Robust shifts in S100a9 expression with aging: A novel mechanism for chronic inflammation

William R. Swindell, Andrew Johnston, Xianying Xing, Andrew Little, Patrick Robichaud, John J. Voorhees, Gary Fisher, Johann E. Gudjonsson

Research output: Contribution to journalArticlepeer-review

67 Scopus citations

Abstract

The S100a8 and S100a9 genes encode a pro-inflammatory protein (calgranulin) that has been implicated in multiple diseases. However, involvement of S100a8/a9 in the basic mechanisms of intrinsic aging has not been established. In this study, we show that shifts in the abundance of S100a8 and S100a9 mRNA are a robust feature of aging in mammalian tissues, involving a range of cell types including the central nervous system. To identify transcription factors that control S100a9 expression, we performed a large-scale transcriptome analysis of 62 mouse and human cell types. We identified cell type-specific trends, as well as robust associations linking S100a9 coexpression to elevated frequency of ETS family motifs, and in particular, to motifs recognized by the transcription factor SPI/PU.1. Sparse occurrence of SATB1 motifs was also a strong predictor of S100a9 coexpression. These findings offer support for a novel mechanism by which a SPI1/PU.1-S100a9 axis sustains chronic inflammation during aging.

Original languageEnglish (US)
Article number1215
JournalScientific reports
Volume3
DOIs
StatePublished - 2013
Externally publishedYes

ASJC Scopus subject areas

  • General

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