Loss of tumor necrosis factor alpha potentiates transforming growth factor beta-mediated pathogenic tissue response during wound healing. - Wikidata - wikimedia - TriplyDB

Loss of tumor necrosis factor alpha potentiates transforming growth factor beta-mediated pathogenic tissue response during wound healing.

Loss of tumor necrosis factor alpha potentiates transforming growth factor beta-mediated pathogenic tissue response during wound healing.

http://www.wikidata.org/entity/Q35088370

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Bone marrow-derived cells in ocular neovascularization: contribution and mechanisms Hypertrophic scar formation following burns and trauma: new approaches to treatment A short-term treatment with tumor necrosis factor-alpha enhances stem cell phenotype of human dental pulp cells.Significance of lipid mediators in corneal injury and repair.Adipocyte inflammation is essential for healthy adipose tissue expansion and remodeling Therapeutic potential of trichostatin A to control inflammatory and fibrogenic disorders of the ocular surface.Dependence of resolvin-induced increases in corneal epithelial cell migration on EGF receptor transactivation TRPV1 involvement in inflammatory tissue fibrosis in mice Decreasing TNF-alpha results in less fibrosis and earlier resolution of granulomatous experimental autoimmune thyroiditis.Corneal Wound Healing Requires IKB kinase β Signaling in Keratocytes Suppression of In Vivo Neovascularization by the Loss of TRPV1 in Mouse Cornea.Loss of TRPV4 Function Suppresses Inflammatory Fibrosis Induced by Alkali-Burning Mouse Corneas Moxifloxacin modifies corneal fibroblast-to-myofibroblast differentiation Sex steroids and cutaneous wound healing: the contrasting influences of estrogens and androgens.Transforming growth factor beta1-mediated activation of the smooth muscle alpha-actin gene in human pulmonary myofibroblasts is inhibited by tumor necrosis factor-alpha via mitogen-activated protein kinase kinase 1-dependent induction of the Egr-1 t Mediators of neovascularization and the hypoxic cornea.Role of platelet-activating factor in cell death signaling in the cornea: A review.Current concepts in scar evolution and control.Cellular/extracellular matrix cross-talk in scar evolution and control.The impact of peri-operative anti-TNF treatment on anastomosis-related complications in Crohn's disease patients. A critical review.Interferon Gamma-treated Dental Pulp Stem Cells Promote Human Mesenchymal Stem Cell Migration In Vitro Macrophage physiology in the eye.TGF-β induction of FGF-2 expression in stromal cells requires integrated smad3 and MAPK pathways.Impaired Healing of a Cutaneous Wound in an Inducible Nitric Oxide Synthase-Knockout Mouse.Tumor necrosis factor-α inhibits transforming growth factor-β-stimulated myofibroblastic differentiation and extracellular matrix production in human gingival fibroblasts.Ocular surface alkali injury damages meibomian glands in mice.Loss of tenascin X gene function impairs injury-induced stromal angiogenesis in mouse corneas.TRPA1 is required for TGF-β signaling and its loss blocks inflammatory fibrosis in mouse corneal stroma.Impaired cornea wound healing in a tenascin C-deficient mouse model.Tumor necrosis factor alpha derived from classically activated "M1" macrophages reduces interstitial cell of Cajal numbers.

P2860

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P2860

Loss of tumor necrosis factor alpha potentiates transforming growth factor beta-mediated pathogenic tissue response during wound healing.

http://www.wikidata.org/entity/Q35088370

description

2006 nî lūn-bûn

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2006 թուականի Յունիսին հրատարակուած գիտական յօդուած

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2006年の論文

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Loss of tumor necrosis factor ...... response during wound healing.

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Loss of tumor necrosis factor ...... response during wound healing.

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Loss of tumor necrosis factor ...... response during wound healing.

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Loss of tumor necrosis factor ...... response during wound healing.

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Loss of tumor necrosis factor ...... response during wound healing.

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The American Journal of Pathology

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Loss of tumor necrosis factor ...... response during wound healing.

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Akira Ooshima

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Kathleen C Flanders

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Kazuo Ikeda

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Osamu Yamanaka

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Yuji Nakajima

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P2860

Tumor necrosis factor alpha suppresses the induction of connective tissue growth factor by transforming growth factor-beta in normal and scleroderma fibroblasts

Tumor necrosis factor-alpha inhibits transforming growth factor-beta /Smad signaling in human dermal fibroblasts via AP-1 activation

Smad-dependent and Smad-independent pathways in TGF-beta family signalling

Myofibroblasts and mechano-regulation of connective tissue remodelling

Therapeutic effect of topical administration of SN50, an inhibitor of nuclear factor-kappaB, in treatment of corneal alkali burns in mice

TGFbeta2 in corneal morphogenesis during mouse embryonic development

Mice lacking Smad3 show accelerated wound healing and an impaired local inflammatory response

Infliximab and methotrexate in the treatment of rheumatoid arthritis. Anti-Tumor Necrosis Factor Trial in Rheumatoid Arthritis with Concomitant Therapy Study Group

Transcriptional control by the TGF-beta/Smad signaling system

TGF-beta signaling and the fibrotic response

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