The role of platelet-derived growth factor on human pluripotent progenitor (CFU-GEMM) growth in vitro

Michalevicz, Rita; Francis, G. E.; Price, Gillian; Hoffbrand, A. V.

doi:10.1016/0145-2126(85)90062-1

Cited by 19 publications

(10 citation statements)

References 18 publications

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“…Mouse splenic erythroid cells express PDGF in vivo after stimulation with erythropoietin, 17,18 demonstrating that precursors of the erythroid lineages are a source of PDGF. In mixed marrow cultures, PDGF stimulates the growth of primitive hematopoietic progenitor cells, such as colony-forming units containing granulocytes, erythroid cells, macrophages, megakaryocytes (CFU-mix, CFU-GEMM), 19,32,33 and lineage-restricted hematopoietic progenitors. 34 Adherent accessory cells are also required for the stimulation of primitive and lineage-restricted hematopoietic progenitors by PDGF, and growth enhancement appears to occur as an indirect effect through the stimulation of interleukin-1 (IL-1) production by PDGFR-positive stromal cells, including macrophages.…”

Section: What Role Does Pdgf Play In Hematopoiesis?mentioning

confidence: 99%

“…19,21,[32][33][34] PDGF promotes in vitro proliferation of erythropoietic progenitors, 20 but stimulation requires the presence of adherent stromal cells, 21 presumably because of PDGF induction of colony-stimulating factor (CSF) release from the stromal cells. Mouse splenic erythroid cells express PDGF in vivo after stimulation with erythropoietin, 17,18 demonstrating that precursors of the erythroid lineages are a source of PDGF.…”

Section: What Role Does Pdgf Play In Hematopoiesis?mentioning

confidence: 99%

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Basis of hematopoietic defects in platelet-derived growth factor (PDGF)-B and PDGF β-receptor null mice

Kaminski

Lindahl

Lin

et al. 2001

Blood

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Platelet-derived growth factor (PDGF)-B and PDGF ␤-receptor (PDGFR␤) deficiency in mice is embryonic lethal and results in cardiovascular, renal, placental, and hematologic disorders. The hematologic disorders are described, and a correlation with hepatic hypocellularity is demonstrated. To explore possible causes, the colony-forming activity of fetal liver cells in vitro was assessed, and hematopoietic chimeras were demonstrated by the transplantation of mutant fetal liver cells into lethally irradiated recipients. It was found that mutant colony formation is equivalent to that of wild-type controls. Hematopoietic chimeras reconstituted with PDGF-B ؊/؊ , PDGFR␤ ؊/؊ , or wild-type fetal liver cells show complete engraftment (greater than 98%) with donor granulocytes, monocytes, B cells, and T cells and display none of the cardiovascular or hematologic abnormalities seen in mutants. In mouse embryos, PDGF-B is expressed by vascular endothelial cells and megakaryocytes. After birth, expression is seen in macrophages and neurons. This study demonstrates that hematopoietic PDGF-B or PDGFR␤ expression is not required for hematopoiesis or integrity of the cardiovascular system. It is argued that metabolic stress arising from mutant defects in the placenta, heart, or blood vessels may lead to impaired liver growth and decreased production of blood cells. The chimera models in this study will serve as valuable tools to test the role of PDGF in inflammatory and immune responses.

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Section: What Role Does Pdgf Play In Hematopoiesis?mentioning

confidence: 99%

Section: What Role Does Pdgf Play In Hematopoiesis?mentioning

confidence: 99%

Basis of hematopoietic defects in platelet-derived growth factor (PDGF)-B and PDGF β-receptor null mice

Kaminski

Lindahl

Lin

et al. 2001

Blood

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“…8–10). Previous studies have demonstrated that PDGF can alter the functional phenotype of stromal cells and modulate normal hematopoiesis (10–17), but its possible role in AML has only been investigated in a small study including 5 patients and reporting no effects of PDGF on AML colony formation (18).…”

mentioning

confidence: 99%

Platelet‐derived growth factor (PDGF) in human acute myelogenous leukemia: PDGF receptor expression, endogenous PDGF release and responsiveness to exogenous PDGF isoforms by in vitro cultured acute myelogenous leukemia blasts

Foss

Ulvestad

Bruserud

2001

European J of Haematology

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We investigated effects of Platelet-derived growth factor (PDGF) and Platelet factor 4 (PF-4) on the functional characteristics of native, human acute myelogenous leukemia (AML) blasts. AML blast expression of the PDGF-receptor alpha-chain was detected for a subset of patients (45%), whereas PDGF-receptor beta-chain expression was detected for most patients (90%). Constitutive AML blast release of the PDGF-AB isoform (the major form also derived from normal platelets) was detected for 43% of patients, whereas PDGF-BB release was not detected for any patient. The PDGF isoforms AA, AB and BB had dose-dependent and divergent effects on spontaneous and cytokine-dependent AML blast proliferation, whereas for constitutive cytokine secretion (IL-1beta, IL-6, TNF-alpha) inhibitory effects were rare and all three isoforms usually had no effect or enhanced the constitutive secretion. The PDGF effects were caused by a direct effect on the AML blasts and were not dependent on the presence of serum. The PDGF effects could also be detected after in vitro culture of AML cells in the presence of IL-4+granulocyte-macrophage colony stimulating factor. PF-4 had divergent effects on proliferation and cytokine secretion by native AML blasts. Our results suggest that exogenous (e.g. platelet-secreted) PDGF and PF-4 can function as regulators of leukemic hematopoiesis and possibly also modulate the function of residual AML cells in peripheral blood stem cell grafts. On the other hand, endogenous release of PDGF-AB by native blasts may modulate the function of normal cells in the bone marrow microenvironment (e.g. bone marrow stromal cells).

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“…Coexpression of PDGF and PDGF receptors has been observed in various human tumors, including meningiomas, melanomas, neuroendocrine tumors, ovarian cancer, pancreatic cancer, gastric cancer, lung cancer and prostate cancer [7]. PDGF can enhance proliferation of normal hematopoietic cells [8, 9] and of hematologic malignancies, such as acute myeloid leukemia [10], chronic myeloid leukemia [11] and myeloproliferative disorders [12]. Tsai et al [13] reported that the pre-B cell line of acute lymphocytic leukemia produces PDGF-A and its receptor in lymphoid malignancies, and they implied that PDGF may function as a lymphokine.…”

Section: Introductionmentioning

confidence: 99%

Autocrine Expression of Platelet-Derived Growth Factor B in B Cell Chronic Lymphocytic Leukemia

Hsu²,

Phyliky³

et al. 2005

Acta Haematol

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Platelet-derived growth factor (PDGF) regulates clonal proliferation of malignant pre-B cell lines, but little is known about its role in normal B lymphocyte differentiation and malignant transformation. To understand the expression of PDGF-A, PDGF-B and the β-receptor (PDGF-Rβ) in B cell lymphoproliferative disorders, we used an immunohistochemical method to stain formalin-fixed, paraffin-embedded tissues in 5 patients with reactive lymphoid hyperplasia, 15 with non-Hodgkin’s lymphoma and 23 with B cell chronic lymphocytic leukemia (B-CLL). Abundant PDGF-A, rather than PDGF-B, was expressed in normal B cell differentiation. There was no difference in the expression of PDGF-A and PDGF-B between patients with reactive lymphoid hyperplasia and patients with malignant lymphoproliferative disorders. Among the patients with B-CLL, the expression of PDGF-B was much stronger than the expression of PDGF-A, and 18 of the patients had coexpression of PDGF-B and PDGF-Rβ. A larger proportion of patients with B-CLL than with non-Hodgkin’s lymphoma had expression of PDGF-B and PDGF-Rβ. In conclusion, PDGF-A expression in all stages of B lymphocyte differentiation suggests that it is important in B cell differentiation and proliferation. Expression of PDGF-B and PDGF-Rβ suggests that autocrine signaling of PDGF may be important in malignant transformation of B-CLL. However, further studies are necessary to confirm these conclusions.

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The role of platelet-derived growth factor on human pluripotent progenitor (CFU-GEMM) growth in vitro

Cited by 19 publications

References 18 publications

Basis of hematopoietic defects in platelet-derived growth factor (PDGF)-B and PDGF β-receptor null mice

Basis of hematopoietic defects in platelet-derived growth factor (PDGF)-B and PDGF β-receptor null mice

Platelet‐derived growth factor (PDGF) in human acute myelogenous leukemia: PDGF receptor expression, endogenous PDGF release and responsiveness to exogenous PDGF isoforms by in vitro cultured acute myelogenous leukemia blasts

Autocrine Expression of Platelet-Derived Growth Factor B in B Cell Chronic Lymphocytic Leukemia

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