Delivery of miR-181a/b-1 enhances endochondral fracture repair by targeting PDK4 and regulating mitochondrial metabolism [dataset]
Description
In this study we showed that local lentiviral delivery of miR-181a/b-1 enhanced ulnar fracture repair in male and female mice, and in vitro osteogenesis in human cartilage precursor cells. Mechanistically, miR-181a/b-1 directly targeted and suppressed pyruvate dehydrogenase kinase 4 (PDK4), thereby increasing mitochondrial respiration. Consistent with this mechanism, treatment with the PDK4 inhibitor diisopropylamine dichloroacetate (DADA) increased osteogenesis and mitochondrial metabolism in vitro and enhanced endochondral fracture repair in vivo, recapitulating the effects of miR-181a/b-1. This dataset comprises 35 .csv files, providing data related to Figures 2, 3, 4, 5, 6, S9 and S12.
Files
Steps to reproduce
A brief description is provided in the Methodological Information section of the Master-README file in the dataset. For detailed methods description, please refer to the associated open-access publication.
Institutions
- Washington University in St. LouisMissouri, St Louis
Categories
Funders
- National Institute of Arthritis and Musculoskeletal and Skin DiseasesNational Institutes of HealthMaryland, BethesdaGrant ID: R01AR075730
- National Institute of Arthritis and Musculoskeletal and Skin DiseasesNational Institutes of HealthMaryland, BethesdaGrant ID: R01AR083421
- National Institute of Arthritis and Musculoskeletal and Skin DiseasesNational Institutes of HealthMaryland, BethesdaGrant ID: F31AR082294
- National Institute of Arthritis and Musculoskeletal and Skin DiseasesNational Institutes of HealthMaryland, BethesdaGrant ID: P30AR074992
- United States Department of DefenseGovernment of the United States of AmericaDistrict of Columbia, WashingtonGrant ID: W81XWH-21-1-0385
Additional Metadata for Digital Commons Data@Becker
| Keywords | microRNA, miR-181a/b, fracture repair, osteogenesis, pyruvate dehydrogenase kinase 4, mitochondrial metabolism |