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dc.contributor.authorBungartz, Gerd
dc.contributor.authorStiller, Sebastian
dc.contributor.authorBauer, Martina
dc.contributor.authorMüller, Werner
dc.contributor.authorSchippers, Angela
dc.contributor.authorWagner, Norbert
dc.contributor.authorFässler, Reinhard
dc.contributor.authorBrakebusch, Cord
dc.date.accessioned2007-11-13T09:30:25Z
dc.date.available2007-11-13T09:30:25Z
dc.date.issued2006-09-15
dc.identifier.citationBlood 2006, 108(6):1857-64en
dc.identifier.issn0006-4971
dc.identifier.pmid16735603
dc.identifier.doi10.1182/blood-2005-10-007658
dc.identifier.urihttp://hdl.handle.net/10033/14518
dc.description.abstractThe function of alpha4beta1 and alpha4beta7 integrins in hematopoiesis is controversial. While some experimental evidence suggests a crucial role for these integrins in retention and expansion of progenitor cells and lymphopoiesis, others report a less important role in hematopoiesis. Using mice with a deletion of the beta1 and the beta7 integrin genes restricted to the hematopoietic system we show here that alpha4beta1 and alpha4beta7 integrins are not essential for differentiation of lymphocytes or myelocytes. However, beta1beta7 mutant mice displayed a transient increase of colony-forming unit (CFU-C) progenitors in the bone marrow and, after phenylhydrazine-induced anemia, a decreased number of splenic erythroid colony-forming units in culture (CFUe's). Array gene expression analysis of CD4(+)CD8(+) double-positive (DP) and CD4(-)CD8(-) double-negative (DN) thymocytes and CD19(+) and CD4(+) splenocytes did not provide any evidence for a compensatory mechanism explaining the mild phenotype. These data show that alpha4beta1 and alpha4beta7 are not required for blood cell differentiation, although in their absence alterations in numbers and distribution of progenitor cells were observed.
dc.format.extent775417 bytes
dc.format.mimetypeapplication/pdf
dc.language.isoenen
dc.titleAdult murine hematopoiesis can proceed without beta1 and beta7 integrins.en
dc.typeArticleen
dc.format.digYES
refterms.dateFOA2018-06-12T17:47:57Z
html.description.abstractThe function of alpha4beta1 and alpha4beta7 integrins in hematopoiesis is controversial. While some experimental evidence suggests a crucial role for these integrins in retention and expansion of progenitor cells and lymphopoiesis, others report a less important role in hematopoiesis. Using mice with a deletion of the beta1 and the beta7 integrin genes restricted to the hematopoietic system we show here that alpha4beta1 and alpha4beta7 integrins are not essential for differentiation of lymphocytes or myelocytes. However, beta1beta7 mutant mice displayed a transient increase of colony-forming unit (CFU-C) progenitors in the bone marrow and, after phenylhydrazine-induced anemia, a decreased number of splenic erythroid colony-forming units in culture (CFUe's). Array gene expression analysis of CD4(+)CD8(+) double-positive (DP) and CD4(-)CD8(-) double-negative (DN) thymocytes and CD19(+) and CD4(+) splenocytes did not provide any evidence for a compensatory mechanism explaining the mild phenotype. These data show that alpha4beta1 and alpha4beta7 are not required for blood cell differentiation, although in their absence alterations in numbers and distribution of progenitor cells were observed.


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