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Overexpression of preeclampsia induced microRNA-26a-5p leads to proteinuria in zebrafish

Journal article
Authors J. Muller-Deile
P. Schroder
L. Beverly-Staggs
R. Hiss
J. Fiedler
Jenny Nyström
T. Thum
H. Haller
M. Schiffer
Published in Scientific Reports
Volume 8
ISSN 2045-2322
Publication year 2018
Published at Institute of Neuroscience and Physiology, Department of Physiology
Language en
Links dx.doi.org/10.1038/s41598-018-22070...
Keywords endothelial growth-factor, vegf-a, actin reorganization, cell-migration, expression, angiogenesis, pregnancies, receptors, podocytes, survival
Subject categories Neurosciences

Abstract

So far the pathomechanism of preeclampsia in pregnancy is focussed on increased circulating levels of soluble fms-like tyrosin kinase-1 (sFLT-1) that neutralizes glomerular VEGF-A expression and prevents its signaling at the glomerular endothelium. As a result of changed glomerular VEGF-A levels endotheliosis and podocyte foot process effacement are typical morphological features of preeclampsia. Recently, microRNA-26a-5p (miR-26a-5p) was described to be also upregulated in the preeclamptic placenta. We found that miR-26a-5p targets VEGF-A expression by means of PIK3C2a in cultured human podocytes and that miR-26a-5p overexpression in zebrafish causes proteinuria, edema, glomerular endotheliosis and podocyte foot process effacement. Interestingly, recombinant zebrafish Vegf-Aa protein could rescue glomerular changes induced by miR-26a-5p. In a small pilot study, preeclamptic patients with podocyte damage identified by podocyturia, expressed significantly more urinary miR-26a-5p compared to healthy controls. Thus, functional and ultrastructural glomerular changes after miR-26a-5p overexpression can resemble the findings seen in preeclampsia and indicate a potential pathophysiological role of miR-26a-5p in addition to sFLT-1 in this disease.

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