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The microRNAs miR-204 and miR-211 maintain joint homeostasis and protect against osteoarthritis progression
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The microRNAs miR-204 and miR-211 maintain joint homeostasis and protect against osteoarthritis progression
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Journal Article
The microRNAs miR-204 and miR-211 maintain joint homeostasis and protect against osteoarthritis progression
2019
Overview
Osteoarthritis (OA) is a common, painful disease. Currently OA is incurable, and its etiology largely unknown, partly due to limited understanding of OA as a whole-joint disease. Here we report that two homologous microRNAs,
miR-204
and
miR-211
, maintain joint homeostasis to suppress OA pathogenesis. Specific knockout of
miR-204/-211
in mesenchymal progenitor cells (MPCs) results in Runx2 accumulation in multi-type joint cells, causing whole-joint degeneration. Specifically,
miR-204/-211
loss-of-function induces matrix-degrading proteases in articular chondrocytes and synoviocytes, stimulating articular cartilage destruction. Moreover,
miR-204
/
-211
ablation enhances NGF expression in a Runx2-dependent manner, and thus hyper-activates Akt signaling and MPC proliferation, underlying multiplex non-cartilaginous OA conditions including synovial hyperplasia, osteophyte outgrowth and subchondral sclerosis. Importantly,
miR-204
/-
211
-deficiency-induced OA is largely rescued by Runx2 insufficiency, confirming the
miR-204
/-
211-
Runx2 axis. Further, intraarticular administration of
miR-204
-expressing adeno-associated virus significantly decelerates OA progression. Collectively,
miR-204
/
-211
are essential in maintaining healthy homeostasis of mesenchymal joint cells to counteract OA pathogenesis.
Osteoarthritis involves whole-joint tissue degeneration. Here, the authors show that miR-204 and miR-211 in mesenchymal joint cells regulate their proliferation, catabolic and osteogenic responses, and that disease progression is ameliorated by intra-articular miR-204 delivery in mice.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
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/ Ablation
/ Animals
/ Core Binding Factor Alpha 1 Subunit - genetics
/ Core Binding Factor Alpha 1 Subunit - metabolism
/ Etiology
/ Homology
/ Humanities and Social Sciences
/ Mesenchymal Stem Cells - physiology
/ Mice
/ miRNA
/ Peptide Hydrolases - genetics
/ Peptide Hydrolases - metabolism
/ Science
/ Viruses
