Interleukin-3 supports growth of mouse pre-B-cell clones in vitro

Palacios, Ronald; Henson, Geoffrey; Steinmetz, Michael; McKearn, John P.

doi:10.1038/309126a0

Cited by 206 publications

(88 citation statements)

References 33 publications

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“…Although the precise role of IL-3 in the early stages of B lymphopoiesis is unknown, the growth factor was required to isolate clonal pro-B and pre-B cell lines (5,21,25,26), and the IL-3 gene is activated in some cases of human acute pro-B cell leukemia associated with the t(5;14) chromosomal translocation (27,28). The apparent leukemogenic effects of IL-3 activation in man strongly suggest that the cytokine mediates cell growth and survival in at least a subset of early B cell progenitors.…”

Section: Resultsmentioning

confidence: 99%

“…This process is greatly influenced by cytokines that act on lymphoid and hematopoietic precursors, including interleukin 3 (IL-3), which supports the in vitro proliferation of multipotent stem cells as well as many progenitor cells already committed to particular lineages (4). When IL-3-dependent cell lines are deprived of growth factor, they not only stop proliferating but undergo apoptosis as well, indicating that IL-3 promotes cell survival by suppression of programmed cell death (5)(6)(7). Thus, it is important to identify the key molecules through which IL-3-generated survival signals are transduced.…”

mentioning

confidence: 99%

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Pivotal role for the NFIL3/E4BP4 transcription factor in interleukin 3-mediated survival of pro-B lymphocytes

Ikushima

Inukai

Inaba

et al. 1997

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

131

142

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The E2A-HLF (hepatic leukemia factor) oncoprotein, generated in pro-B lymphocytes by fusion of the trans-activation domain of E2A to the basic region͞ leucine zipper (bZIP) domain of HLF, functions as an anti-apoptotic transcription factor in leukemic cell transformation. When introduced into interleukin 3 (IL-3)-dependent mouse pro-B lymphocytes, E2A-HLF prevents apoptosis induced by growth factor deprivation, suggesting that IL-3 mediates cell survival through activation of a transcription factor whose activity can be constitutively replaced by the chimeric oncoprotein. We considered four bZIP transcription factors as candidates for this putative IL-3-regulated factor, each of which binds avidly to the DNA consensus sequence recognized by E2A-HLF and is related to the Caenorhabditis elegans CES-2 (cell death specification protein) neuron-specific mediator of cell death. The expression and binding activity of the Nfil3 protein (also called E4bp4), but not of Hlf, Dbp, or Tef, was found to be regulated by IL-3 in mouse pro-B cell lines (Baf-3 and FL5.12). Northern blot analysis showed that Nfil3͞E4bp4 is regulated as a ''delayed-early'' IL-3-responsive gene, requiring de novo protein synthesis. In the absence of IL-3, enforced expression of the human NFIL3͞E4BP4 cDNA promoted the survival but not the growth of IL-3-dependent pro-B cells. Our results implicate NFIL3͞E4BP4 (nuclear factor regulated by IL-3͞adenovirus E4 promoter binding protein) in a distinct growth factor-regulated signaling pathway that is responsible for the survival of early B-cell progenitors, and whose alteration by E2A-HLF leads to childhood B lineage leukemia.

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Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

Pivotal role for the NFIL3/E4BP4 transcription factor in interleukin 3-mediated survival of pro-B lymphocytes

Ikushima

Inukai

Inaba

et al. 1997

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

131

142

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“…Ba/F3 is a murine pro B-cell line established from mouse fetal liver. 18 The cell line grows in suspension (Roswell Park Memorial Institute 1640 medium with 10% fetal bovine serum, 2 mM L-glutamine, MO] and is kept in a cell culture flask at 37°C in 5% carbon dioxide atmosphere. As for the THP-1 cells, they are human monocytic cells derived from a 1-year-old boy with acute monocytic leukemia.…”

Section: Materials and Methods Gd 2 O 3 Nanoparticlesmentioning

confidence: 99%

Gd2O3 nanoparticles in hematopoietic cells for MRI contrast enhancement

Hedlund

Ahrén²,

Gustafsson³

et al. 2011

IJN

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As the utility of magnetic resonance imaging (MRI) broadens, the importance of having specific and efficient contrast agents increases and in recent time there has been a huge development in the fields of molecular imaging and intracellular markers. Previous studies have shown that gadolinium oxide (Gd2O3) nanoparticles generate higher relaxivity than currently available Gd chelates: In addition, the Gd2O3 nanoparticles have promising properties for MRI cell tracking. The aim of the present work was to study cell labeling with Gd2O3 nanoparticles in hematopoietic cells and to improve techniques for monitoring hematopoietic stem cell migration by MRI. Particle uptake was studied in two cell lines: the hematopoietic progenitor cell line Ba/F3 and the monocytic cell line THP-1. Cells were incubated with Gd2O3 nanoparticles and it was investigated whether the transfection agent protamine sulfate increased the particle uptake. Treated cells were examined by electron microscopy and MRI, and analyzed for particle content by inductively coupled plasma sector field mass spectrometry. Results showed that particles were intracellular, however, sparsely in Ba/F3. The relaxation times were shortened with increasing particle concentration. Relaxivities, r1 and r2 at 1.5 T and 21°C, for Gd2O3 nanoparticles in different cell samples were 3.6–5.3 s-1 mM-1 and 9.6–17.2 s-1 mM-1, respectively. Protamine sulfate treatment increased the uptake in both Ba/F3 cells and THP-1 cells. However, the increased uptake did not increase the relaxation rate for THP-1 as for Ba/F3, probably due to aggregation and/or saturation effects. Viability of treated cells was not significantly decreased and thus, it was concluded that the use of Gd2O3 nanoparticles is suitable for this type of cell labeling by means of detecting and monitoring hematopoietic cells. In conclusion, Gd2O3 nanoparticles are a promising material to achieve positive intracellular MRI contrast; however, further particle development needs to be performed.

funding agencies|Swedish Research Council| 621-2007-3810 621-2009-5148 521-2009-3423 |VINNOVA| 2009-00194 |Center in Nanoscience and Technology at LiTH (CeNano)||

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“…This inhibitory effect of IL-3 was very surprising to us since stimulatory roles of IL-3 in B cell development have been reported. For example, several investigators have established IL-3-dependent B220 + pre-B cell lines [29,30] and pro-B cell lines [31][32][33]. It was recently reported that IL-3 can support the proliferation of B220 + c-kit + pre-B cells in the presence of stromal cells [34].…”

Section: Cytokine Regulation Of Lymphohematopoietic Progenitorsmentioning

confidence: 99%