Linked Life Data

18245480

Source:http://linkedlifedata.com/resource/pubmed/id/18245480

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2008-2-4
pubmed:abstractText
B-cell precursor acute lymphoblastic leukemia (BCP-ALL/B-precursor ALL) is characterized by a high rate of tissue infiltration. The mechanism of BCP-ALL cell extravasation is not fully understood. In the present study, we have investigated the major carrier of carbohydrate selectin ligands in the BCP-ALL cell line NALL-1 and its possible role in the extravascular infiltration of the leukemic cells. B-precursor ALL cell lines and clinical samples from patients with BCP-ALL essentially exhibited positive flow cytometric reactivity with E-selectin, and the reactivity was significantly diminished by O-sialoglycoprotein endopeptidase treatment in NALL-1 cells. B-precursor ALL cell lines adhered well to E-selectin but only very weakly to P-selectin with low-shear-force cell adhesion assay. Although BCP-ALL cell lines did not express the well-known core protein P-selectin glycoprotein ligand-1 (PSGL-1), a major proportion of the carbohydrate selectin ligand was carried by a sialomucin, CD43, in NALL-1 cells. Most clinical samples from patients with BCP-ALL exhibited a PSGL-1(neg/low)/CD43(high) phenotype. NALL-1 cells rolled well on E-selectin, but knockdown of CD43 on NALL-1 cells resulted in reduced rolling activity on E-selectin. In addition, the CD43 knockdown NALL-1 cells showed decreased tissue engraftment compared with the control cells when introduced into gamma-irradiated immunodeficient mice. These results strongly suggest that CD43 but not PSGL-1 plays an important role in the extravascular infiltration of NALL-1 cells and that the degree of tissue engraftment of B-precursor ALL cells may be controlled by manipulating CD43 expression.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1538-7445
pubmed:author
pubmed:issnType
Electronic
pubmed:day
1
pubmed:volume
68
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
790-9
pubmed:dateRevised
2011-9-7
pubmed:meshHeading
pubmed-meshheading:18245480-Animals, pubmed-meshheading:18245480-Antigens, CD43, pubmed-meshheading:18245480-CHO Cells, pubmed-meshheading:18245480-Cell Adhesion, pubmed-meshheading:18245480-Cell Line, Tumor, pubmed-meshheading:18245480-Cell Movement, pubmed-meshheading:18245480-Cricetinae, pubmed-meshheading:18245480-Cricetulus, pubmed-meshheading:18245480-Down-Regulation, pubmed-meshheading:18245480-E-Selectin, pubmed-meshheading:18245480-HL-60 Cells, pubmed-meshheading:18245480-Humans, pubmed-meshheading:18245480-Membrane Glycoproteins, pubmed-meshheading:18245480-Mice, pubmed-meshheading:18245480-Mice, Inbred NOD, pubmed-meshheading:18245480-Mice, SCID, pubmed-meshheading:18245480-P-Selectin, pubmed-meshheading:18245480-Precursor B-Cell Lymphoblastic Leukemia-Lymphoma, pubmed-meshheading:18245480-RNA, Small Interfering, pubmed-meshheading:18245480-Sialomucins, pubmed-meshheading:18245480-Transfection
pubmed:year
2008
pubmed:articleTitle
CD43, but not P-selectin glycoprotein ligand-1, functions as an E-selectin counter-receptor in human pre-B-cell leukemia NALL-1.
pubmed:affiliation
Cell Regulation Analysis Team, Research Center for Medical Glycoscience, National Institute of Advanced Industrial Science and Technology, Tsukuba, Japan
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't