期刊
BLOOD
卷 119, 期 22, 页码 5144-5154出版社
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2011-07-368506
关键词
-
类别
资金
- Heimlich Institute of Cincinnati
- Department of Defense [10580355]
- National Institutes of Health (NIH) [R01-HL087159, HL087159S1]
- University of Cincinnati Fellowship Award
- National Blood Foundation
- Spanish Ministry of Science and Technology [Consolider CSD2008-00005]
- Community of Madrid [S2010/BMD-2460]
- NIH [R01 AR041255]
- Hoxworth Blood Center
- Cincinnati Children's Hospital Medical Center
Connexin-43 (Cx43), a gap junction protein involved in control of cell proliferation, differentiation and migration, has been suggested to have a role in hematopoiesis. Cx43 is highly expressed in osteoblasts and osteogenic progenitors (OB/P). To elucidate the biologic function of Cx43 in the hematopoietic microenvironment (HM) and its influence in hematopoietic stem cell (HSC) activity, we studied the hematopoietic function in an in vivo model of constitutive deficiency of Cx43 in OB/P. The deficiency of Cx43 in OB/P cells does not impair the steady state hematopoiesis, but disrupts the directional trafficking of HSC/progenitors (Ps) between the bone marrow (BM) and peripheral blood (PB). OB/P Cx43 is a crucial positive regulator of transstromal migration and homing of both HSCs and progenitors in an irradiated microenvironment. However, OB/P Cx43 deficiency in nonmyeloablated animals does not result in a homing defect but induces increased endosteal lodging and decreased mobilization of HSC/Ps associated with proliferation and expansion of Cxcl12-secreting mesenchymal/osteolineage cells in the BM HM in vivo. Cx43 controls the cellular content of the BM osteogenic microenvironment and is required for homing of HSC/Ps in myeloablated animals. (Blood. 2012; 119(22): 5144-5154)
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据