Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
1991-1-29
pubmed:abstractText
Marrow stromal elements produce as yet uncharacterized soluble growth factors that can stimulate the proliferation of murine pre-B cells, although close contact between these two cell types appears to ensure a better pre-B cell response. We have now shown that freshly isolated normal pre-B cells (ie, the B220+, surface mu- fraction of adult mouse bone marrow) adhere to fibronectin (FN) via an RGD cell-attachment site, as shown in a serum-free adherence assay, and they lose this functional ability on differentiation in vivo into B cells (ie, the B220+, surface mu+ fraction). Similarly, cells from an immortalized but stromal cell-dependent and nontumorigenic murine pre-B cell line originally derived from a Whitlock-Witte culture were also found to adhere to fibronectin (FN) via an RGD cell-attachment site. Moreover, in the presence of anti-FN receptor antibodies, the ability of this immortalized pre-B cell line to proliferate when co-cultured with a supportive stromal cell line (M2-10B4 cells) was markedly reduced (down to 30% of control). This suggests that pre-B cell attachment to FN on stromal cells may be an important component of the mechanism by which stromal cells stimulate normal pre-B cell proliferation and one that is no longer operative to control their more differentiated progeny. Two differently transformed pre-B cell lines, both of which are autocrine, stromal-independent, tumorigenic in vivo, and partially or completely differentiation-arrested at a very early stage of pre-B cell development, did not bind to FN. In addition, anti-FN receptor antibodies were much less effective in diminishing the ability of these tumorigenic pre-B cells to respond to M2-10B4 cell stimulation, which could still be demonstrated when the tumorigenic pre-B cells were co-cultured with M2-10B4 cells at a sufficiently low cell density. Analysis of cell surface molecules immunoprecipitated from both the nontumorigenic and tumorigenic pre-B cell lines by an anti-FN receptor antibody showed an increase in very late antigen (VLA) alpha chain(s) in both tumorigenic pre-B cell lines and a decrease in the beta 1 chain in one. Interestingly, all of the pre-B cell lines expressed similar amounts of messenger RNA for the beta 1 chain of the FN receptor. These results suggest that alteration of FN receptor expression on pre-B cells may represent a mechanism contributing to the outgrowth of leukemic pre-B cells with an autocrine phenotype and capable of stromal cell-independent, autonomous growth.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0006-4971
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
76
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2311-20
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:2147863-Abelson murine leukemia virus, pubmed-meshheading:2147863-Animals, pubmed-meshheading:2147863-Antibodies, pubmed-meshheading:2147863-Bone Marrow Cells, pubmed-meshheading:2147863-Cell Adhesion, pubmed-meshheading:2147863-Cell Differentiation, pubmed-meshheading:2147863-Cell Division, pubmed-meshheading:2147863-Cell Line, pubmed-meshheading:2147863-Cell Transformation, Neoplastic, pubmed-meshheading:2147863-Cell Transformation, Viral, pubmed-meshheading:2147863-Fibronectins, pubmed-meshheading:2147863-Gene Expression, pubmed-meshheading:2147863-Hematopoietic Stem Cells, pubmed-meshheading:2147863-Mice, pubmed-meshheading:2147863-Mice, Inbred C3H, pubmed-meshheading:2147863-Mice, Inbred C57BL, pubmed-meshheading:2147863-Molecular Weight, pubmed-meshheading:2147863-Nucleic Acid Hybridization, pubmed-meshheading:2147863-RNA, Messenger, pubmed-meshheading:2147863-Receptors, Fibronectin, pubmed-meshheading:2147863-Receptors, Immunologic
pubmed:year
1990
pubmed:articleTitle
Transformation-associated alterations in interactions between pre-B cells and fibronectin.
pubmed:affiliation
Terry Fox Laboratory, British Columbia Cancer Agency, Vancouver, Canada.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't