Genome Programme Gen-AU  

Austrian National Bank, Vienna Grant(s): 12601 

Tillgänglig från: 2014-12-12 Skapad: 2014-12-12 Senast uppdaterad: 2019-03-26Bibliografiskt granskad

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American Journal of Pathology
Medicinsk bioteknologi (med inriktning mot cellbiologi (inklusive stamcellsbiologi), molekylärbiologi, mikrobiologi, biokemi eller biofarmaci)

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