Fibronectin promotes the phorbol 12-myristate 13-acetate-induced macrophage differentiation in myeloid leukemia cells

Esendağlı, Güneş; Canpınar, Hande; Yılmaz, Güldal; Kaymaz, Fevziye Figen; Kansu, Emin; Güç, Dicle

doi:10.1007/s12185-008-0243-8

Cited by 5 publications

(4 citation statements)

References 16 publications

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“…Surprisingly, fewer Mk‐p of the myeloid phenotype were observed with TPO or ARP in the presence of FN than in the absence of FN, indicating that accelerated maturation of the CD33 + subpopulation may be facilitated by FN with either TPO or ARP (Grisaru et al , 2001, 2006). Facilitation of myeloid cell maturation by FN has been recently reported (Esendagli et al , 2009). Additionally, different adhesive properties may regulate the proliferation of these cells in the BM.…”

Section: Discussionmentioning

confidence: 96%

Mimicking the haematopoietic niche microenvironment provides a novel strategy for expansion of haematopoietic and megakaryocyte‐progenitor cells from cord blood

et al. 2010

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SummarySevere neutropenia and protracted thrombocytopenia remain serious clinical problems following cord blood transplantation (CBT) due to the paucity of stem and progenitor cells in the grafts. Administration of ex-vivo expanded megakaryocyte progenitor cells may facilitate platelet production. We propose a novel strategy to expand these rare cells ex-vivo, from a small portion of the cord blood (CB) unit, using fibronectin (FN), a major component of hematopoietic niches, combined with cytokines, including thrombopoietin and the hematopoietic stress-associated acetylcholinesterase readthrough peptide (ARP). Application of multiple gates and high definition flow cytometry enabled clear resolution of expanded hematopoietic stem/ precursor cells (HSPC) and megakaryocyte progenitors (Mk-p) and their early subsets while eliminating positively stained non-relevant cells. FN increased viability, expansion of all CD34 + HSPC populations and Mk-p. The combination of FN + thrombopoietin + ARP maintained and expanded very early myeloid and thrombopoietic precursors, increased the proliferation of megakaryocyte, granulocyte-macrophage and multilineage colony-forming progenitors and supported Mk maturation as measured by ploidy and glycoprotein IIb/IIIa expression by quantiative reverse transcription polymerase chain reaction. This approach, which involves expanding HSPC and Mk precursors from a small portion of the CB unit, without sacrificing the coveted stem cells, may lead to improved cell therapy modalities to facilitate earlier myelopoiesis and platelet production post-CBT.

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Section: Discussionmentioning

confidence: 96%

Mimicking the haematopoietic niche microenvironment provides a novel strategy for expansion of haematopoietic and megakaryocyte‐progenitor cells from cord blood

et al. 2010

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“…To investigate whether its presence depends on the proliferative/differentiation status of the cells, CCRF‐CEM were treated by the differentiation agent PMA. PMA is known to activate transcription factors implicated in the differentiation of many leukemic cells via Mitogen‐activated protein (MAP) kinases . Additionally, PMA was previously found to reduce both the growth rate of CCRF‐CEM and the expression of c‐Myc , a pro‐proliferative protein .…”

Section: Resultsmentioning

confidence: 99%

The more basic isoform of eEF1A relates to tumour cell phenotype and is modulated by hyper‐proliferative/differentiating stimuli in normal lymphocytes and CCRF‐CEM T‐lymphoblasts

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et al. 2012

Hematological Oncology

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The elongation factor 1A proteins (eEF1A1/A2) are known to play a role in tumours. We previously found that a more basic isoform of eEF1A (MBI-eEF1A) is present in the cytoskeletal/nuclear-enriched extracts of CCRF-CEM T-lymphoblasts but not in those of normal lymphocytes. To obtain deeper knowledge about MBI-eEF1A biology, we investigate from which of the eEF1A proteins, eEF1A1 or eEF1A2, MBI-eEF1A originates and the possibility that its appearance can be modulated by the differentiated or proliferative cell status. CCRF-CEM T-lymphoblasts and normal lymphocytes were cultured with or without differentiation/pro-proliferative stimuli (Phorbol 12-Myristate 13-Acetate (PMA) alone or the combination of phytohaemagglutinin (PHA) with PMA, respectively), and the presence of MBI-eEF1A evaluated together with that of the eEF1A1/A2 mRNAs. Our data indicate that the MBI-eEF1A may derive from eEF1A1 as eEF1A2 is not expressed in CCRF-CEM and normal lymphocytes. Moreover, MBI-eEF1A is inducible in normal lymphocytes upon hyper-proliferative stimuli application; in CCRF-CEM, its presence can be abrogated by PMA-induced differentiation. Finally, MBI-eEF1A may have a functional role in hyper-proliferating/tumour cells as its disappearance reduces the growth of CCRF-CEM and that of PHA/PMA-stimulated lymphocytes. The presented data suggest that MBI-eEF1A may be related to oncogenic cell phenotype, rising the possibility to use MBI-eEF1A as target for novel therapeutic strategies.

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“…The hard-totransfect cell line HL-60 harboured increased amounts of plasmid DNA compared to its suspension counterparts. The increased ability for the uptake of cationic lipid DNA complexes may be influenced by the potential of HL-60 cells to differentiate into mature leukocytes with an increased ability for endocytosis (Collins 1987;Esendagli et al 2009). …”

Section: Discussionmentioning

confidence: 99%

Transfection of myeloid leukaemia cell lines is distinctively regulated by fibronectin substratum

et al. 2009

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Gene transfer into haematopoietic cells is a challenging approach. The extracellular matrix component fibronectin has been known to modulate the cell cycle dynamics, viability and differentiation of leukaemia cells. Thus, our aim was to investigate the influence of fibronectin substratum on the liposomal transfection of myeloid leukaemia cell lines. Liposomal transfection was performed with K562 and HL-60 as representative lines of transfectioncompetent and -incompetent myeloid leukaemia cells, respectively. Flow cytometry analyses were performed to determine transfection efficiency monitored by green fluorescent protein (GFP) expression and to assess cell viability and cell cycle status. Quantitation of GFP gene expression and DNA uptake was assayed by real time PCR. The current data showed that the adhesion to fibronectin deteriorated the transfection of K562 cells. In contrary, it enhanced the delivery of plasmid DNA into HL-60 cells. Correspondingly, the adhesion to fibronectin influenced the transfection efficiency mainly by modulating the intracellular presence of plasmid DNA. The cell cycle and viability which is regulated by fibronectin had a minor impact on the success of gene delivery. This phenomenon may be considered as an important factor which may modulate the potential gene transfer approaches for myeloid leukaemia.

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Fibronectin promotes the phorbol 12-myristate 13-acetate-induced macrophage differentiation in myeloid leukemia cells

Cited by 5 publications

References 16 publications

Mimicking the haematopoietic niche microenvironment provides a novel strategy for expansion of haematopoietic and megakaryocyte‐progenitor cells from cord blood

Mimicking the haematopoietic niche microenvironment provides a novel strategy for expansion of haematopoietic and megakaryocyte‐progenitor cells from cord blood

The more basic isoform of eEF1A relates to tumour cell phenotype and is modulated by hyper‐proliferative/differentiating stimuli in normal lymphocytes and CCRF‐CEM T‐lymphoblasts

Transfection of myeloid leukaemia cell lines is distinctively regulated by fibronectin substratum

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