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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
Title | 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 |
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Authors | |
Issue Date | 1999 |
Publisher | American 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? |
Abstract | B 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 Identifier | http://hdl.handle.net/10722/148179 |
ISSN | 2023 Impact Factor: 3.6 2023 SCImago Journal Rankings: 1.558 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Lu, L | en_US |
dc.contributor.author | Chaudhury, P | en_US |
dc.contributor.author | Osmond, DG | en_US |
dc.date.accessioned | 2012-05-29T06:11:17Z | - |
dc.date.available | 2012-05-29T06:11:17Z | - |
dc.date.issued | 1999 | en_US |
dc.identifier.citation | Journal Of Immunology, 1999, v. 162 n. 4, p. 1931-1940 | en_US |
dc.identifier.issn | 0022-1767 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/148179 | - |
dc.description.abstract | B 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.language | eng | en_US |
dc.publisher | American Association of Immunologists. The Journal's web site is located at http://www.jimmunol.org | en_US |
dc.relation.ispartof | Journal of Immunology | en_US |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Apoptosis - Genetics - Immunology | en_US |
dc.subject.mesh | B-Lymphocytes - Cytology - Metabolism | en_US |
dc.subject.mesh | Bone Marrow Cells - Cytology - Metabolism | en_US |
dc.subject.mesh | Cell Survival - Genetics - Immunology | en_US |
dc.subject.mesh | Cells, Cultured | en_US |
dc.subject.mesh | Dna-Binding Proteins - Biosynthesis - Genetics | en_US |
dc.subject.mesh | Hematopoiesis - Genetics - Immunology | en_US |
dc.subject.mesh | Hematopoietic Stem Cells - Cytology - Metabolism | en_US |
dc.subject.mesh | Interleukin-7 - Biosynthesis - Deficiency - Genetics | en_US |
dc.subject.mesh | Male | en_US |
dc.subject.mesh | Mice | en_US |
dc.subject.mesh | Mice, Inbred C3h | en_US |
dc.subject.mesh | Mice, Inbred Dba | en_US |
dc.subject.mesh | Mice, Knockout | en_US |
dc.subject.mesh | Mice, Transgenic | en_US |
dc.subject.mesh | Proto-Oncogene Proteins - Biosynthesis - Metabolism | en_US |
dc.subject.mesh | Proto-Oncogene Proteins C-Bcl-2 - Biosynthesis - Metabolism | en_US |
dc.subject.mesh | Transposases - Genetics | en_US |
dc.subject.mesh | Bcl-2-Associated X Protein | en_US |
dc.title | 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 | en_US |
dc.type | Article | en_US |
dc.identifier.email | Lu, L:liweilu@hkucc.hku.hk | en_US |
dc.identifier.authority | Lu, L=rp00477 | en_US |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.pmid | 9973461 | en_US |
dc.identifier.scopus | eid_2-s2.0-0033557693 | en_US |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-0033557693&selection=ref&src=s&origin=recordpage | en_US |
dc.identifier.volume | 162 | en_US |
dc.identifier.issue | 4 | en_US |
dc.identifier.spage | 1931 | en_US |
dc.identifier.epage | 1940 | en_US |
dc.identifier.isi | WOS:000078510800009 | - |
dc.publisher.place | United States | en_US |
dc.identifier.issnl | 0022-1767 | - |