Abstract
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. Weights of CD36KO mice were significantly lower than corresponding wild-type (WT) mice, yet no significant difference was found in femoral nor tibial length between CD36KO and WT mice. Analysis of bone architecture by micro-computed tomography revealed a low bone mass phenotype in CD36KO mice of both genders. Femoral trabecular bone from 1 to 6 month-old CD36KO mice showed lower bone volume, higher trabecular separation and reduced trabeculae number compared to WT mice; similar alterations were noticed for lumbar vertebrae. Plasma levels of osteocalcin (OCN) and N-terminal propeptide of type I procollagen (PINP), two known markers of bone formation, were significantly lower in CD36KO mice than in WT mice, whereas plasma levels of bone resorption markers were similar. Accordingly, histology highlighted lower osteoblast perimeter and reduced bone formation rate. In vitro functional characterization of bone marrow stromal cells and osteoblasts isolated from CD36KO mice showed reduced cell culture expansion and survival, lower gene expression of osteoblastic Runt-related transcription factor 2 (Runx2) and osterix (Osx), as well as bone sialoprotein (BSP) and osteocalcin (OCN). Our results indicate that CD36 is mandatory for adequate bone metabolism, playing a role in osteoblast functions ensuring adequate bone formation.
Highlights
Bone is a dynamic tissue that undergoes continual remodeling through the coordinated processes of bone resorption and formation
We have recently reported the expression of Cluster of Differentiation 36 (CD36) by osteoblasts [10] and we took advantage of the CD36 knockout (CD36KO) mouse model to investigate the role of CD36 in bone remodeling
Since CD36 has been functionally associated with the metabolism of lipoproteins [17,18], we measured the plasma levels of total cholesterol and fractions associated with low density lipoproteins (LDL) and HDL
Summary
Bone is a dynamic tissue that undergoes continual remodeling through the coordinated processes of bone resorption and formation. The equilibrium of both processes ensures the preservation of skeleton structural integrity and mineral homeostasis of the organism [1]. Differentiated osteoblasts synthesize and secrete type I collagen, the main bone matrix protein, and regulate bone mineralization by expressing alkaline phosphatase (ALP) and osteocalcin (OCN). These cells continuously orchestrate bone remodeling by regulating the activation and differentiation of cells from the monocyte/macrophage lineage into osteoclasts [1], required for the resorption process. Any imbalance between the functions of resorptive and formative cell populations that leads to excessive bone resorption or inadequate formation response results in loss of bone density, lower bone mass and increased risk of bone fractures [3] which are the main diagnostic criteria of osteoporosis [4]
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