Inactivation of MAP3K7 in FOXD1-expressing cells results in loss of mesangial PDGFRΒ and juvenile kidney scarring.

Document Type

Article

Publication Date

8-1-2018

Institution/Department

Maine Medical Center Research Institute; Center for Molecular Medicine

Journal Title

American journal of physiology. Renal physiology

MeSH Headings

Animals, Cells, Cultured, Collagen Type IV, Disease Models, Animal, Enzyme Activation, Fibrosis, Forkhead Transcription Factors, Gene Silencing, Genetic Predisposition to Disease, Glomerulonephritis, JNK Mitogen-Activated Protein Kinases, MAP Kinase Kinase Kinases, Mesangial Cells, Mice, Inbred C57BL, Mice, Knockout, Phenotype, Receptor, Platelet-Derived Growth Factor beta, Signal Transduction, p38 Mitogen-Activated Protein Kinases

Abstract

Transforming growth factor-β (TGFβ) plays a central role in renal scarring, controlling extracellular matrix deposition by interstitial cells and mesangial cells. TGFβ signals through Smad and mitogen-activated protein kinase (MAPK) pathways. To understand the role of MAPK in interstitial and mesangial cells, we genetically inactivated TGFβ-activated kinase-1 ( Map3k7) using Foxd1

ISSN

1522-1466

First Page

336

Last Page

336

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