This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Moriguchi, T. Articles by Takahashi, S. Search for Related Content PubMed PubMed Citation Articles by Moriguchi, T. Articles by Takahashi, S.

MafB Is Essential for Renal Development and F4/80 Expression in Macrophages

Takashi Moriguchi,^1,6, Michito Hamada,^1, Naoki Morito,¹ Tsumoru Terunuma,¹ Kazuteru Hasegawa,¹ Chuan Zhang,¹ Tomomasa Yokomizo,¹ Ritsuko Esaki,¹ Etsushi Kuroda,⁵ Keigyou Yoh,³ Takashi Kudo,¹ Michio Nagata,¹ David R. Greaves,⁷ James Douglas Engel,^6* Masayuki Yamamoto,^1,4 and Satoru Takahashi^1,2

Institute of Basic Medical Sciences,¹ Laboratory Animal Resource Center,² Institute of Clinical Medicine,³ Center for Tsukuba Advanced Research Alliance, University of Tsukuba, Tsukuba 305-8575, Japan,⁴ Department of Immunology, University of Occupational and Environmental Health, School of Medicine, Kitakyushu 807-8555, Japan,⁵ Department of Cell and Developmental Biology, University of Michigan, Ann Arbor, Michigan 48109-0616,⁶ Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, United Kingdom⁷

Received 1 January 2006/ Returned for modification 22 February 2006/ Accepted 8 May 2006

MafB is a member of the large Maf family of transcription factors that share similar basic region/leucine zipper DNA binding motifs and N-terminal activation domains. Although it is well known that MafB is specifically expressed in glomerular epithelial cells (podocytes) and macrophages, characterization of the null mutant phenotype in these tissues has not been previously reported. To investigate suspected MafB functions in the kidney and in macrophages, we generated mafB/green fluorescent protein (GFP) knock-in null mutant mice. mafB homozygous mutants displayed renal dysgenesis with abnormal podocyte differentiation as well as tubular apoptosis. Interestingly, these kidney phenotypes were associated with diminished expression of several kidney disease-related genes. In hematopoietic cells, GFP fluorescence was observed in both Mac-1- and F4/80-expressing macrophages in the fetal liver. Interestingly, F4/80 expression in macrophages was suppressed in the homozygous mutant, although development of the Mac-1-positive macrophage population was unaffected. In primary cultures of fetal liver hematopoietic cells, MafB deficiency was found to dramatically suppress F4/80 expression in nonadherent macrophages, whereas the Mac-1-positive macrophage population developed normally. These results demonstrate that MafB is essential for podocyte differentiation, renal tubule survival, and F4/80 maturation in a distinct subpopulation of nonadherent mature macrophages.

T.M. and M.H. contributed equally to this work.

This article has been cited by other articles:

• Kim, K., Kim, J. H., Lee, J., Jin, H. M., Kook, H., Kim, K. K., Lee, S. Y., Kim, N. (2007). MafB negatively regulates RANKL-mediated osteoclast differentiation. Blood 109: 3253-3259 [Abstract] [Full Text]  
• Artner, I., Blanchi, B., Raum, J. C., Guo, M., Kaneko, T., Cordes, S., Sieweke, M., Stein, R. (2007). MafB is required for islet beta cell maturation. Proc. Natl. Acad. Sci. USA 104: 3853-3858 [Abstract] [Full Text]