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Induction of matrix protein synthesis in human glomerular mesangial cells by the terminal complement complex.
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1994
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ImmunologyPathologyCollagen Type IvCellular PhysiologyInflammationProtein ExpressionCell SignalingMatrix Protein SynthesisConnective Tissue DiseaseFibrosisProtein FunctionAutoimmune DiseaseSystemic SclerodermaAutoimmunityVascular BiologySclerodermaCell BiologyComplement SystemSignal TransductionAutoantibody ProductionCell-matrix InteractionTerminal Complement ComplexTerminal ComplementCellular BiochemistryMedicineKidney ResearchExtracellular Matrix
Exposure of human glomerular mesangial cells (GMC) in culture to sublytic doses of the terminal complement proteins C5b-8 and C5b-9 caused a transient increase in abundance of mRNA specific for collagen type IV and fibronectin; mRNA of laminin was not affected. Since C5b-9 is found deposited in inflamed or sclerotic areas we propose that stimulation of matrix protein synthesis by C5b-9 might contribute to the development of glomerular sclerosis.