6/2/2023 0 Comments Kaneva loginSerum elastase inhibitor deficiency and agrl-antitrypsin deficiency in patients with obstructive emphysema. 1 Turino GM, Senior RM, Garg BD, Keller S, Levi MM, Mandl I. ![]() We propose that AAT could be developed for new therapeutic strategies to reduce arthritic pain and repair damaged cartilage. Thus, AAT is endowed with anti-inflammatory, analgesic, and chondroprotective properties that are partially inter-related. In vitro studies using human chondrocytes revealed that SERPINA1 transfection and rAAT protein promoted chondrogenic differentiation through activation of PKA-dependent CREB signaling and inhibition of Wnt/β-catenin pathways. Ex vivo analyses of arthritic joints revealed that AAT promoted transcription of col2a1, acan, and sox9 and downregulated mmp13 and adamts5 gene expression. Intra-articular and systemic administration of AAT reversed joint inflammation, nociception, and cartilage degradation in the KBxN serum and neutrophil elastase models of arthritis. Following an initial identification of α-1-Antitrypsin (AAT) during the resolution phase of acute inflammation, we report here the properties of this protein in the context of cartilage protection, joint inflammation, and associated pain behavior. ![]() ![]() While new treatments have been developed to control joint disease in rheumatoid arthritis, they are partially effective and do not promote structural repair of cartilage.
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