Sex differential gene expression in macrophages and osteoclasts
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE216929 | GEO | 2022/11/03
REPOSITORIES: GEO
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Project description:Osteoclasts are multinucleated giant cells generated by the fusion of precursors in response to stimulation with macrophage colony stimulating factor (MCSF) and receptor activator of NF-kB ligand (RANKL). These cells are the only cells capable of resorbing bone. Tartarate-resistant acid phosphatase is an enzyme secreted by osteoclasts that acts in bone resorption. Mice that are deficient for TRAP have shorter bones and their osteoclasts have decreased resorption capacity. In this project, we will isolate bone marrow macrophages from wild type and TRAP deficient mice, and differentiate the cells in osteoclasts in vitro. RNA will be extracted from macrophages and from macrophages stimulated with RANKL for both mouse lines (n=3/group) yielding 4 groups: Group 1 – macrophages from wild type mice, Group 2 – osteoclasts from wild type mice, Group 3 – macrophages from TRAP deficient mice, Group 4 – osteoclasts from TRAP deficient mice. The differential gene expression will be analyzed by RNAseq.
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Project description:Osteoclasts are the tissue-specific macrophage population of the bone and unique in their bone-resorbing activity. Hence, they are fundamental for bone physiology in health and disease. However, efficient protocols for the isolation and study of primary human osteoclasts are scarce. In this study, we aimed to establish a protocol, which enables the efficient differentiation of functional human osteoclasts from monocytes. To this end, human monocytes were isolated through a double-density gradient from healthy donor blood. The differentiation to macrophages was performed either in cell culture dishes or in Teflon-coated bags. The impact of these two distinct differentiation protocols on the gene expression profile of macrophages was assessed via RNA-Sequencing. The macrophages were then further differentiated to terminal osteoclasts through the addition of Receptor Activator of NF-κB Ligand (RANKL). The yield and function of multinuclear osteoclasts was significantly increased upon initial differentiation of monocytes to macrophages in Teflon-coated bags. Our study has established a novel protocol for the isolation of primary human osteoclasts that improves osteoclastogenesis in comparison to the conventionally used cultivation approach.
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Project description:Purpose: Among the diverse cytokines involved in osteoclast differentiation, IL-3 has been shown to inhibit RANKL-induced osteoclastogenesis. However, the mechanism underlying IL-3-mediated inhibition of osteoclast differentiation is not fully understood. In the present study, we demonstrate that IL-3 activation of STAT5 inhibits RANKL-induced osteoclastogenesis through the induction of Id genes. Methods: To investigate the effect of STAT5 on osteoclast differentiation and IL-3-mediated inhibition of osteoclast differentiation, bone marrow derived macrophages isolated from STAT5 wild-type (Stat5fl/fl) or STAT5 cKO (STAT5;MX1-Cre) were differentiated to osteoclast in the presence of M-CSF and RANKL with or without IL-3; and bone marrow derived macrophges from STAT5 wild-type and STAT5 cKO were overexpressed with PMX-FIG (control) or STAT5A1*6 (constitutively active form of STAT5A) and differentiated to osteoclast. To analyze bone phenotype, femurs and tibiae of 16 week-old STAT5 wild-type and STAT5 cKO were subjected to micro CT analysis and histomorphometry, respectively. Results: Overexpression of STAT5 inhibited RANKL-induced osteoclastogenesis. However, RANKL did not regulate either expression or activation of STAT5 during osteoclast differentiation. STAT5 deficiency prevented IL-3-mediated inhibition of osteoclastogenesis, suggesting that STAT5 plays an important role in IL-3-mediated inhibition of osteoclast differentiation. In addition, IL-3-induced STAT5 activation upregulated expression of the Id1 and Id2 genes, which are negative regulators of osteoclastogenesis. Overexpression of ID1 or ID2 in STAT5-deficient cells reversed osteoclast development recovered from IL-3-mediated inhibition. Moreover, micro-computed tomography and histomorphometric analysis revealed that STAT5 conditional knockout mice showed reduced bone mass, with an increased number of osteoclasts. Furthermore, IL-3 inhibited RANKL-induced osteoclast differentiation less effectively in STAT5 conditional knockout mice than in wild-type mice in a RANKL injection model. Conclusion: Taken together, our results suggest that STAT5 is a key transcription factor for IL-3-mediated inhibition of RANKL-induced osteoclastogenesis through Id gene expression. Examination of 4 different combination of osteoclast differentiation condition of bone marrow derived macrophages.
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