Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
8
|
pubmed:dateCreated |
1989-5-22
|
pubmed:abstractText |
Neurotensin, at less than or equal to 10(-9) M, in the presence of an optimal concentration of macrophage CSF (CSF-1), stimulated a dose-dependent enhancement of colony formation by murine marrow-derived mononuclear phagocyte progenitor cells. The additional colonies arose from the cell cycle and Ia Ag-positive subpopulation previously identified as two-signal-dependent progenitors. Two-signal colony formation diminished when the peptide was added at concentrations greater than 10(-9) M. Neurotensin binds specifically to two distinct receptors, a high affinity receptor (KD approximately 10(-9) M) and a lower affinity (KD approximately 10(-7) M) receptor identified as the tuftsin receptor. Rat liver ferritin and an inhibitory tuftsin analog. (ALA1)-tuftsin, which inhibit two-signal colony formation stimulated by tuftsin and tuftsin-like peptides in combination with CSF-1, did not inhibit colony formation stimulated by CSF-1 and 10(-9) M neurotensin. Both inhibitors, however, reversed the loss of two-signal colony growth in the presence of higher neurotensin concentrations. Neurotensin fragment 1-6, unlike ferritin and (ALA1)-tuftsin, inhibited two-signal colony formation stimulated by 10(-9) M neurotensin. However, like ferritin and (ALA1)-tuftsin, fragment 1-6 permitted full expression of two-signal colony formation in the presence of CSF-1 and 10(-7) M neurotensin. The data indicated that occupancy of both receptors at neurotensin concentrations greater than 10(-9) M might be responsible for the diminished progenitor response. The data further support a potential role for neurotensin as an inflammatory mediator. In addition to direct effects on mature phagocytic leukocytes, neurotensin, at least in vitro can influence the production of new mononuclear phagocytes.
|
pubmed:grant | |
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
AIM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Colony-Stimulating Factors,
http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides,
http://linkedlifedata.com/resource/pubmed/chemical/Neurotensin,
http://linkedlifedata.com/resource/pubmed/chemical/Peptide Fragments,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Immunologic,
http://linkedlifedata.com/resource/pubmed/chemical/Tuftsin,
http://linkedlifedata.com/resource/pubmed/chemical/tuftsin receptor
|
pubmed:status |
MEDLINE
|
pubmed:month |
Apr
|
pubmed:issn |
0022-1767
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:day |
15
|
pubmed:volume |
142
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
2689-94
|
pubmed:dateRevised |
2007-11-14
|
pubmed:meshHeading |
pubmed-meshheading:2784814-Animals,
pubmed-meshheading:2784814-Colony-Stimulating Factors,
pubmed-meshheading:2784814-Dose-Response Relationship, Drug,
pubmed-meshheading:2784814-Female,
pubmed-meshheading:2784814-Hematopoiesis,
pubmed-meshheading:2784814-Hematopoietic Stem Cells,
pubmed-meshheading:2784814-Lipopolysaccharides,
pubmed-meshheading:2784814-Mice,
pubmed-meshheading:2784814-Mice, Inbred C3H,
pubmed-meshheading:2784814-Neurotensin,
pubmed-meshheading:2784814-Peptide Fragments,
pubmed-meshheading:2784814-Phagocytes,
pubmed-meshheading:2784814-Receptors, Immunologic,
pubmed-meshheading:2784814-Tuftsin
|
pubmed:year |
1989
|
pubmed:articleTitle |
Neurotensin regulation of macrophage colony-stimulating factor-stimulated in vitro myelopoiesis.
|
pubmed:affiliation |
Department of Microbiology, University of Tennessee, Knoxville 37996-0845.
|
pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|