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http://dx.doi.org/10.1051/medsci/200521121034DOI Listing

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Article Synopsis
  • The administration of intermittent parathyroid hormone (iPTH) stimulates bone formation by regulating the expression of key enzymes like PHOSPHO1, which is crucial for bone mineralization.
  • In experiments with cultured osteoblasts, PHOSPHO1 expression was significantly inhibited after a few cycles of iPTH, while other enzymes like Alpl required more cycles for similar effects.
  • In vivo studies showed that iPTH-treated wild-type mice had enhanced bone volume and mineralization markers, whereas mice lacking PHOSPHO1 did not exhibit these anabolic responses, indicating the importance of PHOSPHO1 in the bone-building effects of iPTH.
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Beneficial roles of the AhR ligand FICZ on the regenerative potentials of BMSCs and primed cartilage templates.

RSC Adv

April 2022

The State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST), Key Laboratory of Oral Biomedicine Ministry of Education, School and Hospital of Stomatology, Wuhan University 237 Luoyu Road Wuhan 430079 China +86 27 87873260 +86 27 87686318.

Bone marrow-derived mesenchymal stem cells (BMSCs) are commonly used seed cells, and BMSC-derived primed cartilage templates have been shown to achieve bone regeneration in bone tissue engineering. Aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor involved in various cellular processes such as osteogenesis and immune regulation. This study investigated the effects of the AhR endogenous ligand 6-formyl (3,2-) carbazole (FICZ) on the behavior of BMSCs and cartilage templates as well as the possible underlying molecular mechanisms.

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Osteogenesis imperfecta (OI) is a bone fragility disorder that is usually caused by mutations affecting collagen type I. We compared the calvaria bone tissue transcriptome of male 10-week-old heterozygous Jrt ( mutation) and homozygous mice ( mutation) to their respective littermate results. We found that Jrt and mice shared 185 differentially expressed genes (upregulated: 106 genes; downregulated: 79 genes).

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In chronic kidney disease (CKD), hyperphosphatemia is a key factor promoting medial vascular calcification, a common complication associated with cardiovascular events and high mortality. Vascular calcification involves osteo-/chondrogenic transdifferentiation of vascular smooth muscle cells (VSMCs), but the complex signaling events inducing pro-calcific pathways are incompletely understood. The present study investigated the role of acid sphingomyelinase (ASM)/ceramide as regulator of VSMC calcification.

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Neutral Sphingomyelinase 2 (SMPD3) Deficiency in Mice Causes Chondrodysplasia with Unimpaired Skeletal Mineralization.

Am J Pathol

September 2019

Institute of Biomechanics and Orthopedics, German Sport University Cologne, Cologne Center for Musculoskeletal Biomechanics, Faculty of Medicine, University of Cologne, Cologne, Germany.

SMPD3 deficiency in the neutral sphingomyelinase (Smpd3) mouse results in a novel form of juvenile dwarfism, suggesting smpd3 is a polygenetic determinant of body height. SMPD3 controls homeostasis of the sphingomyelin cycle in the Golgi compartment, essential for membrane remodeling, initiating multiform vesicle formation and transport in the Golgi secretory pathway. Using the unbiased Smpd3 genetic model, this study shows that the perturbed Golgi secretory pathway of chondrocytes of the epiphyseal growth zone leads to dysproteostasis, skeletal growth inhibition, malformation, and chondrodysplasia, but showed unimpaired mineralization in primary and secondary enchondral ossification centers.

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