ArticleCell death & disease2016
AIMP1 downregulation restores chondrogenic characteristics of dedifferentiated/degenerated chondrocytes by enhancing TGF-β signal.
Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Microcavitary Alginate Hydrogel Reverses Chondrocyte Dedifferentiation via Temporal Modulation of the p53 Pathway.Annals of biomedical engineering · 2026Article
- AIMP1: multifunctional regulator in physiology and pathology with therapeutic implications.PeerJ · 2025Review
- Brachyury promotes extracellular matrix synthesis through transcriptional regulation of Smad3 in nucleus pulposus.American journal of physiology. Cell physiology · 2024Article
- The mARS complex: a critical mediator of immune regulation and homeostasis.Frontiers in immunology · 2024Review
- Identification of a differential metabolite-based signature in patients with late-stage knee osteoarthritis.Osteoarthritis and cartilage open · 2022Article
- Dedifferentiation alters chondrocyte nuclear mechanics during in vitro culture and expansion.Biophysical journal · 2022Article
- SPRY4 acts as an indicator of osteoarthritis severity and regulates chondrocyte hypertrophy and ECM protease expression.NPJ Regenerative medicine · 2021Article
- Three-dimensional (3D) hydrogel serves as a platform to identify potential markers of chondrocyte dedifferentiation by combining RNA sequencing.Bioactive materials · 2021Article
- Strategies to Modulate the Redifferentiation of Chondrocytes.Frontiers in bioengineering and biotechnology · 2021Review
- Roles of aminoacyl-tRNA synthetase-interacting multi-functional proteins in physiology and cancer.Cell death & disease · 2020Review
- Emerging potential of gene silencing approaches targeting anti-chondrogenic factors for cell-based cartilage repair.Cellular and molecular life sciences : CMLS · 2017Review
- Targeting the reorganization of F-actin for cell-based implantation cartilage repair therapies.Differentiation; research in biological diversityReview
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dedifferentiation and degeneration of chondrocytes critically influences the efficiency of cartilage repair. One of the causes is the defect of transforming growth factor (TGF)-β signaling that promotes chondrogenic differentiation and degeneration. In the present study, we found that aminoacyl-tRNA synthetase-interacting multifunctional protein 1 (AIMP1) negatively regulates TGF-β signaling via interactions with Smad2 and Smad3 in immunoprecipitation assay and luciferase assay. In addition, we observed that the AIMP1 expression level was significantly increased in osteoarthritis (OA) patient-derived degenerated chondrocytes compared with healthy control. So, we hypothesized that downregulation of AIMP1 using small-interfering RNA (siRNA) technology in dedifferentiated (collected at passage #6) and degenerated (obtained from OA-affected areas) chondrocytes could lead to recover TGF-β signaling in both chondrocytes. Indeed, AIMP1 downregulation restored TGF-β signaling by promoting phosphorylation of Smad2 and Smad3, which shows redifferentiated characteristics in both dedifferentiated and degenerated chondrocytes. Additionally, implantation analyses using in vivo mouse model clearly showed that AIMP1 downregulation resulted in the increased chondrogenic potential as well as the enhanced cartilage tissue formation in both dedifferentiated and degenerated chondrocytes. Histological analyses clarified that AIMP1 downregulation increased expression levels of collagen type II (Col II) and aggrecan, but not Col I expression. Taken together, these data indicate that AIMP1 downregulation using siRNA is a novel tool to restore TGF-β signaling and thereby increases the chondrogenic potential of dedifferentiated/degenerated chondrocytes, which could be further developed as a therapeutic siRNA to treat OA.
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