ArticleCell death discovery2026
miR-205a mediated suppression of CDH11 disrupts Wnt/β-catenin signaling and impairs chondrocyte differentiation.
Article in Cell death discovery, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
10 authors.
Funding
Abstract
The precise regulation of chondrocyte differentiation is critical for endochondral ossification, and its disruption underlies a spectrum of skeletal diseases. While the Wnt/β-catenin signaling pathway is a well-established master regulator of skeletal development, its precise regulation during chondrogenesis remains incompletely understood. Here, we identify a novel regulatory axis centered on microRNA-205a and its target, the adhesion molecule Cadherin-11 (CDH11), in avian embryonic models. We demonstrate that CDH11 functions as a positive regulator of chondrocyte differentiation by promoting Wnt/β-catenin signaling. Conversely, miR-205a acts as a potent endogenous inhibitor of this process. Through dual-luciferase reporter assays, we confirm that miR-205a directly binds to the 3'UTR of CDH11 mRNA. Functional studies revealed that miR-205a overexpression suppresses chondrogenesis by downregulating CDH11, thereby inhibiting the Wnt/β-catenin pathway and key chondrogenic markers like Runx2 and BMP2. Silencing miR-205a or overexpressing CDH11 produced the opposite effect, promoting the differentiation program. Critically, rescue experiments using a Wnt/β-catenin pathway agonist substantiated that miR-205a exerts its inhibitory effects primarily through modulating this pathway. Our findings delineate a conserved miR-205a/CDH11/Wnt-β-catenin regulatory circuit that is essential for chondrocyte differentiation, offering fundamental new insights into the molecular etiology of cartilage development and its associated disorders.
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Registered trials
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