Overexpression of a hematopoietic transcriptional regulator EDAG induces myelopoiesis and suppresses lymphopoiesis in transgenic mice

C. Y. Li, Y. Q. Zhan, W. Li, C. W. Xu, W. X. Xu, D. H. Yu, R. Y. Peng, Y. F. Cui, X. Yang, N. Hou, Y. H. Li, B. Dong, Hui (Herb) Sun, X. M. Yang

Research output: Contribution to journalArticle

22 Citations (Scopus)

Abstract

Erythroid differentiation-associated gene (EDAG) is a hematopoietic tissue-specific gene that is highly expressed in the earliest CD34+ lin- bone marrow (BM) cells and involved in the proliferation and differentiation of hematopoietic cells. To investigate the role of EDAG in hematopoiesis, we established an EDAG transgenic mouse model driven by human CD11a promoter. The transgenic mice showed increased mortality with severe organ infiltration by neutrophils, and the homeostasis of hematopoiesis was broken. The myelopoiesis was enhanced with expansion of myeloid cells in BM, increased peripheral granulocytes and extramedullary myelopoiesis in spleen. In contrast to myeloid cells, the lymphoid commitment was severely impaired with the B lymphopoiesis blocked at the transition from pro/pre-B I to pre-B II stage in BM and T thymocytes development blocked at the most immature stage (DN I). Moreover, we showed that EDAG was a transcriptional regulator which had transactivation activity and regulated the expression of several key transcription factors such as PU.1 and Pax5 in transgenic hematopoietic stem cells. These data suggested that EDAG was a key transcriptional regulator in maintaining the homeostasis of hematopoietic lineage commitment.

Original languageEnglish (US)
Pages (from-to)2277-2286
Number of pages10
JournalLeukemia
Volume21
Issue number11
DOIs
StatePublished - Nov 2007
Externally publishedYes

Fingerprint

Lymphopoiesis
Myelopoiesis
Transgenic Mice
Genes
Hematopoiesis
Myeloid Cells
Homeostasis
Bone Marrow
Neutrophil Infiltration
Thymocytes
Hematopoietic Stem Cells
Granulocytes
Bone Marrow Cells
Transcriptional Activation
Cell Differentiation
Transcription Factors
Spleen
Mortality

ASJC Scopus subject areas

  • Hematology
  • Cancer Research

Cite this

Overexpression of a hematopoietic transcriptional regulator EDAG induces myelopoiesis and suppresses lymphopoiesis in transgenic mice. / Li, C. Y.; Zhan, Y. Q.; Li, W.; Xu, C. W.; Xu, W. X.; Yu, D. H.; Peng, R. Y.; Cui, Y. F.; Yang, X.; Hou, N.; Li, Y. H.; Dong, B.; Sun, Hui (Herb); Yang, X. M.

In: Leukemia, Vol. 21, No. 11, 11.2007, p. 2277-2286.

Research output: Contribution to journalArticle

Li, CY, Zhan, YQ, Li, W, Xu, CW, Xu, WX, Yu, DH, Peng, RY, Cui, YF, Yang, X, Hou, N, Li, YH, Dong, B, Sun, HH & Yang, XM 2007, 'Overexpression of a hematopoietic transcriptional regulator EDAG induces myelopoiesis and suppresses lymphopoiesis in transgenic mice', Leukemia, vol. 21, no. 11, pp. 2277-2286. https://doi.org/10.1038/sj.leu.2404901
Li, C. Y. ; Zhan, Y. Q. ; Li, W. ; Xu, C. W. ; Xu, W. X. ; Yu, D. H. ; Peng, R. Y. ; Cui, Y. F. ; Yang, X. ; Hou, N. ; Li, Y. H. ; Dong, B. ; Sun, Hui (Herb) ; Yang, X. M. / Overexpression of a hematopoietic transcriptional regulator EDAG induces myelopoiesis and suppresses lymphopoiesis in transgenic mice. In: Leukemia. 2007 ; Vol. 21, No. 11. pp. 2277-2286.
@article{f064d17a71224c4ea27080707b8776d0,
title = "Overexpression of a hematopoietic transcriptional regulator EDAG induces myelopoiesis and suppresses lymphopoiesis in transgenic mice",
abstract = "Erythroid differentiation-associated gene (EDAG) is a hematopoietic tissue-specific gene that is highly expressed in the earliest CD34+ lin- bone marrow (BM) cells and involved in the proliferation and differentiation of hematopoietic cells. To investigate the role of EDAG in hematopoiesis, we established an EDAG transgenic mouse model driven by human CD11a promoter. The transgenic mice showed increased mortality with severe organ infiltration by neutrophils, and the homeostasis of hematopoiesis was broken. The myelopoiesis was enhanced with expansion of myeloid cells in BM, increased peripheral granulocytes and extramedullary myelopoiesis in spleen. In contrast to myeloid cells, the lymphoid commitment was severely impaired with the B lymphopoiesis blocked at the transition from pro/pre-B I to pre-B II stage in BM and T thymocytes development blocked at the most immature stage (DN I). Moreover, we showed that EDAG was a transcriptional regulator which had transactivation activity and regulated the expression of several key transcription factors such as PU.1 and Pax5 in transgenic hematopoietic stem cells. These data suggested that EDAG was a key transcriptional regulator in maintaining the homeostasis of hematopoietic lineage commitment.",
author = "Li, {C. Y.} and Zhan, {Y. Q.} and W. Li and Xu, {C. W.} and Xu, {W. X.} and Yu, {D. H.} and Peng, {R. Y.} and Cui, {Y. F.} and X. Yang and N. Hou and Li, {Y. H.} and B. Dong and Sun, {Hui (Herb)} and Yang, {X. M.}",
year = "2007",
month = "11",
doi = "10.1038/sj.leu.2404901",
language = "English (US)",
volume = "21",
pages = "2277--2286",
journal = "Leukemia",
issn = "0887-6924",
publisher = "Nature Publishing Group",
number = "11",

}

TY - JOUR

T1 - Overexpression of a hematopoietic transcriptional regulator EDAG induces myelopoiesis and suppresses lymphopoiesis in transgenic mice

AU - Li, C. Y.

AU - Zhan, Y. Q.

AU - Li, W.

AU - Xu, C. W.

AU - Xu, W. X.

AU - Yu, D. H.

AU - Peng, R. Y.

AU - Cui, Y. F.

AU - Yang, X.

AU - Hou, N.

AU - Li, Y. H.

AU - Dong, B.

AU - Sun, Hui (Herb)

AU - Yang, X. M.

PY - 2007/11

Y1 - 2007/11

N2 - Erythroid differentiation-associated gene (EDAG) is a hematopoietic tissue-specific gene that is highly expressed in the earliest CD34+ lin- bone marrow (BM) cells and involved in the proliferation and differentiation of hematopoietic cells. To investigate the role of EDAG in hematopoiesis, we established an EDAG transgenic mouse model driven by human CD11a promoter. The transgenic mice showed increased mortality with severe organ infiltration by neutrophils, and the homeostasis of hematopoiesis was broken. The myelopoiesis was enhanced with expansion of myeloid cells in BM, increased peripheral granulocytes and extramedullary myelopoiesis in spleen. In contrast to myeloid cells, the lymphoid commitment was severely impaired with the B lymphopoiesis blocked at the transition from pro/pre-B I to pre-B II stage in BM and T thymocytes development blocked at the most immature stage (DN I). Moreover, we showed that EDAG was a transcriptional regulator which had transactivation activity and regulated the expression of several key transcription factors such as PU.1 and Pax5 in transgenic hematopoietic stem cells. These data suggested that EDAG was a key transcriptional regulator in maintaining the homeostasis of hematopoietic lineage commitment.

AB - Erythroid differentiation-associated gene (EDAG) is a hematopoietic tissue-specific gene that is highly expressed in the earliest CD34+ lin- bone marrow (BM) cells and involved in the proliferation and differentiation of hematopoietic cells. To investigate the role of EDAG in hematopoiesis, we established an EDAG transgenic mouse model driven by human CD11a promoter. The transgenic mice showed increased mortality with severe organ infiltration by neutrophils, and the homeostasis of hematopoiesis was broken. The myelopoiesis was enhanced with expansion of myeloid cells in BM, increased peripheral granulocytes and extramedullary myelopoiesis in spleen. In contrast to myeloid cells, the lymphoid commitment was severely impaired with the B lymphopoiesis blocked at the transition from pro/pre-B I to pre-B II stage in BM and T thymocytes development blocked at the most immature stage (DN I). Moreover, we showed that EDAG was a transcriptional regulator which had transactivation activity and regulated the expression of several key transcription factors such as PU.1 and Pax5 in transgenic hematopoietic stem cells. These data suggested that EDAG was a key transcriptional regulator in maintaining the homeostasis of hematopoietic lineage commitment.

UR - http://www.scopus.com/inward/record.url?scp=35548941195&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=35548941195&partnerID=8YFLogxK

U2 - 10.1038/sj.leu.2404901

DO - 10.1038/sj.leu.2404901

M3 - Article

C2 - 17690693

AN - SCOPUS:35548941195

VL - 21

SP - 2277

EP - 2286

JO - Leukemia

JF - Leukemia

SN - 0887-6924

IS - 11

ER -