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- Publisher Website: 10.1016/j.exphem.2006.10.014
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- PMID: 17309827
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Article: Hoxb3 deficiency impairs B lymphopoiesis in mouse bone marrow
Title | Hoxb3 deficiency impairs B lymphopoiesis in mouse bone marrow |
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Authors | |
Issue Date | 2007 |
Publisher | Elsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/exphem |
Citation | Experimental Hematology, 2007, v. 35 n. 3, p. 465-475 How to Cite? |
Abstract | Objective: Hox genes are involved in hematopoietic lineage commitment and differentiation. In this study, we investigated the roles of Hoxb3 in hematopoiesis by examining the phenotypes of a Hoxb3 knockout mutant mouse line. Results: Despite previous reports describing the apparently normal phenotype of these mutant mice, we found that by 6 months of age, Hoxb3 -/- mice began to exhibit significantly impaired B lymphopoiesis in the bone marrow (BM). The cellularity was reduced by 30% in mutant BM compared to age- and sex-matched heterozygous and wild-type controls. The population size of B220 +CD43 + progenitor B cells showed a twofold reduction while that of B220 +CD43 -IgM - precursor B cells was decreased fivefold. Sorting-purified Hoxb3 -/- progenitor B cells displayed significantly reduced proliferative response to IL-7 in culture, consistent with our findings of reduced IL-7 receptor expression in Hoxb3 -/- progenitor B cells. However, the peripheral B cell pool in the spleen of Hoxb3 -/- mice was maintained with a similar size as in wild-type littermates. Conclusion: Analysis of T-cell development in the thymus and B1 cell compartment in the peritoneal cavity showed no significant changes. Thus, our findings suggest that the Hoxb3 gene plays an essential role in regulating B lymphopoiesis in the BM of adult mice. © 2007 International Society for Experimental Hematology. |
Persistent Identifier | http://hdl.handle.net/10722/68230 |
ISSN | 2023 Impact Factor: 2.5 2023 SCImago Journal Rankings: 1.157 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
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dc.contributor.author | Ko, KH | en_HK |
dc.contributor.author | Kwan Lam, QL | en_HK |
dc.contributor.author | Zhang, M | en_HK |
dc.contributor.author | Yen Wong, CK | en_HK |
dc.contributor.author | Chun Lo, CK | en_HK |
dc.contributor.author | KahmeyerGabbe, M | en_HK |
dc.contributor.author | Tsang, WH | en_HK |
dc.contributor.author | Tsang, SL | en_HK |
dc.contributor.author | Chan, LC | en_HK |
dc.contributor.author | Sham, MH | en_HK |
dc.contributor.author | Lu, L | en_HK |
dc.date.accessioned | 2010-09-06T06:02:36Z | - |
dc.date.available | 2010-09-06T06:02:36Z | - |
dc.date.issued | 2007 | en_HK |
dc.identifier.citation | Experimental Hematology, 2007, v. 35 n. 3, p. 465-475 | en_HK |
dc.identifier.issn | 0301-472X | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/68230 | - |
dc.description.abstract | Objective: Hox genes are involved in hematopoietic lineage commitment and differentiation. In this study, we investigated the roles of Hoxb3 in hematopoiesis by examining the phenotypes of a Hoxb3 knockout mutant mouse line. Results: Despite previous reports describing the apparently normal phenotype of these mutant mice, we found that by 6 months of age, Hoxb3 -/- mice began to exhibit significantly impaired B lymphopoiesis in the bone marrow (BM). The cellularity was reduced by 30% in mutant BM compared to age- and sex-matched heterozygous and wild-type controls. The population size of B220 +CD43 + progenitor B cells showed a twofold reduction while that of B220 +CD43 -IgM - precursor B cells was decreased fivefold. Sorting-purified Hoxb3 -/- progenitor B cells displayed significantly reduced proliferative response to IL-7 in culture, consistent with our findings of reduced IL-7 receptor expression in Hoxb3 -/- progenitor B cells. However, the peripheral B cell pool in the spleen of Hoxb3 -/- mice was maintained with a similar size as in wild-type littermates. Conclusion: Analysis of T-cell development in the thymus and B1 cell compartment in the peritoneal cavity showed no significant changes. Thus, our findings suggest that the Hoxb3 gene plays an essential role in regulating B lymphopoiesis in the BM of adult mice. © 2007 International Society for Experimental Hematology. | en_HK |
dc.language | eng | en_HK |
dc.publisher | Elsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/exphem | en_HK |
dc.relation.ispartof | Experimental Hematology | en_HK |
dc.rights | Experimental Hematology. Copyright © Elsevier Inc. | en_HK |
dc.subject.mesh | Animals | en_HK |
dc.subject.mesh | Apoptosis - drug effects | en_HK |
dc.subject.mesh | B-Lymphocytes - drug effects - immunology - metabolism | en_HK |
dc.subject.mesh | Bone Marrow Cells - immunology - metabolism | en_HK |
dc.subject.mesh | Cell Proliferation - drug effects | en_HK |
dc.subject.mesh | Disease Models, Animal | en_HK |
dc.subject.mesh | Homeodomain Proteins - genetics - physiology | en_HK |
dc.subject.mesh | Homozygote | en_HK |
dc.subject.mesh | Interleukin-7 - pharmacology | en_HK |
dc.subject.mesh | Lymphopoiesis - immunology | en_HK |
dc.subject.mesh | Mice | en_HK |
dc.subject.mesh | Mice, Knockout | en_HK |
dc.subject.mesh | T-Lymphocytes - immunology - metabolism | en_HK |
dc.title | Hoxb3 deficiency impairs B lymphopoiesis in mouse bone marrow | en_HK |
dc.type | Article | en_HK |
dc.identifier.openurl | http://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0301-472X&volume=35&issue=3&spage=465&epage=75&date=2007&atitle=Hoxb3+deficiency+impairs+B+lymphopoiesis+in+mouse+bone+marrow | en_HK |
dc.identifier.email | Kwan Lam, QL: qlam@pathology.hku.hk | en_HK |
dc.identifier.email | Chan, LC: chanlc@hkucc.hku.hk | en_HK |
dc.identifier.email | Sham, MH: mhsham@hku.hk | en_HK |
dc.identifier.email | Lu, L: liweilu@hkucc.hku.hk | en_HK |
dc.identifier.authority | Kwan Lam, QL=rp00312 | en_HK |
dc.identifier.authority | Chan, LC=rp00373 | en_HK |
dc.identifier.authority | Sham, MH=rp00380 | en_HK |
dc.identifier.authority | Lu, L=rp00477 | en_HK |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1016/j.exphem.2006.10.014 | en_HK |
dc.identifier.pmid | 17309827 | - |
dc.identifier.scopus | eid_2-s2.0-33847069599 | en_HK |
dc.identifier.hkuros | 126175 | en_HK |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-33847069599&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 35 | en_HK |
dc.identifier.issue | 3 | en_HK |
dc.identifier.spage | 465 | en_HK |
dc.identifier.epage | 475 | en_HK |
dc.identifier.isi | WOS:000244605200014 | - |
dc.publisher.place | United States | en_HK |
dc.identifier.scopusauthorid | Ko, KH=7202688627 | en_HK |
dc.identifier.scopusauthorid | Kwan Lam, QL=8722491000 | en_HK |
dc.identifier.scopusauthorid | Zhang, M=8416776200 | en_HK |
dc.identifier.scopusauthorid | Yen Wong, CK=15849791600 | en_HK |
dc.identifier.scopusauthorid | Chun Lo, CK=15847736200 | en_HK |
dc.identifier.scopusauthorid | KahmeyerGabbe, M=55288481400 | en_HK |
dc.identifier.scopusauthorid | Tsang, WH=15849274900 | en_HK |
dc.identifier.scopusauthorid | Tsang, SL=15722984500 | en_HK |
dc.identifier.scopusauthorid | Chan, LC=7403540707 | en_HK |
dc.identifier.scopusauthorid | Sham, MH=7003729109 | en_HK |
dc.identifier.scopusauthorid | Lu, L=7403963552 | en_HK |
dc.identifier.issnl | 0301-472X | - |