Impaired response to GM-CSF and G-CSF, and enhanced apoptosis in C/EBPβ-deficient hematopoietic cells

被引：57

作者：

Akagi, Tadayuki ^{[1
]}

Saitoh, Takayuki ^{[1
]}

O'Kelly, James ^{[1
]}

Akira, Shizuo ^{[2
]}

Gombart, Adrian F. ^{[1
]}

Koeffler, H. Phillip ^{[1
]}

机构：

[1] Univ Calif Los Angeles, Cedars Sinai Med Ctr, Sch Med, Div Hematol & Oncol, Los Angeles, CA 90048 USA

[2] Osaka Univ, Res Inst Microbial Dis, Dept Host Def, Osaka, Japan

来源：

BLOOD | 2008年 / 111卷 / 06期

关键词：

D O I：

10.1182/blood-2007-04-087213

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Transcription factors known as CCAAT enhancer binding proteins (C/EBPs) are involved in hematopoietic differentiation, including myelopolesis and granulopolesis. C/EBP beta-deficient mice develop normally; however, they exhibit detective macrophage function, resulting in increased susceptibility to infection. Little is known about the role of G/EBP beta in granulopoiesis; therefore, we examined granulopoiesis in C/EBP beta-deficient mice. Morphology, the number of peripheral blood and bone marrow cells, and the expression of genes specific for the myeloid lineage were normal in C/EBP beta-deficient mice. Interestingly, the hematopoietic progenitor cells of C/EBP beta-deficient mice did not respond normally to granulocyte/macrophage-colony stimulating factor and granulocyte colony stimulating factor. In addition, C/EBP beta-deficient neutrophils displayed enhanced apoptosis compared with wild-type neutrophils. Our present results indicate that C/EBP beta helps regulate survival of neutrophils, downstream of the granulocyte colony stimulating factor receptor.

引用

页码：2999 / 3004

页数：6

共 37 条

[31] C/EBP-β, C/EBP-δ, PU.1, AML1 genes:: mutational analysis in 381 samples of hematopoietic and solid malignancies [J].

Vegesna, VA ;

Takeuchi, S ;

Hofmann, WK ;

Ikezoe, T ;

Tavor, S ;

Krug, U ;

Fermin, AC ;

Heaney, A ;

Miller, CW ;

Koeffler, HP .

LEUKEMIA RESEARCH, 2002, 26 (05) :451-457

[32] Critical prosurvival roles for C/EBPβ and insulin-like growth factor I in macrophage tumor cells [J].

Wessells, J ;

Yakar, S ;

Johnson, PF .

MOLECULAR AND CELLULAR BIOLOGY, 2004, 24 (08) :3238-3250

[33]

Xie D, 2001, CANCER RES, V61, P8917

[34] Impaired granulopoiesis, myelodysplasia, and early lethality in CCAAT/enhancer binding protein epsilon-deficient mice [J].

Yamanaka, R ;

Barlow, C ;

LekstromHimes, J ;

Castilla, LH ;

Liu, PP ;

Eckhaus, M ;

Decker, T ;

WynshawBoris, A ;

Xanthopoulos, KG .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1997, 94 (24) :13187-13192

[35] Absence of granulocyte colony-stimulating factor signaling and neutrophil development in CCAAT enhancer binding protein alpha-deficient mice [J].

Zhang, DE ;

Zhang, P ;

Wang, ND ;

Hetherington, CJ ;

Darlington, GJ ;

Tenen, DG .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1997, 94 (02) :569-574

[36] Enhancement of hematopoietic stem cell repopulating capacity and self-renewal in the absence of the transcription factor C/EBPα. [J].

Zhang, P ;

Iwasaki-Arai, J ;

Iwasaki, H ;

Fenyus, ML ;

Dayaram, T ;

Owens, BM ;

Shigematsu, H ;

Levantini, E ;

Huettner, CS ;

Lekstrom-Himes, JA ;

Akashi, K ;

Tenen, DG .

IMMUNITY, 2004, 21 (06) :853-863

[37] CCAAT/enhancer binding protein-β is a mediator of keratinocyte survival and skin tumorigenesis involving oncogenic Ras signaling [J].

Zhu, SY ;

Yoon, K ;

Sterneck, E ;

Johnson, PF ;

Smart, RC .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2002, 99 (01) :207-212

← 1 2 3 4 →