2 results match your criteria: "Inserm U1132 and university Paris 7[Affiliation]"
N-acetylcysteine treatment ameliorates the skeletal phenotype of a mouse model of diastrophic dysplasia.
Hum Mol Genet
October 2015
Department of Molecular Medicine, Unit of Biochemistry and
Diastrophic dysplasia (DTD) is a recessive chondrodysplasia caused by mutations in SLC26A2, a cell membrane sulfate-chloride antiporter. Sulfate uptake impairment results in low cytosolic sulfate, leading to cartilage proteoglycan (PG) undersulfation. In this work, we used the dtd mouse model to study the role of N-acetyl-l-cysteine (NAC), a well-known drug with antioxidant properties, as an intracellular sulfate source for macromolecular sulfation.
View Article and Find Full Text PDFLoss of sclerostin promotes osteoarthritis in mice via β-catenin-dependent and -independent Wnt pathways.
Arthritis Res Ther
February 2015
Inserm U1132 and university Paris 7, hopital Lariboisiere, 2 rue Ambroise Pare, 75010, Paris, France.
Introduction: Sclerostin is a Wnt inhibitor produced by osteocytes that regulates bone formation. Because bone tissue contributes to the development of osteoarthritis (OA), we investigated the role of sclerostin in bone and cartilage in a joint instability model in mice.
Methods: Ten-week-old SOST-knockout (SOST-KO) and wild-type (WT) mice underwent destabilization of the medial meniscus (DMM).