Genetic and pharmacological inhibition of microRNA-92a maintains podocyte cell cycle quiescence and limits crescentic glomerulonephritis

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Genetic and pharmacological inhibition of microRNA-92a maintains podocyte cell cycle quiescence and limits crescentic glomerulonephritis. / Henique, Carole; Bollée, Guillaume; Loyer, Xavier; Grahammer, Florian; Dhaun, Neeraj; Camus, Marine; Vernerey, Julien; Guyonnet, Léa; Gaillard, François; Lazareth, Hélène; Meyer, Charlotte; Bensaada, Imane; Legrès, Luc; Satoh, Takashi; Akira, Shizuo; Bruneval, Patrick; Dimmeler, Stefanie; Tedgui, Alain; Karras, Alexandre; Thervet, Eric; Nochy, Dominique; Huber, Tobias B; Mesnard, Laurent; Lenoir, Olivia; Tharaux, Pierre-Louis.

In: NAT COMMUN, Vol. 8, No. 1, 28.11.2017, p. 1829.

Research output: SCORING: Contribution to journalSCORING: Journal articleResearchpeer-review

Harvard

Henique, C, Bollée, G, Loyer, X, Grahammer, F, Dhaun, N, Camus, M, Vernerey, J, Guyonnet, L, Gaillard, F, Lazareth, H, Meyer, C, Bensaada, I, Legrès, L, Satoh, T, Akira, S, Bruneval, P, Dimmeler, S, Tedgui, A, Karras, A, Thervet, E, Nochy, D, Huber, TB, Mesnard, L, Lenoir, O & Tharaux, P-L 2017, 'Genetic and pharmacological inhibition of microRNA-92a maintains podocyte cell cycle quiescence and limits crescentic glomerulonephritis', NAT COMMUN, vol. 8, no. 1, pp. 1829. https://doi.org/10.1038/s41467-017-01885-7

APA

Henique, C., Bollée, G., Loyer, X., Grahammer, F., Dhaun, N., Camus, M., Vernerey, J., Guyonnet, L., Gaillard, F., Lazareth, H., Meyer, C., Bensaada, I., Legrès, L., Satoh, T., Akira, S., Bruneval, P., Dimmeler, S., Tedgui, A., Karras, A., ... Tharaux, P-L. (2017). Genetic and pharmacological inhibition of microRNA-92a maintains podocyte cell cycle quiescence and limits crescentic glomerulonephritis. NAT COMMUN, 8(1), 1829. https://doi.org/10.1038/s41467-017-01885-7

Vancouver

Bibtex

@article{d8a9ad2d7dfa445d93587eace0dd7a0d,
title = "Genetic and pharmacological inhibition of microRNA-92a maintains podocyte cell cycle quiescence and limits crescentic glomerulonephritis",
abstract = "Crescentic rapidly progressive glomerulonephritis (RPGN) represents the most aggressive form of acquired glomerular disease. While most therapeutic approaches involve potentially toxic immunosuppressive strategies, the pathophysiology remains incompletely understood. Podocytes are glomerular epithelial cells that are normally growth-arrested because of the expression of cyclin-dependent kinase (CDK) inhibitors. An exception is in RPGN where podocytes undergo a deregulation of their differentiated phenotype and proliferate. Here we demonstrate that microRNA-92a (miR-92a) is enriched in podocytes of patients and mice with RPGN. The CDK inhibitor p57Kip2 is a major target of miR-92a that constitutively safeguards podocyte cell cycle quiescence. Podocyte-specific deletion of miR-92a in mice de-repressed the expression of p57Kip2 and prevented glomerular injury in RPGN. Administration of an anti-miR-92a after disease initiation prevented albuminuria and kidney failure, indicating miR-92a inhibition as a potential therapeutic strategy for RPGN. We demonstrate that miRNA induction in epithelial cells can break glomerular tolerance to immune injury.",
keywords = "Journal Article",
author = "Carole Henique and Guillaume Boll{\'e}e and Xavier Loyer and Florian Grahammer and Neeraj Dhaun and Marine Camus and Julien Vernerey and L{\'e}a Guyonnet and Fran{\c c}ois Gaillard and H{\'e}l{\`e}ne Lazareth and Charlotte Meyer and Imane Bensaada and Luc Legr{\`e}s and Takashi Satoh and Shizuo Akira and Patrick Bruneval and Stefanie Dimmeler and Alain Tedgui and Alexandre Karras and Eric Thervet and Dominique Nochy and Huber, {Tobias B} and Laurent Mesnard and Olivia Lenoir and Pierre-Louis Tharaux",
year = "2017",
month = nov,
day = "28",
doi = "10.1038/s41467-017-01885-7",
language = "English",
volume = "8",
pages = "1829",
journal = "NAT COMMUN",
issn = "2041-1723",
publisher = "NATURE PUBLISHING GROUP",
number = "1",

}

RIS

TY - JOUR

T1 - Genetic and pharmacological inhibition of microRNA-92a maintains podocyte cell cycle quiescence and limits crescentic glomerulonephritis

AU - Henique, Carole

AU - Bollée, Guillaume

AU - Loyer, Xavier

AU - Grahammer, Florian

AU - Dhaun, Neeraj

AU - Camus, Marine

AU - Vernerey, Julien

AU - Guyonnet, Léa

AU - Gaillard, François

AU - Lazareth, Hélène

AU - Meyer, Charlotte

AU - Bensaada, Imane

AU - Legrès, Luc

AU - Satoh, Takashi

AU - Akira, Shizuo

AU - Bruneval, Patrick

AU - Dimmeler, Stefanie

AU - Tedgui, Alain

AU - Karras, Alexandre

AU - Thervet, Eric

AU - Nochy, Dominique

AU - Huber, Tobias B

AU - Mesnard, Laurent

AU - Lenoir, Olivia

AU - Tharaux, Pierre-Louis

PY - 2017/11/28

Y1 - 2017/11/28

N2 - Crescentic rapidly progressive glomerulonephritis (RPGN) represents the most aggressive form of acquired glomerular disease. While most therapeutic approaches involve potentially toxic immunosuppressive strategies, the pathophysiology remains incompletely understood. Podocytes are glomerular epithelial cells that are normally growth-arrested because of the expression of cyclin-dependent kinase (CDK) inhibitors. An exception is in RPGN where podocytes undergo a deregulation of their differentiated phenotype and proliferate. Here we demonstrate that microRNA-92a (miR-92a) is enriched in podocytes of patients and mice with RPGN. The CDK inhibitor p57Kip2 is a major target of miR-92a that constitutively safeguards podocyte cell cycle quiescence. Podocyte-specific deletion of miR-92a in mice de-repressed the expression of p57Kip2 and prevented glomerular injury in RPGN. Administration of an anti-miR-92a after disease initiation prevented albuminuria and kidney failure, indicating miR-92a inhibition as a potential therapeutic strategy for RPGN. We demonstrate that miRNA induction in epithelial cells can break glomerular tolerance to immune injury.

AB - Crescentic rapidly progressive glomerulonephritis (RPGN) represents the most aggressive form of acquired glomerular disease. While most therapeutic approaches involve potentially toxic immunosuppressive strategies, the pathophysiology remains incompletely understood. Podocytes are glomerular epithelial cells that are normally growth-arrested because of the expression of cyclin-dependent kinase (CDK) inhibitors. An exception is in RPGN where podocytes undergo a deregulation of their differentiated phenotype and proliferate. Here we demonstrate that microRNA-92a (miR-92a) is enriched in podocytes of patients and mice with RPGN. The CDK inhibitor p57Kip2 is a major target of miR-92a that constitutively safeguards podocyte cell cycle quiescence. Podocyte-specific deletion of miR-92a in mice de-repressed the expression of p57Kip2 and prevented glomerular injury in RPGN. Administration of an anti-miR-92a after disease initiation prevented albuminuria and kidney failure, indicating miR-92a inhibition as a potential therapeutic strategy for RPGN. We demonstrate that miRNA induction in epithelial cells can break glomerular tolerance to immune injury.

KW - Journal Article

U2 - 10.1038/s41467-017-01885-7

DO - 10.1038/s41467-017-01885-7

M3 - SCORING: Journal article

C2 - 29184126

VL - 8

SP - 1829

JO - NAT COMMUN

JF - NAT COMMUN

SN - 2041-1723

IS - 1

ER -