期刊
MOLECULAR AND CELLULAR BIOLOGY
卷 23, 期 24, 页码 9349-9360出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/MCB.23.24.9349-9360.2003
关键词
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资金
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL046557, R01HL058734] Funding Source: NIH RePORTER
- NHLBI NIH HHS [R01 HL046557, HL 58734, R01 HL058734, HL 46557] Funding Source: Medline
We have explored the functional implications of inducible alpha4 integrin deletion during adult hematopoiesis by generating a conditional-knockout mouse model, and we show that alpha4 integrin-deficient hematopoietic progenitor cells accumulate in the peripheral blood soon after interferon-induced gene deletion. Although their numbers gradually stabilize at a lower level, progenitor cell influx into the circulation continues at above-normal levels for more than 50 weeks. Concomitantly, a progressive accumulation of progenitors occurs within the spleen. In addition, the regeneration of erythroid and myeloid progenitor cells is delayed during stress hematopoiesis induced by phenylhydrazine or by 5-fluorouracil, suggesting impairment in early progenitor expansion in the absence of alpha4 integrin. Moreover, in transplantation studies, homing of alpha4(-/-) cells to the bone marrow, but not to the spleen, is selectively impaired, and short-term engraftment is critically delayed in the early weeks after transplantation. Thus, conditional deletion of alpha4 integrin in adult mice is accompanied by a novel hematopoietic phenotype during both homeostasis and recovery from stress, a phenotype that is distinct from the ones previously described in alpha4 integrin-null chimeras and beta1 integrin-conditional knockouts.
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