Histone variant H2A.J accumulates in senescent cells and promotes inflammatory gene expression View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2017-05-10

AUTHORS

Kévin Contrepois, Clément Coudereau, Bérénice A. Benayoun, Nadine Schuler, Pierre-François Roux, Oliver Bischof, Régis Courbeyrette, Cyril Carvalho, Jean-Yves Thuret, Zhihai Ma, Céline Derbois, Marie-Claire Nevers, Hervé Volland, Christophe E. Redon, William M. Bonner, Jean-François Deleuze, Clotilde Wiel, David Bernard, Michael P. Snyder, Claudia E. Rübe, Robert Olaso, François Fenaille, Carl Mann

ABSTRACT

The senescence of mammalian cells is characterized by a proliferative arrest in response to stress and the expression of an inflammatory phenotype. Here we show that histone H2A.J, a poorly studied H2A variant found only in mammals, accumulates in human fibroblasts in senescence with persistent DNA damage. H2A.J also accumulates in mice with aging in a tissue-specific manner and in human skin. Knock-down of H2A.J inhibits the expression of inflammatory genes that contribute to the senescent-associated secretory phenotype (SASP), and over expression of H2A.J increases the expression of some of these genes in proliferating cells. H2A.J accumulation may thus promote the signalling of senescent cells to the immune system, and it may contribute to chronic inflammation and the development of aging-associated diseases. More... »

PAGES

14995

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ncomms14995

DOI

http://dx.doi.org/10.1038/ncomms14995

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1085378071

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/28489069


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