title: miR-29a modulates tumor necrosis factor-α-induced osteogenic inhibition by targeting Wnt antagonists.
abstract: We previously found that miR-29a was significantly downregulated in Ankylosing spondylitis (AS) patients, a chronic inflammatory disease associated with bone metabolic disorder, however, the underlying mechanism remains unclear. In this study, we demonstrated that miR-29a regulates tumor necrosis factor-α (TNF-α) mediated bone loss mainly by targeting DKK1 and GSK3β, thus activating the Wnt/β-catenin pathway. Our findings may provide new insight into the pathogenesis of the bone metabolism disorder in inflammation environment and provide promising therapeutic target.
authors.affiliation: Department of Rheumatology, Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510630, Guangdong, China.
authors.forename: Caixia
authors.initials: C
authors.lastname: Li
authors.forename: Pingping
authors.initials: P
authors.lastname: Zhang
authors.forename: Jieruo
authors.initials: J
authors.lastname: Gu
mesh_terms: D000880:Anthraquinones; D015153:Blotting, Western; D001862:Bone Resorption / Q000378:metabolism*; D038362:Glycogen Synthase Kinase 3 / Q000378:metabolism; D000071679:Glycogen Synthase Kinase 3 beta; D006801:Humans; D036341:Intercellular Signaling Peptides and Proteins / Q000378:metabolism; D008156:Luciferases; D035683:MicroRNAs / Q000378:metabolism*; D009841:Oligonucleotides / Q000235:genetics; D060888:Real-Time Polymerase Chain Reaction; D013167:Spondylitis, Ankylosing / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*; D060449:Wnt Signaling Pathway / Q000502:physiology*
chemical_list: D000880:Anthraquinones; C501126:DKK1 protein, human; D036341:Intercellular Signaling Peptides and Proteins; C532045:MIRN29a microRNA, human; D035683:MicroRNAs; D009841:Oligonucleotides; D014409:Tumor Necrosis Factor-alpha; C010078:alizarin; D008156:Luciferases; C000605506:GSK3B protein, human; D000071679:Glycogen Synthase Kinase 3 beta; D038362:Glycogen Synthase Kinase 3
keywords: TNF-α; Wnt antagonists; miR-29a