ArticleThe Journal of biological chemistry2012
Matrix disruptions, growth, and degradation of cartilage with impaired sulfation.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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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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Who cites it
17 citing papers in PubMed, 30 citations in OpenAlex.
- Review
- Article
- Large-scale integrative analysis of juvenile idiopathic arthritis for new insight into its pathogenesis.Arthritis research & therapy · 2024Article
- Targeting FGFR3 signaling and drug repurposing for the treatment of SLC26A2-related chondrodysplasia in mouse model.Journal of orthopaedic translation · 2024Article
- Cryopreserved, Thin, Laser-Etched Osteochondral Allograft maintains the functional components of articular cartilage after 2 years of storage.Journal of orthopaedic surgery and research · 2020Article
- Suppressing UPR-dependent overactivation of FGFR3 signaling ameliorates SLC26A2-deficient chondrodysplasias.EBioMedicine · 2019Article
- Microscale mapping of extracellular matrix elasticity of mouse joint cartilage: an approach to extracting bulk elasticity of soft matter with surface roughness.Soft matter · 2018Article
- Article
- Sulfated hydrogel matrices direct mitogenicity and maintenance of chondrocyte phenotype through activation of FGF signaling.Advanced functional materials · 2016Article
- Altered signaling in the G1 phase deregulates chondrocyte growth in a mouse model with proteoglycan undersulfation.Journal of cellular biochemistry · 2014Article
- FACE analysis as a fast and reliable methodology to monitor the sulfation and total amount of chondroitin sulfate in biological samples of clinical importance.Molecules (Basel, Switzerland) · 2014Article
- Multiple roles of the SO4(2-)/Cl-/OH- exchanger protein Slc26a2 in chondrocyte functions.The Journal of biological chemistry · 2014Article
- Current understanding on the molecular basis of chondrogenesis.Clinical pediatric endocrinology : case reports and clinical investigations : official journal of the Japanese Society for Pediatric Endocrinology · 2014Review
- Regulatory mechanisms for the development of growth plate cartilage.Cellular and molecular life sciences : CMLS · 2013Review
- Canine chondrodysplasia caused by a truncating mutation in collagen-binding integrin alpha subunit 10.PloS one · 2013Article
- Ageing affects chondroitin sulfates and their synthetic enzymes in the intervertebral disc.Signal transduction and targeted therapyArticle
- Makings of a brittle bone: Unexpected lessons from a low protein diet study of a mouse OI model.Matrix biology : journal of the International Society for Matrix BiologyArticle
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Diastrophic dysplasia (DTD) is an incurable recessive chondrodysplasia caused by mutations in the SLC26A2 transporter responsible for sulfate uptake by chondrocytes. The mutations cause undersulfation of glycosaminoglycans in cartilage. Studies of dtd mice with a knock-in Slc26a2 mutation showed an unusual progression of the disorder: net undersulfation is mild and normalizing with age, but the articular cartilage degrades with age and bones develop abnormally. To understand underlying mechanisms, we studied newborn dtd mice. We developed, verified and used high-definition infrared hyperspectral imaging of cartilage sections at physiological conditions, to quantify collagen and its orientation, noncollagenous proteins, and chondroitin chains, and their sulfation with 6-μm spatial resolution and without labeling. We found that chondroitin sulfation across the proximal femur cartilage varied dramatically in dtd, but not in the wild type. Corresponding undersulfation of dtd was mild in most regions, but strong in narrow articular and growth plate regions crucial for bone development. This undersulfation correlated with the chondroitin synthesis rate measured via radioactive sulfate incorporation, explaining the sulfation normalization with age. Collagen orientation was reduced, and the reduction correlated with chondroitin undersulfation. Such disorientation involved the layer of collagen covering the articular surface and protecting cartilage from degradation. Malformation of this layer may contribute to the degradation progression with age and to collagen and proteoglycan depletion from the articular region, which we observed in mice already at birth. The results provide clues to in vivo sulfation, DTD treatment, and cartilage growth.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.