Profiling of genes which are differentially expressed in mouse liver in response to adenoviral vectors and delivered genes

Tc, Haberberger; K, Kupfer; Je, Murphy

doi:10.1038/sj.gt.3301181

Cited by 32 publications

(17 citation statements)

References 27 publications

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“…6, 8, and 14; this study) may allow pDCs to roll on resting or on minimally activated ECs and, thus, to constantly screen peripheral sites and lymph nodes for chemokine signatures of viral infection. In this respect, the CXCR3Ls may be of particular significance as they are among the gene products that are extremely rapidly and robustly up-regulated after viral encounter (42,43). In aggregate, these observations allow for speculation that pDC traffic into virally infected sites is maximal at early time points and may decrease with the onset of overt EC activation and EC activationdependent recruitment of effector cells of the innate and adaptive immune system.…”

Section: Discussionmentioning

confidence: 96%

Plasmacytoid Dendritic Cell Recruitment by Immobilized CXCR3 Ligands

Kohrgruber

Gröger

Meraner

et al. 2004

The Journal of Immunology

109

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Plasmacytoid dendritic cells (pDCs) recognize microbes, viruses in particular, and provide unique means of innate defense against them. The mechanism of pDC tissue recruitment remained enigmatic because the ligands of CXCR3, the cardinal chemokine receptor on pDCs, have failed to induce in vitro chemotaxis of pDCs in the absence of additional chemokines. In this study, we demonstrate that CXCR3 is sufficient to induce pDC migration, however, by a migratory mechanism that amalgamates the features of haptotaxis and chemorepulsion. To mediate “haptorepulsion” of pDCs, CXCR3 requires the encounter of its cognate ligands immobilized, optimally by heparan sulfate, in a form of a negative gradient. This is the first report of the absolute requirement of chemokine immobilization and presentation for its in vitro promigratory activity. The paradigmatic example of pDC haptorepulsion described here may represent a new pathophysiologically relevant migratory mechanism potentially used by other cells in response to other chemokines.

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Section: Discussionmentioning

confidence: 96%

Plasmacytoid Dendritic Cell Recruitment by Immobilized CXCR3 Ligands

Kohrgruber

Gröger

Meraner

et al. 2004

The Journal of Immunology

109

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“…Normal human fibroblasts were grown to 50% confluence and infected with adenovirus-encoding CTGF as described previously (26). Cells were infected with 500 viral particles per cell.…”

Section: Methodsmentioning

confidence: 99%

Iloprost suppresses connective tissue growth factor production in fibroblasts and in the skin of scleroderma patients

Stratton¹,

Xu²,

Martini³

et al. 2001

J. Clin. Invest.

156

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Patients with scleroderma receiving Iloprost as a treatment for severe Raynaud's phenomenon report a reduction in skin tightness, suggesting that this drug inhibits skin fibrosis. Connective tissue growth factor (CTGF), a recently described profibrotic cytokine, acts downstream and in concert with TGF-β to stimulate the fibrotic process and is involved in the fibrosis seen in scleroderma. Here we show that Iloprost, acting by elevation of cAMP, blocks the induction of CTGF and the increase in collagen synthesis in fibroblasts exposed to TGF-β. The potency of Iloprost with respect to suppression of CTGF far exceeds that of other prostanoid receptor agonists, suggesting that its effect is mediated by the prostacyclin receptor IP. By sampling dermal interstitial fluid using a suction blister device, we show that CTGF levels are greatly elevated in the dermis of scleroderma patients compared with healthy controls and that Iloprost infusion causes a marked decrease in dermal CTGF levels. These studies suggest that Iloprost could be reducing the level of a key profibrotic cytokine in scleroderma patients and that endogenous production of eicosanoids may limit the fibrotic response to TGF-β.

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“…It has been reported to have mitogenic activity (17) and to mediate cell adhesion (18), angiogenesis (19), increased cell migration (20,21) and cell survival (22), induction of apoptosis (23), and regulation of gene expression (17,24 -27). Its expression in mesangial cells is induced by exposure to high glucose or to TGF-␤, and it mediates some of the biologic effects of the latter (27).…”

mentioning

confidence: 99%

Connective Tissue Growth Factor and Regulation of the Mesangial Cell Cycle

Abdel-Wahab

Weston

Roberts

et al. 2002

Journal of the American Society of Nephrology

108

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Abstract. Connective tissue growth factor (CTGF) is now considered to be one of the important driver molecules for the pathogenesis of diabetic nephropathy (DN) and possibly many other fibrotic disorders. However, the molecular mechanisms by which CTGF functions remain to be established. In an attempt to define these mechanisms, this study was designed to investigate whether CTGF has any effect on the cell cycle of human mesangial cells (HMC), which are known to undergo hypertrophy in DN. This report provides the first evidence that CTGF is a hypertrophic factor for HMC. CTGF stimulates HMC to actively enter the G 1 phase from G 0 , but they do not then progress further through the cell cycle. The molecular mechanisms underlying this G 1 phase arrest appear to be due to the induction of the cyclin-dependent kinase inhibitors (CDKI) p15 INK4

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Profiling of genes which are differentially expressed in mouse liver in response to adenoviral vectors and delivered genes

Cited by 32 publications

References 27 publications

Plasmacytoid Dendritic Cell Recruitment by Immobilized CXCR3 Ligands

Plasmacytoid Dendritic Cell Recruitment by Immobilized CXCR3 Ligands

Iloprost suppresses connective tissue growth factor production in fibroblasts and in the skin of scleroderma patients

Connective Tissue Growth Factor and Regulation of the Mesangial Cell Cycle

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