ArticleThe Journal of biological chemistry2014
Multiple roles of the SO4(2-)/Cl-/OH- exchanger protein Slc26a2 in chondrocyte functions.
Article in The Journal of biological chemistry, 2014. 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, 37 citations in OpenAlex.
- Biallelic variants in SLC26A2 cause multiple epiphyseal dysplasia-4 by disturbing chondrocyte homeostasis.Orphanet journal of rare diseases · 2024Article
- Digital spatial profiling of segmental outflow regions in trabecular meshwork reveals a role for ADAM15.PloS one · 2024Article
- Targeting FGFR3 signaling and drug repurposing for the treatment of SLC26A2-related chondrodysplasia in mouse model.Journal of orthopaedic translation · 2024Article
- SLC26 Anion Transporters.Handbook of experimental pharmacology · 2024Review
- Uremic Toxin-Induced Exosome-like Extracellular Vesicles Contain Enhanced Levels of Sulfated Glycosaminoglycans which Facilitate the Interaction with Very Small Superparamagnetic Iron Oxide Particles.International journal of molecular sciences · 2023Article
- Single-cell transcriptomic atlas of mouse cochlear aging.Protein & cell · 2023Article
- Oxalate secretion is stimulated by a cAMP-dependent pathway in the mouse cecum.Pflugers Archiv : European journal of physiology · 2023Article
- Hypomorphic and dominant-negative impact of truncated SOX9 dysregulates Hedgehog-Wnt signaling, causing campomelia.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Anatomical characteristics and potential gene mutation sites of a familial recurrent patellar dislocation.BMC medical genomics · 2022Article
- Integrated RNA-Seq Analysis Uncovers the Potential Mechanism of the "Kidney Governing Bones" Theory of TCM.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Genomic adaptation of Ethiopian indigenous cattle to high altitude.Frontiers in genetics · 2022Article
- Role of NEAT1/MiR-9-5p/SLC26A2 Pathway on Human Airway Smooth Muscle Cell.Yonsei medical journal · 2021Article
- Review
- The role of NHE3 (Slc9a3) in oxalate and sodium transport by mouse intestine and regulation by cAMP.Physiological reports · 2021Article
- Recessive multiple epiphyseal dysplasia and Stargardt disease in two sisters.Molecular genetics & genomic medicine · 2021Article
- ClAmerican journal of physiology. Cell physiology · 2020Review
- Suppressing UPR-dependent overactivation of FGFR3 signaling ameliorates SLC26A2-deficient chondrodysplasias.EBioMedicine · 2019Article
- A New Look at Causal Factors of Idiopathic Scoliosis: Altered Expression of Genes Controlling Chondroitin Sulfate Sulfation and Corresponding Changes in Protein Synthesis in Vertebral Body Growth Plates.International journal of medical sciences · 2019Article
- Human mesenchymal stem cells induced to differentiate as chondrocytes follow a biphasic pattern of extracellular matrix production.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2018Article
- Loss of the anion exchanger DRA (Slc26a3), or PAT1 (Slc26a6), alters sulfate transport by the distal ileum and overall sulfate homeostasis.American journal of physiology. Gastrointestinal and liver physiology · 2017Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
Mutations in the SO4(2-)/Cl(-)/OH(-) exchanger Slc26a2 cause the disease diastrophic dysplasia (DTD), resulting in aberrant bone development and, therefore, skeletal deformities. DTD is commonly attributed to a lack of chondrocyte SO4(2-) uptake and proteoglycan sulfation. However, the skeletal phenotype of patients with DTD is typified by reduction in cartilage and osteoporosis of the long bones. Chondrocytes of patients with DTD are irregular in size and have a reduced capacity for proliferation and terminal differentiation. This raises the possibility of additional roles for Slc26a2 in chondrocyte function. Here, we examined the roles of Slc26a2 in chondrocyte biology using two distinct systems: mouse progenitor mesenchymal cells differentiated to chondrocytes and freshly isolated mouse articular chondrocytes differentiated into hypertrophic chondrocytes. Slc26a2 expression was manipulated acutely by delivery of Slc26a2 or shSlc26a2 with lentiviral vectors. We demonstrate that slc26a2 is essential for chondrocyte proliferation and differentiation and for proteoglycan synthesis. Slc26a2 also regulates the terminal stage of chondrocyte cell size expansion. These findings reveal multiple roles for Slc26a2 in chondrocyte biology and emphasize the importance of Slc26a2-mediated protein sulfation in cell signaling, which may account for the complex phenotype of DTD.
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