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ماتریس متالوپروتئیناز
, interleukins; iNOS, inducible nitric oxide synthase; LPS, lipopolysaccharide; M-CSF, macrophage colony-stimulating factor; MCP-1/5, monocyte chemoattractant protein-1/5 (CCL2/CCL12); MHCII, major histocompatibility complex class II; MIP- 1α/β, macrophage inflammatory protein-1 alpha/beta (CCL3/CCL4); MNCs, mononuclear cells; MMPs, matrix metalloproteinases; MSCs, mesenchymal stromal cells; NF-κβ, nuclear factor kappa beta; PAMPs, pathogen-associated molecular patterns; PDGF, platelet-derived growth factor; PGE-2, prostaglandin E-2; ROS, reactive oxygen species; TAMs, tumor-associated macrophages; TGF- β1, transforming growth factor beta 1; TNF-α, tumor necrosis factor-alpha; VEGF, vascular endothelial growth factor.
In the beginning of the final remodeling phase, macrophages release matrix metalloproteinases (MMPs) to breakdown the provisional extracellular matrix, and then apoptose so that the skin can mature to its original, non-wounded state (Vannella and Wynn, 2017).
Interferon-gamma differentially regulates monocyte matrix metalloproteinase-1 and−9 through tumor necrosis factor-α and caspase 8.
Macrophages are an important source of chemokines, matrix metalloproteinases (MMPs), and other in- flammatory mediators that drive the initial cellular response following injury (Wynn and Barron, 2010).
Matrix metalloproteinase 12-deficiency augments extracellular matrix degrading metalloproteinases and attenuates IL-13-dependent fibrosis.
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