pubmed-article:1384785 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:1384785 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
pubmed-article:1384785 | lifeskim:mentions | umls-concept:C0600251 | lld:lifeskim |
pubmed-article:1384785 | lifeskim:mentions | umls-concept:C0018951 | lld:lifeskim |
pubmed-article:1384785 | lifeskim:mentions | umls-concept:C0080095 | lld:lifeskim |
pubmed-article:1384785 | lifeskim:mentions | umls-concept:C1280500 | lld:lifeskim |
pubmed-article:1384785 | lifeskim:mentions | umls-concept:C1709059 | lld:lifeskim |
pubmed-article:1384785 | lifeskim:mentions | umls-concept:C1515655 | lld:lifeskim |
pubmed-article:1384785 | pubmed:issue | 10 | lld:pubmed |
pubmed-article:1384785 | pubmed:dateCreated | 1992-12-22 | lld:pubmed |
pubmed-article:1384785 | pubmed:abstractText | To determine the mechanism(s) by which interleukin-1 (IL-1) promotes granulopoiesis in vivo, we examined the effect of in vivo administration of IL-1 alpha on colony-stimulating factor (CSF) receptor expression on bone marrow cells (BMCs) and whether this directly correlated with progenitor cell responsiveness. Administration of IL-1 alpha to mice induced the upregulation of both granulocyte-macrophage-CSF (GM-CSF) and IL-3 receptors, which reached a maximum 24 hours after IL-1 alpha injection on unfractionated BMCs. This upregulation was more pronounced on the progenitor-enriched cell population (lineage-negative [Lin(-)]). The enhanced GM-CSF and IL-3 receptor expression directly correlated with enhanced IL-3- or GM-CSF-induced growth of colony-forming unit-culture (CFU-c) or CFU-mixture (CFU-Mix; colonies containing macrophages, granulocytes, and erythroid cells). In addition, the absolute number of high proliferative potential-colony-forming cells (HPP-CFC) was increased fivefold. In contrast, granulocyte-CSF (G-CSF)-specific binding on unfractionated BMCs was rapidly (4 hours) reduced after IL-1 alpha administration and returned to control levels by 24 hours. This reduction correlated with IL-1 alpha-induced margination of mature granulocytes (RBC-8C5hi cells), which express high levels of G-CSF receptors. IL-1 alpha treatment did not affect G-CSF receptor expression on Lin- cells. Pretreatment of mice with anti-type I IL-1 receptor antibody blocked the IL-1 alpha-induced upregulation of GM-CSF and IL-3 receptor expression on BMCs. Taken together, as one possible mechanism, IL-1 alpha in vivo may stimulate the expression of functional GM-CSF and IL-3 receptors on BMCs indirectly, and, in concert with the induction of circulating CSF levels, may account for the ability of IL-1 alpha to stimulate hematopoiesis in vivo. | lld:pubmed |
pubmed-article:1384785 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1384785 | pubmed:language | eng | lld:pubmed |
pubmed-article:1384785 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1384785 | pubmed:citationSubset | AIM | lld:pubmed |
pubmed-article:1384785 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1384785 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1384785 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1384785 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1384785 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1384785 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1384785 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:1384785 | pubmed:month | Nov | lld:pubmed |
pubmed-article:1384785 | pubmed:issn | 0006-4971 | lld:pubmed |
pubmed-article:1384785 | pubmed:author | pubmed-author:LongoD LDL | lld:pubmed |
pubmed-article:1384785 | pubmed:author | pubmed-author:OppenheimJ... | lld:pubmed |
pubmed-article:1384785 | pubmed:author | pubmed-author:RuscettiF WFW | lld:pubmed |
pubmed-article:1384785 | pubmed:author | pubmed-author:KellerJ RJR | lld:pubmed |
pubmed-article:1384785 | pubmed:author | pubmed-author:JacobsenS ESE | lld:pubmed |
pubmed-article:1384785 | pubmed:author | pubmed-author:DuboisC MCM | lld:pubmed |
pubmed-article:1384785 | pubmed:author | pubmed-author:ChizzoniteRR | lld:pubmed |
pubmed-article:1384785 | pubmed:author | pubmed-author:HestdalKK | lld:pubmed |
pubmed-article:1384785 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:1384785 | pubmed:day | 15 | lld:pubmed |
pubmed-article:1384785 | pubmed:volume | 80 | lld:pubmed |
pubmed-article:1384785 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:1384785 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:1384785 | pubmed:pagination | 2486-94 | lld:pubmed |
pubmed-article:1384785 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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pubmed-article:1384785 | pubmed:year | 1992 | lld:pubmed |
pubmed-article:1384785 | pubmed:articleTitle | In vivo effect of interleukin-1 alpha on hematopoiesis: role of colony-stimulating factor receptor modulation. | lld:pubmed |
pubmed-article:1384785 | pubmed:affiliation | Biological Response Modifiers, Program Resources, Inc/DynCorp, Inc, National Cancer Institute, Frederick Cancer Research and Development Center, MD 21702-1201. | lld:pubmed |
pubmed-article:1384785 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:1384785 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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