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Am J Physiol Cell Physiol 291: C104-C113, 2006. First published February 15, 2006; doi:10.1152/ajpcell.00614.2005
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GROWTH, DIFFERENTIATION, AND APOPTOSIS

Activation of hypoxia-inducible factor 1 during macrophage differentiation

Tomoyuki Oda,1,2 Kiichi Hirota,1,3 Kenichiro Nishi,1,4 Satoshi Takabuchi,1,3 Seiko Oda,1,3 Hiroko Yamada,5 Toshiyuki Arai,3 Kazuhiko Fukuda,3 Toru Kita,2 Takehiko Adachi,1 Gregg L. Semenza,6 and Ryuji Nohara1

1The Tazuke Kofukai Medical Research Institute, Kitano Hospital, Osaka; 2Department of Cardiovascular Medicine, Graduate School of Medicine, Kyoto University, Kyoto; 3Department of Anesthesia, Kyoto University Hospital, Kyoto; 4Department of Anesthesiology, Kansai Medical University, Osaka; 5Department of Hematology and Oncology, Kyoto University Hospital, Kyoto University, Kyoto, Japan; and 6Vascular Biology Program, Institute for Cell Engineering, The Johns Hopkins University School of Medicine, Baltimore, Maryland

Submitted 12 December 2005 ; accepted in final form 7 February 2006

Monocytes/macrophages of the myeloid lineage are the main cellular effectors of innate immunity. Hypoxia-inducible factor 1 (HIF-1) is essential for myeloid cell activation in response to inflammatory stimuli. However, it has not been established whether HIF-1 activity is induced during differentiation from monocyte to macrophage. We demonstrate that macrophage differentiation of THP-1 cells or monocytes from peripheral blood induces increased expression of both HIF-1{alpha} and HIF-1beta as well as increased HIF-1 transcriptional activity leading to increased expression of HIF-1 target genes. The increased HIF-1 activity in differentiated THP-1 cells resulted from the combined effect of increased HIF-1{alpha} mRNA levels and increased HIF-1{alpha} protein synthesis. Differentiation-induced HIF-1{alpha} protein and mRNA and HIF-1-dependent gene expression was blocked by treating cells with an inhibitor of the protein kinase C or MAP kinase signaling pathway. THP-1 cell differentiation was also associated with increased phosphorylation of the translational regulatory proteins p70 S6 kinase, S6 ribosomal protein, eukaryotic initiation factor 4E, and 4E binding protein 1, thus providing a possible mechanism for the modulation of HIF-1{alpha} protein synthesis. RNA interference studies demonstrated that HIF-1{alpha} is dispensable for macrophage differentiation but is required for functional maturation.

translation; RNA interference


Address for reprint requests and other correspondence: K. Hirota, Dept. of Anesthesia, Kyoto Univ. Hospital, Sakyo-ku, Kyoto, 606-8507, Japan (e-mail: hif1{at}mac.com)




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