PLX146228

GSE152677: Transcriptional profiling of intramembranous and endochondral ossification afterfracturein mice

• Organsim mouse
• Type RNASEQ
• Target gene
• Project ARCHS4

Bonefracturerepair represents an important clinical challenge with nearly 1 million non-union fractures occurring annually in the U.S. Gene expression differs between non-union and healthy repair, suggesting there is a pattern of gene expression that is indicative of optimal repair. Despite this, the gene expression profile offracturerepair remains incompletely understood. In this work, we used RNA-seq of two well-establishedmurinefracturemodels to describe gene expression of intramembranous and endochondralboneformation. We used top differentially expressed genes, enriched gene ontology terms and pathways,calluscellular phenotyping, and histology to describe and contrast theseboneformation processes across time. Intramembranous repair, as modeled by ulnar stressfracture, and endochondral repair, as modeled by femur fullfracture, exhibited vastly different transcriptional profiles throughout repair. Stressfracturehealinghad enriched differentially expressed genes associated withbonerepair and osteoblasts, highlighting the strong osteogenic repair process of thismodel. Interestingly, the PI3K-Akt signaling pathway was one of only a few pathways uniquely enriched in stressfracturerepair. Fullfracturerepair involved a higher level of inflammatory and immunecellrelated genes than did stressfracturerepair. Fullfracturerepair also differed from stressfracturein a robust downregulation of ion channel genes following injury, the role of which infracturerepair is unclear. This study offers a broad description of gene expression in intramembranous and endochondral ossification across several time points throughout repair and suggests several potentially intriguing genes, pathways, and cells whose role infracturerepair requires further study SOURCE: Jennifer,Ann,McKenzieMatthew Silva Washington University in St. Louis