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Blood, 1 August 2007, Vol. 110, No. 3, pp. 870-876. Prepublished online as a Blood First Edition Paper on April 12, 2007; DOI 10.1182/blood-2007-01-068528. This Article Full Text Full Text (PDF) Supplemental Figures All Versions of this Article: blood-2007-01-068528v1 110/3/870    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Liu, X.-S. Articles by Wang, Z.-G. Search for Related Content PubMed PubMed Citation Articles by Liu, X.-S. Articles by Wang, Z.-G. Related Collections Hematopoiesis and Stem Cells Cytoskeleton Stem Cells in Hematology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMATOPOIESIS Disruption of palladin leads to defects in definitive erythropoiesis by interfering with erythroblastic island formation in mouse fetal liver Xue-Song Liu1,2, Xi-Hua Li1, Yi Wang1, Run-Zhe Shu1,2, Long Wang1,3,4, Shun-Yuan Lu1,3,4, Hui Kong4, Yue-E Jin1, Li-Jun Zhang1, Jian Fei4, Sai-Juan Chen3, Zhu Chen3, Ming-Min Gu1, Zhen-Yu Lu1, and Zhu-Gang Wang1,3,4 1 Laboratory of Genetic Engineering, Department of Medical Genetics, Institute of Health Sciences, Shanghai Institutes for Biological Sciences of Chinese Academy of Sciences, and Shanghai Jiao Tong University School of Medicine, Shanghai; 2 Graduate School of Chinese Academy of Sciences, Shanghai; 3 State Key Laboratory of Medical Genomics, Rui-jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai; and 4 Shanghai Research Center for Model Organisms, Shanghai, People's Republic of China Palladin was originally found up-regulated with NB4 cell differentiation induced by all-trans retinoic acid. Disruption of palladin results in neural tube closure defects, liver herniation, and embryonic lethality. Here we further report that Palld–/– embryos exhibit a significant defect in erythropoiesis characterized by a dramatic reduction in definitive erythrocytes derived from fetal liver but not primitive erythrocytes from yolk sac. The reduction of erythrocytes is accompanied by increased apoptosis of erythroblasts and partial blockage of erythroid differentiation. However, colony-forming assay shows no differences between wild-type (wt) and mutant fetal liver or yolk sac in the number and size of colonies tested. In addition, Palld–/– fetal liver cells can reconstitute hematopoiesis in lethally irradiated mice. These data strongly suggest that deficient erythropoiesis in Palld–/– fetal liver is mainly due to a compromised erythropoietic microenvironment. As expected, erythroblastic island in Palld–/– fetal liver was found disorganized. Palld–/– fetal liver cells fail to form erythroblastic island in vitro. Interestingly, wt macrophages can form such units with either wt or mutant erythroblasts, while mutant macrophages lose their ability to bind wt or mutant erythroblasts. These data demonstrate that palladin is crucial for definitive erythropoiesis and erythroblastic island formation and, especially, required for normal function of macrophages in fetal liver. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: K. E. McGrath, P. D. Kingsley, A. D. Koniski, R. L. Porter, T. P. Bushnell, and J. Palis Enucleation of primitive erythroid cells generates a transient population of "pyrenocytes" in the mammalian fetus Blood, February 15, 2008; 111(4): 2409 - 2417. [Abstract] [Full Text] [PDF]

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