Growth factor-dependent inhibition of normal hematopoiesis by N-ras antisense oligodeoxynucleotides.
Open accessAbstract
To determine whether N-ras expression is required at specific stages of the process of in vitro normal human hematopoiesis, adherent- and T lymphocyte-depleted mononuclear marrow cells (A-T-MNC) or highly purified progenitors (CD34+ cells) were cultured in semisolid medium, under conditions that favor the growth of specific progenitor cell types, after exposure to N-ras sense and antisense oligodeoxynucleotides. N-ras antisense, but not sense, oligodeoxynucleotide treatment of A-T-MNC and CD34+ cells resulted in a significantly decreased number of granulocyte/macrophage colony-forming units (CFU-GM) induced by interleukin 3 (IL-3) or granulocyte/macrophage colony-stimulating factor (GM-CSF) and of macrophage colonies (CFU-M) induced by M-CSF, but not of granulocytic colonies induced with G-CSF or IL-5. However, the same treatment significantly inhibited colony formation induced by each of the above factors in combination with IL-3. Megakaryocytic colony (CFU-Meg) formation from A-T-MNC or CD34+ cells in the presence of IL-6 + IL-3 + erythropoietin (Epo) was also markedly decreased after antisense oligodeoxynucleotide treatment. Erythroid colonies derived from A-T-MNC in the presence of Epo (CFU-E) were not inhibited upon antisense treatment, whereas those arising from A-T-MNC or CD34+ cells in the presence of IL-3 + Epo (BFU-E) were markedly affected. These results are consistent with the hypothesis that distinct signal transduction pathways, involving N-ras or not, are activated by different growth factors in different hematopoietic progenitor cells.
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Ras signal transduction plays an important role in myeloid differentiation.
“Ras signal transduction has been demonstrated to play an important role in myeloid differentiation (47)(48)(49)(50)”
From c-Jun Is a JNK-independent Coactivator of the PU.1 Transcription Factor (1999) · cites this paper as [50]
The discussion (pp. 747–748) links N-ras to growth-factor-dependent signaling and reports that it is required for the growth of some myeloid progenitors. It describes a role in coordinating proliferation and differentiation as likely, but the reported experiments measure colony growth rather than directly demonstrating a role in myeloid differentiation. (LLM, conf=0.84)
Experimental — accuracy not yet measuredM-CSF, granulocyte-macrophage colony-stimulating factor, or interleukin-3-induced monocytopoiesis of CD34+ cells is inhibited by N-Ras antisense oligonucleotides.
“In addition, M-CSF, granulocyte-macrophage colony-stimulating factor, or interleukin-3-induced monocytopoiesis of CD34ϩ cells is inhibited by N-Ras antisense oligonucleotides (50).”
From c-Jun Is a JNK-independent Coactivator of the PU.1 Transcription Factor (1999) · cites this paper as [50]
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- Authors
- Skorski, T., Szczylik, C., Ratajczak, M. Z., Malaguarnera, L., Gewirtz, A. M., & Calabretta, B.
- Affiliations
- Jefferson Cancer Institute, Thomas Jefferson University, Philadelphia, Pennsylvania 19107.
- Thomas Jefferson University (US)
- Venue
- The Journal of experimental medicine
- Publisher
- Rockefeller University Press
- Published
- 1992-03-01
- Volume
- 175
- Issue
- 3
- Pages
- 743-750
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- PMC
- PMC2119161
- OpenAlex
- W2106064881
- Cited by
- 52
- References
- 36
- Citations by year
- 2015: 1
- FWCI
- 4.73
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- cc-by-nc-sa
- Locations
- The Journal of Experimental Medicine (publishedVersion)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- IRIS UNIMORE (University of Modena and Reggio Emilia) (submittedVersion, cc-by)
- Funders
- National Institutes of Health (5r01ca046782-11)
- National Cancer Institute (CA36896, CA46782)
- Topics
- Health Sciences › Medicine › Hematology › Hematopoietic Stem Cell Transplantation
- Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Keywords
- NRAS, antisense oligodeoxynucleotides, hematopoiesis, hematopoietic progenitor cells, CD34+ cells, CFU-GM, CFU-M, CFU-Meg, CFU-E, BFU-E, interleukin-3, GM-CSF, macrophage colony-stimulating factor, erythropoietin, interleukin-6, signal transduction, megakaryopoiesis, erythroid colony formation
- MeSH terms
- Base Sequence, Bone Marrow, Bone Marrow Cells, Depression, Chemical, Growth Substances, Hematopoiesis, Humans, Megakaryocytes, Molecular Sequence Data, Genes, ras, RNA, Messenger, Stem Cells, Transcription, Genetic, Erythroid Precursor Cells, Antigens, CD, Granulocyte-Macrophage Colony-Stimulating Factor, Oligonucleotides, Antisense, Antigens, CD34
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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