Y Box-Binding Factor Promotes Eosinophil Survival by Stabilizing Granulocyte-Macrophage Colony-Stimulating Factor mRNA

Capowski, Elizabeth E.; Esnault, Stéphane; Bhattacharya, Saswati; Malter, James S.

doi:10.4049/jimmunol.167.10.5970

Cited by 101 publications

(74 citation statements)

References 50 publications

(42 reference statements)

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“…Specific binding of YB-1 to VEGF and GM-CSF mRNAs was independently confirmed by other researchers. 23,24 Consistent with the idea that Akt phosphorylation reduces the repressor activity of YB-1, association of several of these mRNAs with YB-1 was reduced in cells treated with IGF-1. 19 Moreover, a total of 93 transcripts identified in our study were among the 343 messages previously reported to be translationally activated by combined Ras/Akt signaling.…”

Section: Eif4esupporting

confidence: 67%

Y-box Binding Protein 1: Providing a New Angle on Translational Regulation

Evdokimova

Ovchinnikov²,

Sorensen³

2006

Cell Cycle

108

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Section: Eif4esupporting

confidence: 67%

Y-box Binding Protein 1: Providing a New Angle on Translational Regulation

Evdokimova

Ovchinnikov²,

Sorensen³

2006

Cell Cycle

108

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“…The time course of the cytoplasmic localization closely correlated with the mesangioproliferative phase of the disease, which peaks between days 3 and 6 (33). This close correlation may suggest that YB-1 acts predominantly as regulator of translational processes at this stage of disease, e.g., by affecting the half-life of cytokine messenger RNA (7,17), or by nonspecifically binding to the 5Ј RNA cap structure (16). Notably, YB-1 regulates the translation of its own mRNA (50), which may explain differences in YB-1 protein and mRNA synthesis after stimulation with PDGF-B.…”

Section: Subcellular Shuttling Of Yb-1 In Inflammatory Glomerular Dismentioning

confidence: 79%

“…Depending on the cellular context, YB-1 may transactivate or -repress target gene transcription (9,10,14,15). In addition, YB-1 binds to mRNA in a nonspecific as well as a specific way, which has profound effects on mRNA translation (16) and mRNA half-lives, e.g., of the IL-2 and GM-CSF genes (7,17). Finally, by means of direct interaction with specific mRNA sequences, YB-1 may affect mRNA splicing, as has been demonstrated for the CD44 and E1A genes (18 -20).…”

mentioning

confidence: 99%

Y-Box Protein 1 Mediates PDGF-B Effects in Mesangioproliferative Glomerular Disease

Roeyen

Eitner

Martinkus

et al. 2005

Journal of the American Society of Nephrology

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The pivotal role of PDGF-B for mesangioproliferative glomerular disease is well established. Here, Y-box protein-1 (YB-1) was identified as a downstream signaling target of PDGF-B. In healthy kidney cells, YB-1 was located predominantly within the nuclear compartment. Subsequent to PDGF-B infusion and in the course of anti-Thy1.1-induced mesangioproliferative glomerulonephritis, relocalization of YB-1 into the cytoplasm was observed. In experimental models that lack profound mesangial cell proliferation (e.g., Puromycin-nephrosis, passive Heyman nephritis, spontaneous normotensive nephrosclerosis, hyperlipidemic diabetic nephropathy), YB-1 remained nuclear. This translocation coincided with upregulation of YB-1 protein levels within the mesangial compartment. Increased YB-1 expression and subcellular shuttling was dependent on PDGF-B signaling via the mitogen-activated protein kinase pathway because these alterations were prevented by specific PDGF aptamers and the mitogen-activated protein kinase pathway inhibitor U0126. Furthermore, PDGF-B strongly induced YB-1 expression in vitro. This induction was important because RNAi-dependent knockdown of YB-1 abolished the mitogenic PDGF-B effect. Taken together, YB-1 seems to represent a specific and necessary PDGF-B target in mesangioproliferative glomerular disease.

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“…27,36 It has been reported that YB-1 affects the expression of various proliferative and inflammatory proteins, such as granulocyte-macrophage colony-stimulating factor and matrix metalloproteinase-2, at both the transcriptional and translational level. 15,35 YB-1 can herein act both as a transrepressor and a transactivator. The present study shows that as opposed to SMCs, YB-1 overexpression inhibited the expression of CCL5 induced by inflammatory stimulation in macrophages.…”

Section: Discussionmentioning

confidence: 99%

“…An increased expression of YB-1 in certain inflammatory diseases has been described (eg, by activated eosinophils in allergic asthma, 15 in which YB-1 prolonged their survival and thus exacerbated disease, or by mesangial cells in mesangioproliferative disease 16 ). YB-1 preferentially binds to DNA containing the so-called Y-box or inverted CCAAT box (CTGATTGGC/ TC/TAA).…”

Section: Clinical Perspective P 1820mentioning

confidence: 99%

Y-Box Binding Protein-1 Controls CC Chemokine Ligand-5 (CCL5) Expression in Smooth Muscle Cells and Contributes to Neointima Formation in Atherosclerosis-Prone Mice

et al. 2007

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Background-The CC chemokine CCL5/Regulated on Activation, Normal T Cell Expressed and Secreted (RANTES) is upregulated in mononuclear cells or deposited by activated platelets during inflammation and has been implicated in atherosclerosis and neointimal hyperplasia. We investigated the influence of the transcriptional regulator Y-box binding protein (YB)-1 on CCL5 expression and wire-induced neointimal hyperplasia. Methods and Results-Analysis of the CCL5 promoter revealed potential binding sites for YB-1, and interaction of YB-1 with a sequence at position Ϫ204/Ϫ173 was confirmed by DNA binding assays. Both YB-1 expression and CC chemokine ligand-5 (CCL5) mRNA expression were increased in neointimal versus medial smooth muscle cells, as analyzed by real-time polymerase chain reaction. Overexpression of YB-1 in smooth muscle cells (but not macrophages) enhanced CCL5 transcriptional activity in reporter assays, mRNA and protein expression, and CCL5-mediated monocyte arrest. Carotid arteries of hyperlipidemic apolipoprotein E-deficient mice were subjected to intraluminal transfection with a lentivirus encoding YB-1 short hairpin RNA or empty vector directly after wire injury. Double immunofluorescence revealed YB-1 expression in neointimal smooth muscle cells but not macrophages and colocalization with neointimal CCL5, which was downregulated by YB-1 short hairpin RNA. Neointima formation was decreased significantly after YB-1 knockdown compared with controls and was associated with a diminished content of lesional macrophages. A reduction of lesion formation by YB-1 knockdown was not observed in apolipoprotein E-deficient mice deficient in the CCL5 receptor CCR5 or after treatment with the CCL5 antagonist Met-RANTES, which indicates that YB-1 effects were dependent on CCL5. Conclusions-The transcriptional regulator YB-1 mediates CCL5 expression in smooth muscle cells and thereby contributes to neointimal hyperplasia, thus representing a novel target with which to limit vascular remodeling.

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Y Box-Binding Factor Promotes Eosinophil Survival by Stabilizing Granulocyte-Macrophage Colony-Stimulating Factor mRNA

Cited by 101 publications

References 50 publications

Y-box Binding Protein 1: Providing a New Angle on Translational Regulation

Y-box Binding Protein 1: Providing a New Angle on Translational Regulation

Y-Box Protein 1 Mediates PDGF-B Effects in Mesangioproliferative Glomerular Disease

Y-Box Binding Protein-1 Controls CC Chemokine Ligand-5 (CCL5) Expression in Smooth Muscle Cells and Contributes to Neointima Formation in Atherosclerosis-Prone Mice

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