To the top

Page Manager: Webmaster
Last update: 9/11/2012 3:13 PM

Tell a friend about this page
Print version

Overexpression of preecla… - University of Gothenburg, Sweden Till startsida
To content Read more about how we use cookies on

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
Keywords endothelial growth-factor, vegf-a, actin reorganization, cell-migration, expression, angiogenesis, pregnancies, receptors, podocytes, survival
Subject categories Neurosciences


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.

Page Manager: Webmaster|Last update: 9/11/2012

The University of Gothenburg uses cookies to provide you with the best possible user experience. By continuing on this website, you approve of our use of cookies.  What are cookies?