Publications by authors named "Morgane Bourmaud"

Article Synopsis
  • Early-onset osteoporosis (EOOP) is linked to specific genetic variants, particularly the V667M variant, which is associated with low bone mineral density (BMD) and an increased risk of fractures.
  • Research included both human patients with the V667M variant and mice with the same mutation, showing that both groups exhibited reduced BMD and impaired bone quality, as well as altered bone structure.
  • Additionally, the study revealed retinal vascular abnormalities in the mutant mice, suggesting a connection between bone health and eye condition related to this genetic variant.
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Osteocytes are mechanosensitive cells that control bone remodeling in response to mechanical loading. To date, specific signaling pathways modulated by mechanical loading in osteocytes are not well understood. Yes associated protein (YAP) and transcriptional coactivator with PDZ-binding motif (TAZ), the main effectors of the Hippo pathway, are reported to play a role in mechanotransduction and during osteoblastogenesis.

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Osteoarthritis is characterized by cartilage loss resulting from the activation of chondrocytes associated with a synovial inflammation. Activated chondrocytes promote an increased secretion of matrix proteases and proinflammatory cytokines leading to cartilage breakdown. Since natural products possess anti-inflammatory properties, we investigated the direct effect of extracts (RIE) in chondrocyte metabolism and cartilage loss.

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Diastrophic dysplasia (DTD) is a recessive chondrodysplasia caused by mutations in the SLC26A2 gene encoding for a sulfate/chloride transporter. When SLC26A2 is impaired intracellular level of sulfate is reduced leading to the synthesis of undersulfated proteoglycans. In normal chondrocytes, the main source of intracellular sulfate is the extracellular uptake through SLC26A2, but a small amount comes from the catabolism of sulfur-containing amino acids and other thiols.

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