ArticleOsteoarthritis and cartilage2015
Early postnatal ablation of the microRNA-processing enzyme, Drosha, causes chondrocyte death and impairs the structural integrity of the articular cartilage.
Article in Osteoarthritis and cartilage, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 38 citations in OpenAlex.
- miRNA-based regulation in growth plate cartilage: mechanisms, targets, and therapeutic potential.Frontiers in endocrinology · 2025Review
- microRNA-124 directly suppresses Nodal and Notch to regulate mesodermal development.Developmental biology · 2023Article
- MicroRNA Signatures in Cartilage Ageing and Osteoarthritis.Biomedicines · 2023Article
- Review
- Ablation of the miRNA cluster 24 in cartilage and osteoblasts impairs bone remodeling.Scientific reports · 2022Article
- Tendon-Specific Dicer Deficient Mice Exhibit Hypoplastic Tendon Through the Downregulation of Tendon-Related Genes and MicroRNAs.Frontiers in cell and developmental biology · 2022Article
- Article
- Review
- Epigenetic Regulation of Skeletal Tissue Integrity and Osteoporosis Development.International journal of molecular sciences · 2020Review
- Exosomal miRNAs in osteoarthritis.Molecular biology reports · 2020Review
- The Transcription Factor-microRNA Regulatory Network during hESC-chondrogenesis.Scientific reports · 2020Article
- Lin28a overexpression reveals the role of Erk signaling in articular cartilage development.Development (Cambridge, England) · 2018Article
- Evidence that miR-146a attenuates aging- and trauma-induced osteoarthritis by inhibiting Notch1, IL-6, and IL-1 mediated catabolism.Aging cell · 2018Article
- Anti-Inflammatory Effects of p-Coumaric Acid, a Natural Compound ofEvidence-based complementary and alternative medicine : eCAM · 2018Article
- MicroRNAs in orthopaedic research: Disease associations, potential therapeutic applications, and perspectives.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2018Review
- MicroRNAs and Autophagy: Fine Players in the Control of Chondrocyte Homeostatic Activities in Osteoarthritis.Oxidative medicine and cellular longevity · 2017Review
- Role of Osterix and MicroRNAs in Bone Formation and Tooth Development.Medical science monitor : international medical journal of experimental and clinical research · 2016Review
- The Role of MicroRNAs and Their Targets in Osteoarthritis.Current rheumatology reports · 2016Review
- Mechanical and IL-1β Responsive miR-365 Contributes to Osteoarthritis Development by Targeting Histone Deacetylase 4.International journal of molecular sciences · 2016Article
- Review
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
objectiveIn growth plate chondrocytes, loss of Dicer, a microRNA (miRNA)-processing enzyme, causes defects in proliferation and differentiation, leading to a lethal skeletal dysplasia. However roles of miRNAs in articular chondrocytes have not been defined in vivo. To investigate the role of miRNAs in articular chondrocytes and to explore the possibility of generating a novel mouse osteoarthritis (OA) model caused by intrinsic cellular dysfunction, we ablated Drosha, another essential enzyme for miRNA biogenesis, exclusively in articular chondrocytes of postnatal mice.
designFirst, to confirm that the essential role of miRNAs in skeletal development, we ablated the miRNA biogenesis pathway by deleting Drosha or DGCR8 in growth plate chondrocytes. Next, to investigate the role of miRNAs in articular cartilage, we deleted Drosha using Prg4-CreER(T) transgenic mice expressing a tamoxifen-activated Cre recombinase (CreER(T)) exclusively in articular chondrocytes. Tamoxifen was injected at postnatal days, 7, 14, 21, and 28 to ablate Drosha.
resultsDeletion of Drosha or DGCR8 in growth plate chondrocytes caused a lethal skeletal defect similar to that of Dicer deletion, confirming the essential role of miRNAs in normal skeletogenesis. Early postnatal Drosha deletion in articular chondrocytes significantly increased cell death and decreased Safranin-O staining. Mild OA-like changes, including surface erosion and cleft formation, were found in male mice at 6 months of age; however such changes in females were not observed even at 9 months of age.
conclusionsEarly postnatal Drosha deficiency induces articular chondrocyte death and can cause a mild OA-like pathology.
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