Abstract
Angiopoietin-1 (Ang-1) is known to have hematoprotective effects by increasing the quiescence of hematopoietic stem cells. However, it remains to be determined if the upregulation of Ang-1 and the subsequent increase in the quiescence of hematopoietic stem cells are also involved in the dexamethasone (Dex)-mediated bone marrow protection. Here Western blotting and flow cytometric analyses demonstrate that Dex increases the levels of Ang-1 in mouse bone marrow and the quiescence of hematopoietic stem cells. Our data for the first time suggest that the increased quiescence of hematopoietic stem cells provides a novel mechanism of Dex-induced hematoprotection.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Angiopoietin-1 / biosynthesis*
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Angiopoietin-1 / genetics
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Animals
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Base Sequence
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Bone Marrow / drug effects
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Bone Marrow / metabolism
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Cytoprotection*
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Dexamethasone / pharmacology*
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Glucocorticoids / pharmacology*
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Humans
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Mice
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Mice, Inbred C57BL
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Myeloid Progenitor Cells / cytology
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Myeloid Progenitor Cells / drug effects*
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Myeloid Progenitor Cells / metabolism
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RNA Stability / drug effects
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RNA, Messenger / biosynthesis
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Receptors, Glucocorticoid / biosynthesis
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Receptors, Glucocorticoid / genetics
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Response Elements
Substances
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Angiopoietin-1
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Glucocorticoids
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RNA, Messenger
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Receptors, Glucocorticoid
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Dexamethasone