Kruppel-like factor 2 (KLF2) regulates proinflammatory activation of monocytes.

Proceedings of the National Academy of Sciences of the United States of America
Hiranmoy DasMukesh K Jain

Abstract

The mechanisms regulating activation of monocytes remain incompletely understood. Herein we provide evidence that Kruppel-like factor 2 (KLF2) inhibits proinflammatory activation of monocytes. In vitro, KLF2 expression in monocytes is reduced by cytokine activation or differentiation. Consistent with this observation, KLF2 expression in circulating monocytes is reduced in patients with chronic inflammatory conditions such as coronary artery disease. Adenoviral overexpression of KLF2 inhibits the LPS-mediated induction of proinflammatory factors, cytokines, and chemokines and reduces phagocytosis. Conversely, short interfering RNA-mediated reduction in KLF2 increased inflammatory gene expression. Reconstitution of immunodeficient mice with KLF2-overexpressing monocytes significantly reduced carrageenan-induced acute paw edema formation. Mechanistically, KLF2 inhibits the transcriptional activity of both NF-kappaB and activator protein 1, in part by means of recruitment of transcriptional coactivator p300/CBP-associated factor. These observations identify KLF2 as a novel negative regulator of monocytic activation.

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Citations

Jun 30, 2012·Biomechanics and Modeling in Mechanobiology·Beth L Roman, Kerem Pekkan
Aug 2, 2012·Current Atherosclerosis Reports·Mohamad Amer AlaitiMukesh K Jain
May 28, 2013·Journal of Dermatological Science·Chang-Joon BaeWoon-Kyu Lee
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