Scavenger receptor class B, type I (Scarb1) deficiency promotes osteoblastogenesis but stunts terminal osteocyte differentiation.

Scavenger receptor class B type I (SR-BI), the Scarb1 gene product, is a high-density lipoprotein (HDL) receptor which was shown to influence bone metabolism. Its absence in mice is associated with alterations of the glucocorticoid/adrenocorticotropic hormone axis, and translated in high bone mass and enhanced bone formation. Since the cellular alterations underlying the enhanced bone formation remain unknown, we investigated Scarb1-deficient marrow stromal cells (MSC) behavior in vitro.

Low-bone-mass phenotype of deficient mice for the cluster of differentiation 36 (CD36).

Bone tissue is continuously remodeled by bone cells and maintenance of its mass relies on the balance between the processes of resorption and formation. We have reported the expression of numerous scavenger receptors, namely scavenger receptor (SR) class B type I and II (SR-BI and SR-BII), and CD36, in bone-forming osteoblasts but their physiological roles in bone metabolism are still unknown. To unravel the role of CD36 in bone metabolism, we determined the bone phenotype of CD36 knockout (CD36KO) mice and characterized the cell functions of osteoblasts lacking CD36.

Expression of macrophage migration inhibitory factor by osteoblastic cells: protection against cadmium toxicity.

Exposition to cadmium (Cd) has been linked to bone metabolism alterations and occurrence of osteoporosis. Despite its known renal toxicity which indirectly disrupts bone metabolism through impairment of vitamin D synthesis, increasing evidence argues for the direct action of Cd on bone-forming osteoblasts. Indeed, accumulation of Cd in osteoblasts and metal-induced cell death has been documented but little is known about the intracellular mechanisms of protection against this stress.

Alterations in bone and erythropoiesis in hemolytic anemia: comparative study in bled, phenylhydrazine-treated and Plasmodium-infected mice.

Sustained erythropoiesis and concurrent bone marrow hyperplasia are proposed to be responsible for low bone mass density (BMD) in chronic hemolytic pathologies. As impaired erythropoiesis is also frequent in these conditions, we hypothesized that free heme may alter marrow and bone physiology in these disorders. Bone status and bone marrow erythropoiesis were studied in mice with hemolytic anemia (HA) induced by phenylhydrazine (PHZ) or Plasmodium infection and in bled mice.

Differential expression of glucose transporters in rabbit placenta: effect of hypercholesterolemia in dams.

Low birth weight is observed in rabbit offspring when maternal hypercholesterolemia is induced during gestation, but the related etiology is still unknown. Glucose is one of the most important substances during fetal development, and defect in glucose supply to fetus was related to pathophysiological mechanisms in intrauterine growth restriction. Thus, the aim of this work was to evaluate the impact of maternal hypercholesterolemia during rabbit gestation on the glucose metabolism and the routing of glucose transporters (SLC2 and SLC5 [previously known as GLUT and SGLT]) in placenta.