Author:
Rodriguez Patricia Q.,Unnersjö-Jess David,Zambrano Sonia S.,Guo Jing,Möller-Hackbarth Katja,Blom Hans,Jahnukainen Timo,Ebarasi Lwaki,Patrakka Jaakko
Abstract
AbstractPodocytes are critical for the maintenance of kidney ultrafiltration barrier and play a key role in the progression of glomerular diseases. Although mediator complex proteins have been shown to be important for many physiological and pathological processes, their role in kidney tissue has not been studied. In this study, we identified a mediator complex protein 22 (Med22) as a renal podocyte cell-enriched molecule. Podocyte-specific Med22 knockout mouse showed that Med22 was not needed for normal podocyte maturation. However, it was critical for the maintenance of podocyte health as the mice developed progressive glomerular disease and died due to renal failure. Detailed morphological analyses showed that Med22-deficiency in podocytes resulted in intracellular vacuole formation followed by podocyte loss. Moreover, Med22-deficiency in younger mice promoted the progression of glomerular disease, suggesting Med22-mediated processes may have a role in the development of glomerulopathies. This study shows for the first time that mediator complex has a critical role in kidney physiology.
Funder
AstraZeneca
Swedish Diabetes Foundation
Swedish Kidney Foundation
CIMED
Marianne and Marcus Wallenberg Foundation
Karolinska Insitute
Karolinska Institute
Publisher
Springer Science and Business Media LLC
Cited by
1 articles.
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