Identification of Flk-1 target genes in vasculogenesis: Pim-1 is required for endothelial and mural cell differentiation in vitro

Zippo, Alessio; Robertis, Alessandra De; Bardelli, Monia; Galvagni, Federico; Oliviero, Salvatore

doi:10.1182/blood-2003-11-3827

Cited by 108 publications

(104 citation statements)

References 51 publications

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“…Anp32b +/− mice were intercrossed and embryos were genotyped at time E17.5. Our histological examinations did not show any defects in vascular endothelium or smooth muscle, as might have been expected from previous reports on ANP32B functions (32,40). However, our data regarding the incidence of hematomas in Anp32b −/− embryos do support a potential role for ANP32B in vascular development.…”

Section: Discussioncontrasting

confidence: 37%

Acidic nuclear phosphoprotein 32kDa (ANP32)B-deficient mouse reveals a hierarchy of ANP32 importance in mammalian development

Reilly

Afzal²,

Gorrini³

et al. 2011

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

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The highly conserved ANP32 proteins are proposed to function in a broad array of physiological activities through molecular mechanisms as diverse as phosphatase inhibition, chromatin regulation, caspase activation, and intracellular transport. On the basis of previous analyses of mice bearing targeted mutations of Anp32a or Anp32e, there has been speculation that all ANP32 proteins play redundant roles and are dispensable for normal development. However, more recent work has suggested that ANP32B may in fact have functions that are not shared by other ANP32 family members. Here we report that ANP32B expression is associated with a poor prognosis in human breast cancer, consistent with the increased levels of Anp32b mRNA present in proliferating wild-type (WT) murine embryonic fibroblasts and stimulated WT B and T lymphocytes. Moreover, we show that, contrary to previous assumptions, Anp32b is very important for murine embryogenesis. In a mixed genetic background, ANP32B-deficient mice displayed a partially penetrant perinatal lethality that became fully penetrant in a pure C57BL/6 background. Surviving ANP32B-deficient mice showed reduced viability due to variable defects in various organ systems. Study of compound mutants lacking ANP32A, ANP32B, and/or ANP32E revealed previously hidden roles for ANP32A in mouse development that became apparent only in the complete absence of ANP32B. Our data demonstrate a hierarchy of importance for the mammalian Anp32 genes, with Anp32b being the most critical for normal development.cell growth | mouse embryogenesis | premature aging

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Section: Discussioncontrasting

confidence: 37%

Acidic nuclear phosphoprotein 32kDa (ANP32)B-deficient mouse reveals a hierarchy of ANP32 importance in mammalian development

Reilly

Afzal²,

Gorrini³

et al. 2011

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

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“…It has also been shown that Pim-1 activates the cyclin-dependent kinase inhibitor p21 (24) and that the antiapoptotic factor Bcl-2 is regulated downstream of Pim-1 (25), suggesting that Pim-1 is involved in cell cycle regulation and apoptosis in hematopoietic cells. In addition, functional analysis by RNA interference in embryonic stem cells has recently demonstrated that Pim-1 is required for their differentiation into endothelial cells and VSMCs (26). In this study, we show that Pim-1 expression is observed in ballooninjured rat carotid arteries and human coronary arteries and that dominant negative Pim-1 markedly suppresses VSMC proliferation in the balloon-injured model and in a cell culture system.…”

mentioning

confidence: 58%

“…These findings suggest that Pim-1 plays a critical role in VSMC proliferation under certain conditions. Because functional analysis by RNA interference in embryonic stem cells has recently demonstrated that Pim-1 is required for their differentiation into VSMCs (26), it is likely that Pim-1 plays at least two roles in VSMCs; one is a physiological role in differentiation into VSMCs, and another is a role in VSMC proliferation under certain conditions.…”

Section: Discussionmentioning

confidence: 99%

Role of Pim-1 in Smooth Muscle Cell Proliferation

Katakami

Kaneto

Hao

et al. 2004

Journal of Biological Chemistry

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“…However, this function is thought to occur by SHIP inhibiting formation of a complex between TLR4 and MyD88. 150 SHIP1 is expressed in endothelial cells, 151 and thus may play a role in the regulation of LPS signaling in these cells.…”

Section: Toll-interacting Protein (Tollip)mentioning

confidence: 99%

Lipopolysaccharide signaling in endothelial cells

Dauphinee

Karsan

2006

Laboratory Investigation

534

433

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Sepsis is the systemic immune response to severe bacterial infection. The innate immune recognition of bacterial and viral products is mediated by a family of transmembrane receptors known as Toll-like receptors (TLRs). In endothelial cells, exposure to lipopolysaccharide (LPS), a major cell wall constituent of Gramnegative bacteria, results in endothelial activation through a receptor complex consisting of TLR4, CD14 and MD2. Recruitment of the adaptor protein myeloid differentiation factor (MyD88) initiates an MyD88-dependent pathway that culminates in the early activation of nuclear factor-jB (NF-jB) and the mitogen-activated protein kinases. In parallel, a MyD88-independent pathway results in a late-phase activation of NF-jB. The outcome is the production of various proinflammatory mediators and ultimately cellular injury, leading to the various vascular sequelae of sepsis. This review will focus on the signaling pathways initiated by LPS binding to the TLR4 receptor in endothelial cells and the coordinated regulation of this pathway.

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Identification of Flk-1 target genes in vasculogenesis: Pim-1 is required for endothelial and mural cell differentiation in vitro

Cited by 108 publications

References 51 publications

Acidic nuclear phosphoprotein 32kDa (ANP32)B-deficient mouse reveals a hierarchy of ANP32 importance in mammalian development

Acidic nuclear phosphoprotein 32kDa (ANP32)B-deficient mouse reveals a hierarchy of ANP32 importance in mammalian development

Role of Pim-1 in Smooth Muscle Cell Proliferation

Lipopolysaccharide signaling in endothelial cells

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