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Article: Regulation of cell survival during B lymphopoiesis in mouse bone marrow: Enhanced pre-B-cell apoptosis in CSF-1-deficient op/op mutant mice

TitleRegulation of cell survival during B lymphopoiesis in mouse bone marrow: Enhanced pre-B-cell apoptosis in CSF-1-deficient op/op mutant mice
Authors
Issue Date2001
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/exphem
Citation
Experimental Hematology, 2001, v. 29 n. 5, p. 596-601 How to Cite?
AbstractObjective. Osteopetrotic (op/op) mice are deficient in macrophages and osteoclasts due to a CSF-1 gene mutation. The aim of this study was to evaluate the effect of these deficiencies and of CSF-1-dependent mechanisms on B lymphopoiesis in bone marrow, with special reference to the apoptotic activity of precursor B cells. Materials and Methods. B-cell development and apoptosis were examined in the bone marrow of op/op mice using immunofluorescence labeling and flow cytometry. Short-term cultures of bone marrow were used to evaluate the effect of recombinant CSF-1 on the rate of B-cell apoptosis. Results. Bone marrow cellularity was greatly reduced in op/op mice compared with normal littermates. However, precursor B cells were disproportionately decreased, most markedly at the pre-B-cell stage. Precursor B cells, particularly pre-B cells, displayed elevated apoptotic incidences both ex vivo and in short-term culture. Addition of recombinant CSF-1 reduced the incidence of apoptosis among precursor B cells in short-term cultures of whole bone marrow suspensions from normal mice but not in cultures of sorted B220+ B-lineage cells. Conclusions. The finding of increased pre-B-cell apoptosis in op/op mice provides evidence that CSF-1-dependent mechanisms can strongly influence the survival of precursor B cells in mouse bone marrow, particularly at the pro-B/pre-B cell transition. It is proposed that the local or systemic levels of CSF-1 during ontogeny may thus play a role in regulating B-cell production within the bone marrow microenvironment. © 2001 International Society for Experimental Hematology.
Persistent Identifierhttp://hdl.handle.net/10722/88701
ISSN
2015 Impact Factor: 2.303
2015 SCImago Journal Rankings: 1.341
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLu, Len_HK
dc.contributor.authorOsmond, DGen_HK
dc.date.accessioned2010-09-06T09:46:50Z-
dc.date.available2010-09-06T09:46:50Z-
dc.date.issued2001en_HK
dc.identifier.citationExperimental Hematology, 2001, v. 29 n. 5, p. 596-601en_HK
dc.identifier.issn0301-472Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/88701-
dc.description.abstractObjective. Osteopetrotic (op/op) mice are deficient in macrophages and osteoclasts due to a CSF-1 gene mutation. The aim of this study was to evaluate the effect of these deficiencies and of CSF-1-dependent mechanisms on B lymphopoiesis in bone marrow, with special reference to the apoptotic activity of precursor B cells. Materials and Methods. B-cell development and apoptosis were examined in the bone marrow of op/op mice using immunofluorescence labeling and flow cytometry. Short-term cultures of bone marrow were used to evaluate the effect of recombinant CSF-1 on the rate of B-cell apoptosis. Results. Bone marrow cellularity was greatly reduced in op/op mice compared with normal littermates. However, precursor B cells were disproportionately decreased, most markedly at the pre-B-cell stage. Precursor B cells, particularly pre-B cells, displayed elevated apoptotic incidences both ex vivo and in short-term culture. Addition of recombinant CSF-1 reduced the incidence of apoptosis among precursor B cells in short-term cultures of whole bone marrow suspensions from normal mice but not in cultures of sorted B220+ B-lineage cells. Conclusions. The finding of increased pre-B-cell apoptosis in op/op mice provides evidence that CSF-1-dependent mechanisms can strongly influence the survival of precursor B cells in mouse bone marrow, particularly at the pro-B/pre-B cell transition. It is proposed that the local or systemic levels of CSF-1 during ontogeny may thus play a role in regulating B-cell production within the bone marrow microenvironment. © 2001 International Society for Experimental Hematology.en_HK
dc.languageengen_HK
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/exphemen_HK
dc.relation.ispartofExperimental Hematologyen_HK
dc.rightsExperimental Hematology. Copyright © Elsevier Inc.en_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshApoptosis - drug effectsen_HK
dc.subject.meshB-Lymphocytes - pathologyen_HK
dc.subject.meshBone Marrow - pathologyen_HK
dc.subject.meshCell Lineageen_HK
dc.subject.meshCells, Cultured - drug effectsen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshHematopoiesisen_HK
dc.subject.meshHematopoietic Stem Cells - drug effects - pathologyen_HK
dc.subject.meshMacrophage Colony-Stimulating Factor - deficiency - genetics - pharmacologyen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Mutant Strainsen_HK
dc.subject.meshOsteopetrosis - pathologyen_HK
dc.subject.meshReceptor, Macrophage Colony-Stimulating Factor - analysisen_HK
dc.subject.meshRecombinant Proteins - pharmacologyen_HK
dc.titleRegulation of cell survival during B lymphopoiesis in mouse bone marrow: Enhanced pre-B-cell apoptosis in CSF-1-deficient op/op mutant miceen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0301-472X&volume=29&spage=596&epage=601&date=2001&atitle=Regulation+of+cell+survival+during+B+lymphopoiesis+in+mouse+bone+marrow:+enhanced+pre-B-cell+apoptosis+in+CSF-1-deficient+op/op+mutant+miceen_HK
dc.identifier.emailLu, L:liweilu@hkucc.hku.hken_HK
dc.identifier.authorityLu, L=rp00477en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/S0301-472X(01)00621-Xen_HK
dc.identifier.pmid11376872-
dc.identifier.scopuseid_2-s2.0-0035006699en_HK
dc.identifier.hkuros59748en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0035006699&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume29en_HK
dc.identifier.issue5en_HK
dc.identifier.spage596en_HK
dc.identifier.epage601en_HK
dc.identifier.isiWOS:000168760100007-
dc.publisher.placeUnited Statesen_HK

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