Extracellular matrix promotes the growth and differentiation of murine hematopoietic cells in vitro.

Campbell, Alan D.; Wicha, Max S.; Long, Michael W.

doi:10.1172/jci111928

Cited by 88 publications

(28 citation statements)

References 18 publications

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“…Also, fibronectin has an instructive and permissive effect on the proliferation and differentiation of erythroid (54), myeloid (55), and lymphoid (56, 57) precursors, as well as on the in vivo medullary hematopoiesis (58). In addition, VCAM-1 may help to promote lympho-and myelopoiesis (56,59).…”

Section: Discussionmentioning

confidence: 99%

Bcr/Abl expression stimulates integrin function in hematopoietic cell lines.

Bazzoni¹,

Carlesso²,

Griffin³

et al. 1996

J. Clin. Invest.

119

101

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Cell adhesion to the extracellular matrix is largely mediated by adhesion molecules of the integrin family and is often diminished upon oncogenic transformation. However, we show here that the chronic myelogenous leukemia oncogene Bcr/ Abl has positive effects on VLA-4 and VLA-5 integrin function. The presence of Bcr/Abl in the GM-CSF-or IL-3-dependent hematopoietic cell lines MO7e, 32D, and BaF/3 enhanced cell binding to both soluble and immobilized fibronectin.

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Section: Discussionmentioning

confidence: 99%

Bcr/Abl expression stimulates integrin function in hematopoietic cell lines.

Bazzoni¹,

Carlesso²,

Griffin³

et al. 1996

J. Clin. Invest.

119

101

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“…In mice, blocking anti-␤ 1 -chain antibodies reduce in vivo colony formation in the spleen and medullar hematopoiesis from allogeneic hematopoietic progenitor cells (2). In cultures of purified CD34 ϩ progenitors, fibronectin has been shown to stimulate, in cooperation with interleukin 3 (IL-3), the formation of colonies derived from colony-forming unit (CFU)-granulocyte, erythroid, monocyte, megakaryocyte, burstforming unit-erythroid, CFU-erythroid, and CFU-macrophage, an effect reversed by RGDS-containing peptides that block fibronectin͞␣ 5 ␤ 1 -integrin interaction (3)(4)(5). In addition, cytokines such as IL-3, granulocyte-monocyte colonystimulating factor, and stem cell factor are transient and selective activators of both ␣ 4 ␤ 1 and ␣ 5 ␤ 1 integrins expressed by normal CD34 ϩ progenitor cells and cytokine-dependent myeloid cell lines MO7e and TF1, thus conferring on these cells a transient adherent phenotype to fibronectin (6).…”

mentioning

confidence: 99%

Adhesion to fibronectin stimulates proliferation of wild-type and bcr/abl -transfected murine hematopoietic cells

Krämer

Hörner

Willer

et al. 1999

Proc. Natl. Acad. Sci. U.S.A.

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Cells of most tissues require adhesion to a surface to grow. However, for hematopoietic cells, both stimulation and inhibition of proliferation by adhesion to extracellular matrix components have been described. Furthermore, it has been suggested that progenitor cells from chronic myelogenous leukemia show decreased ␤ 1 integrin-mediated adhesion to fibronectin, resulting in increased proliferation and abnormal trafficking. However, we show here that the chronic myelogenous leukemia-specific fusion protein p210bcr͞abl stimulates the expression of ␣ 5 ␤ 1 integrins and induces adhesion to fibronectin when expressed in the myeloid cell line 32D. Moreover, proliferation of both p210bcr͞abl-transfected 32D (32Dp210) cells and untransfected 32D cells is stimulated by immobilized fibronectin. Cell cycle analysis revealed that nonadherent 32D and 32Dp210 cells are arrested in late G 1 or early S phase, whereas the adherent fractions continue cycling. Although both adherent and nonadherent p210bcr͞abl-transfected and parental 32D cells express equal amounts of cyclin A, a protein necessary for cell cycle progression at the G 1 ͞S boundary, cyclin A complexes immunoprecipitated from 32D cells cultured on immobilized fibronectin were found to be catalytically inactive in nonadherent but not in adherent cells. In addition, as compared with untransfected 32D cells, cyclin A immunoprecipitates from 32Dp210 cells exhibited a greatly elevated kinase activity and remained partially active irrespective of the adhesion status. The lack of cyclin A͞cyclin-dependent kinase (CDK) 2 activity in nonadherent 32D cells appeared to result from increased expression and cyclin A complex formation of the CDK inhibitor p27 Kip1 . Taken together, our results indicate that adhesion stimulates cell cycle progression of hematopoietic cells by downregulation of p27 Kip1 , resulting in activation of cyclin A͞CDK2 complexes and subsequent transition through the G 1 ͞S adhesion checkpoint.

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“…6 The proliferation and differentiation of HSCs to B-lineage cells requires vital signals from the BM microenviroment, including cytokines, growth factors, and adhesion molecules secreted by stromal cells and the ECM. [38][39][40] Previous investigation of the mechanism responsible for the observed arrest of B lymphopoiesis in rabbits led Kalis et al 7 to suggest that the BM stroma in adult rabbits loses its potential to support B lymphopoiesis. Surprisingly, IL-7, a cytokine critical for B lymphopoiesis, was found to be up-regulated in adult rabbits.…”

Section: Discussionmentioning

confidence: 99%