PAD4 Deficiency Decreases Inflammation and Susceptibility to Pregnancy Loss in a Mouse Model

Erpenbeck, L. and Chowdhury, C. S. and Zsengeller, Z. K. and Gallant, M. and Burke, S. D. and Cifuni, S. and Hahn, S. and Wagner, D. D. and Karumanchi, S. A.. (2016) PAD4 Deficiency Decreases Inflammation and Susceptibility to Pregnancy Loss in a Mouse Model. Biol Reprod, 95 (6). p. 132.

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Official URL: https://edoc.unibas.ch/61787/

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Inflammation is thought to play a critical role in the pathogenesis of placentation disorders such as recurrent miscarriages, growth restriction, and preeclampsia. Recently, neutrophil extracellular traps (NETs) have emerged as a potential mechanism for promoting inflammation in both infectious and noninfectious disorders. To investigate a pathogenic role for NETs in placentation disorders, we studied a model of antiangiogenic factor-mediated pregnancy loss in wild-type (WT) mice and in mice deficient in peptidylarginine deiminase 4 (Padi4-/-) that are unable to form NETs. Overexpression of soluble fms-like tyrosine kinase 1 (sFlt-1), an antiangiogenic protein that is pathogenically linked with abnormal placentation disorders during early gestation, resulted in pregnancy loss and large accumulation of neutrophils and NETs in WT placentas. Interestingly, sFlt-1 overexpression in Padi4-/- mice resulted in dramatically lower inflammatory and thrombotic response, which was accompanied by significant reduction in pregnancy losses. Inhibition of NETosis may serve as a novel target in disorders of impaired placentation.
Faculties and Departments:03 Faculty of Medicine > Departement Biomedizin > Department of Biomedicine, University Hospital Basel > Prenatal Medicine (Hahn)
UniBasel Contributors:Hahn, Sinuhe
Item Type:Article, refereed
Article Subtype:Research Article
ISSN:1529-7268 (Electronic) 0006-3363 (Linking)
Note:Publication type according to Uni Basel Research Database: Journal article
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Last Modified:31 May 2020 21:32
Deposited On:31 May 2020 21:32

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