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Article: Regulation of cell survival during B lymphopoiesis: Apoptosis and Bcl- 2/Bax content of precursor B cells in bone marrow of mice with altered expression of IL-7 and recombinase-activating gene-2

TitleRegulation of cell survival during B lymphopoiesis: Apoptosis and Bcl- 2/Bax content of precursor B cells in bone marrow of mice with altered expression of IL-7 and recombinase-activating gene-2
Authors
Issue Date1999
PublisherAmerican Association of Immunologists. The Journal's web site is located at http://www.jimmunol.org
Citation
Journal Of Immunology, 1999, v. 162 n. 4, p. 1931-1940 How to Cite?
AbstractB cell development in mouse bone marrow depends critically upon IL-7. To examine the possible in vivo trophic role of IL-7, we have quantitated apoptosis and Bcl-2 family proteins in populations of phenotypically defined B lineage cells in IL-7-deficient and IL-7-overexpressing mice. Using immunofluorescence labeling, multiparameter flow cytometry, and a short-term culture assay, we show that the apoptotic rates of precursor B cells, but not of more mature B cells, are enhanced by IL-7 gene deletion, associated with increased intracellular content of Bax and decreased Bcl-2, while, conversely, an IL-7 transgene suppresses precursor B cell apoptosis and produces low Bax and high Bcl-2 levels. During normal B cell development, high Bax/Bcl-2 ratios characterize cells undergoing greatest apoptotic cell death. Pro-B cells in RAG-2(-/-) mice, all destined to abort, show elevated Bax levels and Bax/Bcl-2 ratios. By comparison with the elevated rate of pro- B cell apoptosis in RAG-2(-/-) mice, provisional estimates have been made for the fraction of pro-B cells undergoing apoptosis in normal mice (70%), IL- 7(-/-) mice (85%), and IL-7 transgenic mice (35%). The results demonstrate that IL-7 strongly promotes in vivo cell survival and maintains antiapoptotic Bcl-2/Bax ratios during the development of precursor B cells in mouse bone marrow.
Persistent Identifierhttp://hdl.handle.net/10722/148179
ISSN
2015 Impact Factor: 4.985
2015 SCImago Journal Rankings: 3.549
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLu, Len_US
dc.contributor.authorChaudhury, Pen_US
dc.contributor.authorOsmond, DGen_US
dc.date.accessioned2012-05-29T06:11:17Z-
dc.date.available2012-05-29T06:11:17Z-
dc.date.issued1999en_US
dc.identifier.citationJournal Of Immunology, 1999, v. 162 n. 4, p. 1931-1940en_US
dc.identifier.issn0022-1767en_US
dc.identifier.urihttp://hdl.handle.net/10722/148179-
dc.description.abstractB cell development in mouse bone marrow depends critically upon IL-7. To examine the possible in vivo trophic role of IL-7, we have quantitated apoptosis and Bcl-2 family proteins in populations of phenotypically defined B lineage cells in IL-7-deficient and IL-7-overexpressing mice. Using immunofluorescence labeling, multiparameter flow cytometry, and a short-term culture assay, we show that the apoptotic rates of precursor B cells, but not of more mature B cells, are enhanced by IL-7 gene deletion, associated with increased intracellular content of Bax and decreased Bcl-2, while, conversely, an IL-7 transgene suppresses precursor B cell apoptosis and produces low Bax and high Bcl-2 levels. During normal B cell development, high Bax/Bcl-2 ratios characterize cells undergoing greatest apoptotic cell death. Pro-B cells in RAG-2(-/-) mice, all destined to abort, show elevated Bax levels and Bax/Bcl-2 ratios. By comparison with the elevated rate of pro- B cell apoptosis in RAG-2(-/-) mice, provisional estimates have been made for the fraction of pro-B cells undergoing apoptosis in normal mice (70%), IL- 7(-/-) mice (85%), and IL-7 transgenic mice (35%). The results demonstrate that IL-7 strongly promotes in vivo cell survival and maintains antiapoptotic Bcl-2/Bax ratios during the development of precursor B cells in mouse bone marrow.en_US
dc.languageengen_US
dc.publisherAmerican Association of Immunologists. The Journal's web site is located at http://www.jimmunol.orgen_US
dc.relation.ispartofJournal of Immunologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshApoptosis - Genetics - Immunologyen_US
dc.subject.meshB-Lymphocytes - Cytology - Metabolismen_US
dc.subject.meshBone Marrow Cells - Cytology - Metabolismen_US
dc.subject.meshCell Survival - Genetics - Immunologyen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshDna-Binding Proteins - Biosynthesis - Geneticsen_US
dc.subject.meshHematopoiesis - Genetics - Immunologyen_US
dc.subject.meshHematopoietic Stem Cells - Cytology - Metabolismen_US
dc.subject.meshInterleukin-7 - Biosynthesis - Deficiency - Geneticsen_US
dc.subject.meshMaleen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Inbred C3hen_US
dc.subject.meshMice, Inbred Dbaen_US
dc.subject.meshMice, Knockouten_US
dc.subject.meshMice, Transgenicen_US
dc.subject.meshProto-Oncogene Proteins - Biosynthesis - Metabolismen_US
dc.subject.meshProto-Oncogene Proteins C-Bcl-2 - Biosynthesis - Metabolismen_US
dc.subject.meshTransposases - Geneticsen_US
dc.subject.meshBcl-2-Associated X Proteinen_US
dc.titleRegulation of cell survival during B lymphopoiesis: Apoptosis and Bcl- 2/Bax content of precursor B cells in bone marrow of mice with altered expression of IL-7 and recombinase-activating gene-2en_US
dc.typeArticleen_US
dc.identifier.emailLu, L:liweilu@hkucc.hku.hken_US
dc.identifier.authorityLu, L=rp00477en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid9973461en_US
dc.identifier.scopuseid_2-s2.0-0033557693en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0033557693&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume162en_US
dc.identifier.issue4en_US
dc.identifier.spage1931en_US
dc.identifier.epage1940en_US
dc.identifier.isiWOS:000078510800009-
dc.publisher.placeUnited Statesen_US

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