Complement C3a and C5a modulate osteoclast formation and inflammatory response of osteoblasts in synergism with IL-1β. - Wikidata - wikimedia - TriplyDB

Complement C3a and C5a modulate osteoclast formation and inflammatory response of osteoblasts in synergism with IL-1β.

Complement C3a and C5a modulate osteoclast formation and inflammatory response of osteoblasts in synergism with IL-1β.

http://www.wikidata.org/entity/Q35172785

about

Mesenchymal Stem Cells after Polytrauma: Actor and Target Complement activation in the context of stem cells and tissue repair Genetic and intervention studies implicating complement C3 as a major target for the treatment of periodontitis.Identification of candidate genes for myeloma-induced osteocyte death based on microarray data Early intra-articular complement activation in ankle fractures.A Memory of Early Life Physical Activity Is Retained in Bone Marrow of Male Rats Fed a High-Fat Diet.Mesenchymal stromal cells engage complement and complement receptor bearing innate effector cells to modulate immune responses Mesenchymal stem cells engineered to inhibit complement-mediated damage.Complement C3 and C5 deficiency affects fracture healing The immunological contribution to heterotopic ossification disorders.Prophylactic and therapeutic treatment with a synthetic analogue of a parasitic worm product prevents experimental arthritis and inhibits IL-1β production via NRF2-mediated counter-regulation of the inflammasome Human Monocyte-Derived Osteoclasts Are Targeted by Staphylococcal Pore-Forming Toxins and Superantigens.Osteoblast-specific overexpression of complement receptor C5aR1 impairs fracture healing.Neutrophils orchestrate their own recruitment in murine arthritis through C5aR and FcγR signaling.Deletion of the membrane complement inhibitor CD59a drives age and gender-dependent alterations to bone phenotype in mice.Abrogated RANKL expression in properdin-deficient mice is associated with better outcome from collagen-antibody-induced arthritis.Efficient production of multi-modified pigs for xenotransplantation by 'combineering', gene stacking and gene editing.Biomarkers of inflammation and innate immunity in atrophic nonunion fracture.Inhibition of Complement Retards Ankylosing Spondylitis Progression The complement system is activated in synovial fluid from subjects with knee injury and from patients with osteoarthritis.C5aR inhibition in the early inflammatory phase does not affect bone regeneration in a model of uneventful fracture healing A bone substitute with high affinity for vitamin D-binding protein--relationship with niche of osteoclasts.Complement-triggered pathways orchestrate regenerative responses throughout phylogenesis.Urokinase receptor mediates osteogenic differentiation of mesenchymal stem cells and vascular calcification via the complement C5a receptor.Acute murine antigen-induced arthritis is not affected by disruption of osteoblastic glucocorticoid signalling.Pathways for bone loss in inflammatory disease.Regenerative medicine: prospects for the treatment of inflammatory bowel disease.Bone and the innate immune system.Emerging therapeutic targets for osteoporosis treatment.Foreign Body Reaction to Biomaterials: On Mechanisms for Buildup and Breakdown of Osseointegration.Identification of Hip BMD Loss and Fracture Risk Markers Through Population-Based Serum Proteomics.C5L2 Receptor Represses Brain-Derived Neurotrophic Factor Secretion in Lipoteichoic Acid-Stimulated Pulp Fibroblasts.Nerve Growth Factor Secretion From Pulp Fibroblasts is Modulated by Complement C5a Receptor and Implied in Neurite Outgrowth.Pulp Fibroblasts Control Nerve Regeneration through Complement Activation.Osteoimmunology: memorandum for rheumatologists.Flesh-eating Streptococcus pyogenes triggers the expression of receptor activator of nuclear factor-κB ligand.Rapid-onset clinical and mechanistic effects of anti-C5aR treatment in the mouse collagen-induced arthritis model.Treatment with anti-C5aR mAb leads to early-onset clinical and mechanistic effects in the murine delayed-type hypersensitivity arthritis model.Clinical, cellular, microscopic, and ultrastructural studies of a case of fibrogenesis imperfecta ossium.Complement receptors C5aR1 and C5aR2 act differentially during the early immune response after bone fracture but are similarly involved in bone repair.

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Complement C3a and C5a modulate osteoclast formation and inflammatory response of osteoblasts in synergism with IL-1β.

http://www.wikidata.org/entity/Q35172785

description

2011 nî lūn-bûn

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2011 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած

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2011 թվականի սեպտեմբերին հրատարակված գիտական հոդված

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2011年の論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年论文

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Complement C3a and C5a modulat ...... lasts in synergism with IL-1β.

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Complement C3a and C5a modulat ...... lasts in synergism with IL-1β.

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Complement C3a and C5a modulat ...... lasts in synergism with IL-1β.

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Complement C3a and C5a modulat ...... lasts in synergism with IL-1β.

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Journal of Cellular Biochemistry

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Complement C3a and C5a modulat ...... lasts in synergism with IL-1β.

@en

P2093

Astrid Liedert

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Ludwika Kreja

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Marion Schneider

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Philipp Schoengraf

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Rolf E Brenner

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Sebastian Kandert

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Stefan Recknagel

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P2860

Identification of subpopulations with characteristics of mesenchymal progenitor cells from human osteoarthritic cartilage using triple staining for cell surface markers

Multilineage potential of adult human mesenchymal stem cells

Minimal criteria for defining multipotent mesenchymal stromal cells. The International Society for Cellular Therapy position statement

Modulation of C3a activity: internalization of the human C3a receptor and its inhibition by C5a

Osteoimmunology: shared mechanisms and crosstalk between the immune and bone systems

Osteoclast differentiation and activation

Complement: a key system for immune surveillance and homeostasis

Complement regulators and inhibitory proteins.

Membrane complement regulatory proteins: insight from animal studies and relevance to human diseases.

Efficient osteoclast differentiation requires local complement activation.

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2594-2605

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10.1002/JCB.23186

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9

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112

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John D. Lambris

Markus S Huber-Lang

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2011-09-01T00:00:00Z

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230228881

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21598302

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3158833

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