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Excess glucocorticoids inhibit murine bone turnover via modulating the immunometabolism of the skeletal microenvironment

ABSTRACT: Excess glucocorticoids inhibit murine bone turnover via modulating the immunometabolism of the skeletal microenvironment

PROVIDER: PRJNA1085221 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28256452_1.fastq.gz	Fastqsanger.gz
	SRR28256452_2.fastq.gz	Fastqsanger.gz
	SRR28256453_1.fastq.gz	Fastqsanger.gz
	SRR28256453_2.fastq.gz	Fastqsanger.gz
	SRR28256454_1.fastq.gz	Fastqsanger.gz

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Excess glucocorticoids inhibit murine bone turnover via modulating the immunometabolism of the skeletal microenvironment

Project description:Elevated bone resorption and diminished bone formation have been recognized as the primary features of glucocorticoid-associated skeletal disorders. However, the direct effects of excess glucocorticoids on bone turnover remains unclear. Here, we explored the outcomes of exogenous glucocorticoid treatment on bone loss and delayed fracture healing in mice and found that reduced bone turnover was a dominant feature, resulting in a net loss of bone mass. We investigated the single-cell gene expression profiles of these two models. In the glucocorticoid-induced bone loss model, we sequenced the cell population digested from the bone surface. In the glucocorticoid-associated fracture healing model, we sequenced the cell population digested from the callus. Overall, the cell population on the bone surface was predominantly composed of hematopoietic cells, while only a small fraction represented the bone progenitor cells. In the fracture healing model, the callus contained a significant number of osteogenic and osteoclastic lineage cells. We primarily analyzed the gene expression of functional genes in the fracture healing model and characterized the metabolic profiles. These data provide insights into the multifactorial metabolic mechanisms by which glucocorticoids generate skeletal disorders.

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Project description:Glucocorticoids are the cornerstone of asthma and other inflammatory disease therapy. Resistance or insensitivity to glucocorticoids presents a substantial and challenging clinical problem. MicroRNAs are emerging as central regulators of inflammation, but it is not clear whether they could augment or attenuate glucocorticoid responses. We aimed to identify microRNAs that regulate cytokine and chemokine expression in airway epithelial cells and whether these miRNAs are subject to the effects of glucocorticoids. MicroRNAomic analyses of primary bronchial epithelial cells and the A549 airway epithelial cell line identified 7 miRNAs that were altered by inflammatory cytokine treatment and 22 that were regulated by glucocorticoids (n=3 for each treatment). miR-146a emerged as a central candidate, whose expression was induced by TNF-alpha and repressed by glucocorticoids. Its role as a candidate in asthmatic inflammation was supported by expression profiling in human asthmatics, which showed that plasma miR-146a expression was elevated in asthma and associated with measures related to worse asthma outcomes, including elevated blood eosinophil counts, higher asthma control questionnaire scores, and need for higher doses of inhaled glucocorticoids. However, transfection of miR-146a in A549 cells treated with TNF-alpha +/- glucocorticoids produced an anti-inflammatory effect and with increased efficacy of glucocorticoids. We propose a model whereby miR-146a is induced by inflammatory conditions as a feedback mechanism to limit inflammation. Glucocorticoids may limit this regulatory pathway by preventing miR-146a expression. Consequently, exogenous administration of miR-146a could be a novel therapeutic strategy to enhance effects of glucocorticoids.

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