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Suppressor of cytokine signaling-1 is essential for suppressing dendritic cell activation and systemic autoimmunity.
It is found that SOCS1-deficient dendritic cells (DCs) were also hyperresponsive to interferon-gamma and interleukin-4, and efficiently stimulated B cell proliferation in vitro and autoantibody production in vivo.
Regulation of Cytokine-Induced Nitric Oxide Synthesis by Asymmetric Dimethylarginine: Role of Dimethylarginine Dimethylaminohydrolase
The results indicate two mechanisms of IL-1&bgr;–induced NO synthesis: the direct stimulation of the expression of iNOS and the indirect stimulation ofiNOS activity by upregulating DDAH and reducing ADMA.
Molecular mechanism for elevation of asymmetric dimethylarginine and its role for hypertension in chronic kidney disease.
Investigation of the molecular mechanism for the elevation of ADMA levels in CKD using a rat remnant kidney model suggests that substitution of DDAH protein or enhancement of its activity may become a novel therapeutic strategy for the treatment of hypertension-related vascular injury in CKd.
Periostin, a matricellular protein, plays a role in the induction of chemokines in pulmonary fibrosis.
It is concluded that periostin plays a unique role as an inducer of chemokines to recruit neutrophils and macrophages important in the process of pulmonary fibrosis in BLM-administered model mice, suggesting a therapeutic potential for periastin in IPF and drug-induced ILD.
IFNγ-dependent, spontaneous development of colorectal carcinomas in SOCS1-deficient mice
Data strongly suggest that SOCS1 is a unique antioncogene which prevents chronic inflammation-mediated carcinogenesis by regulation of the IFNγ/STAT1 pathways.
Interleukin-18 production and pulmonary function in COPD
Overproduction of interleukin-18 in the lungs may be involved in the pathogenesis of chronic obstructive pulmonary disease.
Role of proinflammatory cytokines IL-18 and IL-1beta in bleomycin-induced lung injury in humans and mice.
Evidence is provided for an important role of IL-1beta and IL-18 in chemotherapy-induced lung injury in patients with bleomycin-induced lethal lung injury.
AGEs activate mesangial TGF-beta-Smad signaling via an angiotensin II type I receptor interaction.
It is suggested that AGE-RAGE-mediated ROS generation activates TGF-beta-Smad signaling and subsequently induces mesangial cell hypertrophy and fibronectin synthesis by autocrine production of Ang II, which may provide an important link between metabolic and haemodynamic factors in promoting the development and progression of diabetic nephropathy.
Redox-active protein thioredoxin prevents proinflammatory cytokine- or bleomycin-induced lung injury.
It is suggested that TRX modulates pulmonary inflammatory responses and acts to prevent lung injury, and may have clinical benefits in human ILD, including lung fibrosis, for which no effective therapeutic strategy currently exists.
Advanced Glycation End‐Products Attenuate Human Mesenchymal Stem Cells and Prevent Cognate Differentiation Into Adipose Tissue, Cartilage, and Bone
  • S. Kume, S. Kato, +6 authors K. Nagata
  • Biology, Medicine
    Journal of bone and mineral research : the…
  • 1 September 2005
AGEs inhibited the proliferation of MSCs, induced apoptosis, and prevented cognate differentiation into adipose tissue, cartilage, and bone, suggesting a deleterious effect of AGEs in the pathogenesis of musculoskeletal disorders in aged and diabetic patients.