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Regulation of the MAFF Transcription Factor by Proinflammatory Cytokines in Myometrial Cells¹

Lady Davis Institute for Medical Research³ and Department of Medicine,⁴ McGill University, Montreal, Quebec, Canada H3T 1E2 Departments of Biochemistry and Molecular Biology,⁵ University of Texas Medical School, Houston, Texas 77030 Biomedical Sciences,⁶ Colorado State University, Fort Collins, Colorado 80523

ABSTRACT

The MAF (proto-)oncogene family of basic-leucine zipper transcription factors plays crucial roles in the control of mammalian gene expression and development. Here we analyzed the regulation of the human MAFF gene, coding for a small MAF transcription factor, in uterine smooth muscle cells. We found that MAFF transcript levels are induced by proinflammatory cytokines in PHM1–31 myometrial cells. We observed an important induction by interleukin 1 beta (IL1B) and a weaker upregulation by tumor necrosis factor (TNF), whereas interleukin 6 (IL6) treatment had no effect. Time course experiments revealed a rapid induction of MAFF transcripts within 30 min following IL1B treatment. The presence of actinomycin D inhibited the upregulation, suggesting that regulation of MAFF mRNA levels occurs at the transcriptional level. We generated a MAFF-specific antiserum and determined that MAFF protein was also induced by TNF and IL1B in PHM1–31 cells. In contrast, it was particularly interesting that the transcript and protein levels of the highly homologous MAFG and MAFK genes are not modulated by these cytokines. Our results suggest a possible specific role for MAFF in proinflammatory cytokine-mediated control of myometrial gene expression and provide the first link between a small MAF transcription factor and the inflammatory response.

CNC, cytokines, gene regulation, IL1B, MAF, parturition, signal transduction, TNF, transcription factor, uterus

¹ Supported by McGill Cancer Consortium and J.W. McConnell McGill Major Research studentships to W.M. Also supported by NIH award (HD09618) to B.M.S. V.B. supported by a Chercheur Boursier Fonds de la Recherche en Santé du Quebec and a McGill University Charles O. Monat award. Also supported by grants from the Hospital for Sick Children Foundation/Institute for Human Development, Child and Youth Health-CIHR and from the Cancer Research Society Inc. to V.B.

² Correspondence: Volker Blank, Lady Davis Institute for Medical Research, Department of Medicine, McGill University, 3755 Cote Sainte-Catherine Road, Montreal, Quebec, Canada H3T 1E2. FAX: 514 340 7573; volker.blank{at}mcgill.ca

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