Hematopoietic developmental pathways: on cellular basis

Iwasaki, Hiromi; Akashi, Koichi

doi:10.1038/sj.onc.1210754

Cited by 96 publications

(71 citation statements)

References 99 publications

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“…Fukuda et al 8 demonstrated that apoE Ϫ/Ϫ mice repopulated with Agtr1 Ϫ/Ϫ marrow showed a modest but significant reduction of atherosclerotic lesion development, whereas ablation of BM-AT 1 receptor in LDLr Ϫ/Ϫ mice had no effect on atherosclerosis, 7,21 suggesting that the different models used may differ in their consequence of BM-AT 1 14,15 M-CSF is the principal regulator of proliferation and terminal differentiation of monocyte-lineage cells. 22 We found that M-CSFinduced colony forming activity was dramatically attenuated in BM cells from Agtr1 Ϫ/Ϫ mice, and that in vitro differentiation of HSCs from Agtr1 Ϫ/Ϫ mice was significantly reduced in the presence of M-CSF.…”

Section: Discussionmentioning

confidence: 99%

Bone Marrow Angiotensin AT ₁ Receptor Regulates Differentiation of Monocyte Lineage Progenitors From Hematopoietic Stem Cells

Tsubakimoto

Yamada

Yokoi

et al. 2009

ATVB

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Background-The angiotensin II (Ang II) type 1 (AT 1 ) receptor is expressed in bone marrow (BM) cells, whereas it remains poorly defined how Ang II regulates differentiation/proliferation of monocyte-lineage cells to exert proatherogenic actions. Methods and Results-We generated BM chimeric apoE Ϫ/Ϫ mice repopulated with AT 1 -deficient (Agtr1 Key Words: bone marrow progenitors Ⅲ angiotensin Ⅲ monocyte Ⅲ atherosclerosis Ⅲ M-CSF T he angiotensin II (Ang II) type 1 (AT 1 ) receptor exerts proatherogenic actions. 1 AT 1 receptor-deficient (Agtr1 Ϫ/Ϫ ) mice showed a significant reduction of atherosclerotic development, 2,3 and treatment with AT 1 receptor blocker (ARB) reduced the size of atherosclerotic lesions both in experimental animals and humans. 4 AT 1 receptors are present in a variety of cells, including endothelial cells, vascular smooth muscle cells, and bone marrow (BM) stem cells and progenitors. 5,6 Recently, Cassis et al demonstrated that Ang II-induced atherosclerosis was significantly attenuated in LDL receptor-deficient (LDLr Ϫ/Ϫ ) mice whose BM cells were repopulated with Agtr1 Ϫ/Ϫ cells. 7 Fukuda et al also reported that atherosclerotic lesion development was significantly reduced in apoE-deficient (apoE Ϫ/Ϫ ) mice with Agtr1 Ϫ/Ϫ marrow. 8 However, no information regarding the role of the BM-AT 1 receptor on the differentiation/proliferation and properties of BM stem cells and progenitors has been reported in these previous studies.Monocytes and macrophages play a crucial role in the pathogenesis of atherosclerosis, which is characterized by plaque progression, destabilization, and subsequent plaque rupture, through foam cell formation, migration/proliferation of resident vascular smooth muscle cells, and degradation of extracellular matrix. 9 Along with the previous studies showing the effect of diet-induced hypercholesterolemia on BM and leukocyte, 10 Swirski et al reported that hypercholesterolemia induced a surprisingly profound expansion of blood monocytes as well as BM monocyte-lineage cells. 11 However, the relative contribution of the BM renin-angiotensin system to hypercholesterolemia-associated monocytosis has not been fully investigated. 12 In the present study, we focused on the action of the AT 1 receptor expressed in BM cells and studied whether (1) Ang II affects the differentiation/proliferation from BM stem cells into monocyte-lineage cells, and (2) MethodsA full description of all methods can be found in the Data Supplement (available online at http://atvb.ahajournals.org). Animal PreparationApoE Ϫ/Ϫ mice (C57BL/6) and AT1a receptor-deficient (Agtr1 Ϫ/Ϫ ) mice (C57BL/6) were obtained from Taconic Co Ltd (Germantown, NY) and Tanabe Seiyaku Co Ltd (Osaka, Japan), respectively. BM cells of 2-month-old female apoE Ϫ/Ϫ recipient mice were repopulated with male Agtr1 Ϫ/Ϫ or Agtr1 ϩ/ϩ cells. The percentage chimerism determined by transplanting GFP-overexpressing BM cells was 96Ϯ2% of peripheral blood mononuclear cells. 13 Furthermore, BM CD45 Ϫ CD34 Ϫ stromal cells, HSCs, and myeloid ...

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Section: Discussionmentioning

confidence: 99%

Bone Marrow Angiotensin AT ₁ Receptor Regulates Differentiation of Monocyte Lineage Progenitors From Hematopoietic Stem Cells

Tsubakimoto

Yamada

Yokoi

et al. 2009

ATVB

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“…Since all lineages of blood cells are derived from bone marrow progenitor cells in adult mice, we examined whether loss of Ubc13 affected the bone marrow progenitors. Two major populations of progenitor cells, LSK and LK, could be detected by flow cytometry based on their expression of IL-7 receptor alpha chain (IL-7R␣), lineage markers (Lin), stem cell antigen-1 (Sca-1), and the receptor tyrosine kinase c-Kit (31). The LSK population (IL-7R␣ Ϫ Lin Ϫ Sca-1 ϩ c-Kit ϩ ) contains the multipotent HSCs that can further produce lineage-specific progenitors, whereas the LK population (IL-7R␣ Ϫ Lin Ϫ Sca-1 Ϫ c-Kit ϩ ) contains common myeloid progenitors (CMP).…”

Section: Ubc13 Iko Mice Display Bone Marrow Atrophy and Deficiency Inmentioning

confidence: 99%

Regulation of hematopoiesis by the K63-specific ubiquitin-conjugating enzyme Ubc13

Yamamoto

Akira

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

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“…1 Mechanisms that regulate myeloid lineage choice are relevant to host defense mechanisms and also to leukemic transformation of immature cells. Several transcription factors contribute to myeloid lineage specification.…”

Section: Introductionmentioning

confidence: 99%

M-CSF elevates c-Fos and phospho-C/EBPα(S21) via ERK whereas G-CSF stimulates SHP2 phosphorylation in marrow progenitors to contribute to myeloid lineage specification

Jack

Zhang

Friedman

2009

Blood

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The role of hematopoietic cytokines in lineage commitment remains uncertain. To gain insight into the contribution of cytokine signaling to myeloid lineage specification, we compared granulocyte colony-stimulating factor (G-CSF) and macrophage colony-stimulating factor (M-CSF) signaling in Ba/F3 cells expressing both the G-CSF and M-CSF receptors and in lineage-negative murine marrow cells. G-CSF and M-CSF serve as prototypes for additional cytokines that also influence immature myeloid cells. G-CSF specifically activated signal transducer and activator of transcription 3 and induced Src homology region 2 domain-containing phosphatase 2 (SHP2) phosphorylation, whereas M-CSF preferentially activated phospholipase Cγ2, and thereby extracellular signal-regulated kinase (ERK), to stabilize c-Fos and stimulate CCAAT/enhancer-binding protein (C/EBP)α(S21) phosphorylation. In contrast, activation of Jun kinase or c-Jun was similar in response to either cytokine. Inhibition of ERK prevented induction of c-Fos by M-CSF and reduced C/EBPα phosphorylation and formation of colony-forming unit–monocytes. SHP2 inhibition reduced ERK activation in G-CSF, but not M-CSF, and reduced colony-forming unit–granulocytes, underscoring divergent pathways to ERK activation. Phorbol ester mimicked the effect of M-CSF, activating ERK independent of SHP2. In summary, M-CSF activates ERK more potently than G-CSF, and thereby induces higher levels of c-Fos and phospho-C/EBPα(S21), which may directly interact to favor monopoiesis, whereas G-CSF activates signal transducer and activator of transcription 3 and SHP2, potentially shifting the balance to granulopoiesis via gene induction by C/EBPα homodimers and via effects of SHP2 on regulators besides ERK.

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Hematopoietic developmental pathways: on cellular basis

Cited by 96 publications

References 99 publications

Bone Marrow Angiotensin AT ₁ Receptor Regulates Differentiation of Monocyte Lineage Progenitors From Hematopoietic Stem Cells

Bone Marrow Angiotensin AT ₁ Receptor Regulates Differentiation of Monocyte Lineage Progenitors From Hematopoietic Stem Cells

Regulation of hematopoiesis by the K63-specific ubiquitin-conjugating enzyme Ubc13

M-CSF elevates c-Fos and phospho-C/EBPα(S21) via ERK whereas G-CSF stimulates SHP2 phosphorylation in marrow progenitors to contribute to myeloid lineage specification

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Hematopoietic developmental pathways: on cellular basis

Cited by 96 publications

References 99 publications

Bone Marrow Angiotensin AT 1 Receptor Regulates Differentiation of Monocyte Lineage Progenitors From Hematopoietic Stem Cells

Bone Marrow Angiotensin AT 1 Receptor Regulates Differentiation of Monocyte Lineage Progenitors From Hematopoietic Stem Cells

Regulation of hematopoiesis by the K63-specific ubiquitin-conjugating enzyme Ubc13

M-CSF elevates c-Fos and phospho-C/EBPα(S21) via ERK whereas G-CSF stimulates SHP2 phosphorylation in marrow progenitors to contribute to myeloid lineage specification

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Bone Marrow Angiotensin AT ₁ Receptor Regulates Differentiation of Monocyte Lineage Progenitors From Hematopoietic Stem Cells

Bone Marrow Angiotensin AT ₁ Receptor Regulates Differentiation of Monocyte Lineage Progenitors From Hematopoietic Stem Cells