Focal segmental glomerulosclerosis is induced by microRNA-193a and its downregulation of WT1 | Zendy

Christoph A. Gebeshuber | Zendy; Christoph Kornauth | Zendy; Lihua Dong | Zendy; Ralph Sierig | Zendy; Jost Seibler | Zendy; Martina Reiss | Zendy; Stefanie Tauber | Zendy; Martin Bilban | Zendy; Shijun Wang | Zendy; Renate Kain | Zendy; Georg A. Böhmig | Zendy; Marcus J. Moeller | Zendy; Hermann Josef Gröne | Zendy; Christoph Englert | Zendy; Javier Martı́nez | Zendy; Dontscho Kerjaschki | Zendy

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Focal segmental glomerulosclerosis is induced by microRNA-193a and its downregulation of WT1

Author(s) -

Christoph A. Gebeshuber,

Christoph Kornauth,

Lihua Dong,

Ralph Sierig,

Jost Seibler,

Martina Reiss,

Stefanie Tauber,

Martin Bilban,

Shijun Wang,

Renate Kain,

Georg A. Böhmig,

Marcus J. Moeller,

Hermann Josef Gröne,

Christoph Englert,

Javier Martı́nez,

Dontscho Kerjaschki

Publication year - 2013

Publication title -

nature medicine

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 19.536

H-Index - 547

eISSN - 1546-170X

pISSN - 1078-8956

DOI - 10.1038/nm.3142

Subject(s) - podocyte , downregulation and upregulation , podocalyxin , nephrin , focal segmental glomerulosclerosis , glomerulosclerosis , cancer research , microrna , nephrosis , biology , transcription factor , microbiology and biotechnology , glomerulonephritis , kidney , endocrinology , gene , proteinuria , genetics

Focal segmental glomerulosclerosis (FSGS) is a frequent and severe glomerular disease characterized by destabilization of podocyte foot processes. We report that transgenic expression of the microRNA miR-193a in mice rapidly induces FSGS with extensive podocyte foot process effacement. Mechanistically, miR-193a inhibits the expression of the Wilms' tumor protein (WT1), a transcription factor and master regulator of podocyte differentiation and homeostasis. Decreased expression levels of WT1 lead to downregulation of its target genes PODXL (podocalyxin) and NPHS1 (nephrin), as well as several other genes crucial for the architecture of podocytes, initiating a catastrophic collapse of the entire podocyte-stabilizing system. We found upregulation of miR-193a in isolated glomeruli from individuals with FSGS compared to normal kidneys or individuals with other glomerular diseases. Thus, upregulation of miR-193a provides a new pathogenic mechanism for FSGS and is a potential therapeutic target.

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