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Toxicology

Title:		MAPK- and PKC/CREB-dependent induction of interleukin-11 by the environmental contaminant formaldehyde in human bronchial epithelial cells
Author(s):		Lecureur V; Arzel M; Ameziane S; Houlbert N; Le Vee M; Jouneau S; Fardel O;
Address:		"EA4427-SeRAIC, IFR140, Universite de Rennes 1, Faculte des Sciences Pharmaceutiques et Biologiques, Rennes, France. valerie.lecureur@univ-rennes1.fr"
Journal Title:		Toxicology
Year:		2012
Volume:		20111128
Issue:		1
Page Number:		13 - 22
DOI:		10.1016/j.tox.2011.11.011
ISSN/ISBN:		1879-3185 (Electronic) 0300-483X (Linking)
Abstract:		"Formaldehyde (FA) is a volatile organic compound (VOC), considered as a major indoor air pollutant and suspected to favor the development of inflammatory lung diseases. The present study was aimed at identifying cytokines/chemokines targeted by FA in human lung cells. This VOC was demonstrated to up-regulate interleukin-11 (IL-11) mRNA and secretion levels in a dose-dependent manner in cultured lung epithelial BEAS-2B cells. It concomitantly induced mRNA expression of transforming growth factor (TGF)-beta1, a fibrogenic marker regulated by IL-11. FA was also found to trigger an early phosphorylation of p38 and extracellular signal-regulated kinase (ERK)1/2 mitogen-activated protein kinases (MAPKs) in BEAS-2B cells, whose inhibition by ERK and p38 MAPK chemical inhibitors (U0126 and SB203580, respectively) counteracted FA-mediated induction of IL-11. In addition, FA increased phosphorylation of cAMP response element binding protein (CREB) and the use of small-interfering RNA targeting CREB demonstrated that this transcription factor was required for the up-regulation of IL-11 by FA. Implication of protein kinase C (PKC) in FA-induced IL-11 expression was moreover demonstrated by using RO-31-8220, a PKC inhibitor. We finally showed using SB203580 and RO-31-8220 that phosphorylation of CREB and CREB-promoter activity induced by FA are under the control of both p38 MAPK and PKC. Taken together, the results showed that FA uses different pathways to induce IL-11 expression in lung BEAS-2B cells. IL-11, well-known to contribute to lung inflammatory diseases, appears thus as a molecular target of FA, which could be involved in putative deleterious inflammatory and fibrogenic pulmonary effects of this VOC"
Keywords:		"Cell Line Cell Line, Tumor Cyclic AMP Response Element-Binding Protein/*physiology Environmental Pollutants/*toxicity Formaldehyde/*toxicity Humans Interleukin-11/*biosynthesis Mitogen-Activated Protein Kinases/*physiology Protein Kinase C/*physiology Rec;"
Notes:		"MedlineLecureur, Valerie Arzel, Matthieu Ameziane, Sarah Houlbert, Noemie Le Vee, Marc Jouneau, Stephane Fardel, Olivier eng Comparative Study Research Support, Non-U.S. Gov't Ireland 2011/12/06 Toxicology. 2012 Feb 6; 292(1):13-22. doi: 10.1016/j.tox.2011.11.011. Epub 2011 Nov 28"