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Blood, Vol. 93 No. 5 (March 1), 1999:
pp. 1586-1594
Structural and Functional Abnormalities in the Spleen of an
mFtz-F1 Gene-Disrupted Mouse
Ken-ichirou Morohashi,
Hisae Tsuboi-Asai,
Sumie Matsushita,
Masahiro Suda,
Manabu Nakashima,
Hironobu Sasano,
Yoshiaki Hataba,
Chun-Lin Li,
Junichi Fukata,
Junji Irie,
Takeshi Watanabe,
Hiroshi Nagura, and
En Li
From the Division of Cell Differentiation, Department of
Developmental Biology, National Institute for Basic Biology,
Myodaiji-cho, Okazaki; the Department of Molecular Biomechanics, School
of Life Science, The Graduate University for Advanced Studies,
Myodaiji-cho, Okazaki; the Department of Molecular Biology, Graduate
School of Medical Science, Kyushu University, Higashi-ku, Fukuoka; the
Clinical Laboratory, Kyushu University Hospital, Higashi-ku, Fukuoka;
the Department of Molecular Immunology, Medical Institute of
Bioregulation, Kyushu University, Higashi-ku, Fukuoka; the Department
of Pathology, Tohoku University School of Medicine, Sendai; the
Department of Molecular Cell Biology, Institute of DNA Medicine, Jikei
University School of Medicine, Minatoku, Tokyo; the First Department of
Internal Medicine, Kochi Medical School, Nankoku, Kochi; the Department
of Pathology, Nagasaki University School of Medicine, Nagasaki,
Japan; and the Cardiovascular Research Center, Massachusetts General
Hospital-East, Harvard Medical School, Charlestown, MA.
The spleen has two main functions. The first is to provide a proper
microenvironment to lymphoid and myeloid cells, whereas the second
involves clearance of abnormal erythrocytes. Ad4BP/SF-1, a product of
the mammalian FTZ-F1 gene (mFTZ-F1), was originally identified as a steroidogenic, tissue-specific transcription factor. Immunohistochemical examination of the mammalian spleens confirmed the
expression of Ad4BP/SF-1 in endothelial cells of the splenic venous
sinuses and pulp vein. In mFtz-F1 gene-disrupted (KO) mice, several structural abnormalities were detected in the spleen, including
underdevelopment and nonuniform distribution of erythrocytes. Examination of the spleen of KO fetuses showed failure of development of certain tubular structures during embryogenesis. These structures are normally assembled by Ad4BP/SF-1 immunoreactive cells, and most
likely form the vascular system during later stages of development. Other structural abnormalities in the spleen of the KO mice included defects in the tissue distribution of type-IV collagen, laminin, c-kit, and vimentin. These morphologic defects in
the vascular system were associated with a decrease in the proportion
of hematopoietic cells, although differentiation of these cells was not
affected significantly. A high number of abnormal red blood cells
containing Howell-Jolly bodies were noted in the KO mice, indicating
impaired clearance by the splenic vascular system. We also detected the presence of an mRNA-encoding cholesterol side-chain cleavage P450 in
the spleen, resembling the findings in steroidogenic tissues such as
the gonads and adrenal cortex. The mRNA transcript was not involved in
splenic structural defects as it was detected in the spleens of both
normal and KO mice, indicating that the regulatory mechanism of the
P450 gene in the spleen is different from that in steroidogenic
tissues. Our results indicate that a lack of the mFtz-F1 gene
in mice is associated with structural and functional abnormalities of
the splenic vascular system.
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