Lineage-restricted expression of bone morphogenetic protein genes in human hematopoietic cell lines

被引:39
作者
Detmer, K
Steele, TA
Shoop, MA
Dannawi, H
机构
[1] Mercer Univ, Sch Med, Div Basic Med Sci, Macon, GA 31207 USA
[2] Med Ctr Cent Georgia, Dept Pediat, Macon, GA USA
关键词
bone morphogenetic proteins; lineage-restricted expression; hematopoiesis; differentiation; hematopoietic cell lines; neoplasia;
D O I
10.1006/bcmd.1999.0259
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
To explore the possibility that bone morphogenetic proteins (BMPs) are autocrine/paracrine regulators of hematopoietic differentiation and function, we screened a panel of human cell lines encompassing the hematopoietic lineages for expression of members of this family of genes. Expression of BMP-2, BMP-4, BMP-6, BMP-7, Growth and Differentiation Factor-1 (GDF-1), Placental Bone Morphogenetic Protein (PLAB), and Transforming Growth Factor-beta 3 (TGF-beta 3) was detected in one or more cell lines. BMP-2, BMP-1, BMP-7, and TGF-beta 3 expression was also found in normal hemaropoietic tissue. Expression of BMP-5 and BMP-S was not seen. Lineage-restricted patterns of expression were found for BMP-4 (T-lymphoid), BMP-7 (lymphoid), PLAB (macrophage/monocyte), and GDF-1 (myeloid), Expression of BMP-2, CDF-1, and PLAB could be modulated by treatment with differentiating agents. Marked variations in the levels of BMP-4, BMP-7, and PLAB expression were encountered, indicating that disorders in BMP signaling pathways may play a role in the development of hematopoietic neoplasia.
引用
收藏
页码:310 / 323
页数:14
相关论文
共 56 条
  • [1] AMEDEE J, 1994, DIFFERENTIATION, V58, P157
  • [2] An J, 1996, EXP HEMATOL, V24, P768
  • [3] TRANSCRIPTS FOR TRANSFORMING GROWTH-FACTORS IN HUMAN BREAST-CANCER - CLINICAL CORRELATES
    BARRETTLEE, P
    TRAVERS, M
    LUQMANI, Y
    COOMBES, RC
    [J]. BRITISH JOURNAL OF CANCER, 1990, 61 (04) : 612 - 617
  • [4] Bone morphogenetic proteins regulate the developmental program of human hematopoietic stem cells
    Bhatia, M
    Bonnet, D
    Wu, DM
    Murdoch, B
    Wrana, J
    Gallacher, L
    Dick, JE
    [J]. JOURNAL OF EXPERIMENTAL MEDICINE, 1999, 189 (07) : 1139 - 1147
  • [5] Overexpression of bone morphogenetic protein-6 (BMP-6) in the epidermis of transgenic mice: Inhibition or stimulation of proliferation depending on the pattern of transgene expression and formation of psoriatic lesions
    Blessing, M
    Schirmacher, P
    Kaiser, S
    [J]. JOURNAL OF CELL BIOLOGY, 1996, 135 (01) : 227 - 239
  • [6] MIC-1, a novel macrophage inhibitory cytokine, is a divergent member of the TGF-beta superfamily
    Bootcov, MR
    Bauskin, AR
    Valenzuela, SM
    Moore, AG
    Bansal, M
    He, XY
    Zhang, HP
    Donnellan, M
    Mahler, S
    Pryor, K
    Walsh, BJ
    Nicholson, RC
    Fairlie, WD
    Por, SB
    Robbins, JM
    Breit, SN
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1997, 94 (21) : 11514 - 11519
  • [7] The Smad5 gene is involved in the intracellular signaling pathways that mediate the inhibitory effects of transforming growth factor-β on human hematopoiesis
    Bruno, E
    Horrigan, SK
    Van Den Berg, D
    Rozler, E
    Fitting, PR
    Moss, ST
    Westbrook, C
    Hoffman, R
    [J]. BLOOD, 1998, 91 (06) : 1917 - 1923
  • [8] CHOMCZYNSKI P, 1987, ANAL BIOCHEM, V162, P156, DOI 10.1016/0003-2697(87)90021-2
  • [9] TERMINAL DIFFERENTIATION OF HUMAN PROMYELOCYTIC LEUKEMIA-CELLS INDUCED BY DIMETHYL-SULFOXIDE AND OTHER POLAR COMPOUNDS
    COLLINS, SJ
    RUSCETTI, FW
    GALLAGHER, RE
    GALLO, RC
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1978, 75 (05) : 2458 - 2462
  • [10] Loss of functional cell surface transforming growth factor beta (TGF-beta) type 1 receptor correlates with insensitivity to TGF-beta in chronic lymphocytic leukemia
    DeCoteau, JF
    Knaus, PI
    Yankelev, H
    Reis, MD
    Lowsky, R
    Lodish, HF
    Kadin, ME
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1997, 94 (11) : 5877 - 5881