Summary of Study ST002242

This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench,, where it has been assigned Project ID PR001431. The data can be accessed directly via it's Project DOI: 10.21228/M8RD8W This work is supported by NIH grant, U2C- DK119886.


This study contains a large results data set and is not available in the mwTab file. It is only available for download via FTP as data file(s) here.

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Study IDST002242
Study TitleHypoxia promotes osteogenesis via regulating the acetyl-CoA-mediated mito-nuclear communication.
Study SummaryBone-mesenchymal stem cells (MSCs) reside in a hypoxic niche that maintains their differentiation potential. Although the role of hypoxia (low oxygen concentration) in the regulation of stem cell function has been previously reported, with normoxia (high oxygen concentration) leading to impaired osteogenesis, the molecular events triggering changes in stem cell fate decisions in response to high oxygen remain elusive. Here, we study the impact of normoxia on the mito-nuclear communication with regards to stem cell differentiation. We show that normoxia-cultured MSCs undergo profound transcriptional alterations which cause irreversible osteogenesis defects. Mechanistically, high oxygen promotes chromatin compaction and histone hypo-acetylation, particularly on promoters and enhancers of osteogenic genes. Although normoxia induces metabolic rewiring resulting in high acetyl-CoA levels, histone hypo-acetylation occurs due to trapping of acetyl-CoA inside mitochondria, owing to lower CiC activity. Strikingly, restoring the cytosolic acetyl-CoA pool remodels the chromatin landscape and rescues the osteogenic defects. Collectively, our results demonstrate that the metabolism-chromatin-osteogenesis axis is heavily perturbed in response to high oxygen and identify CiC as a novel, oxygen-sensitive regulator of the MSC function.
CECAD Research Center
Last NameYang
First NameMing
AddressJoseph-Stelzmann-Straße 26, Köln, Koeln, 50931, Germany
Submit Date2022-08-01
Raw Data AvailableYes
Raw Data File Type(s)raw(Thermo)
Analysis Type DetailLC-MS
Release Date2022-08-17
Release Version1
Ming Yang Ming Yang application/zip

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Subject type: Cultured cells; Subject species: Mus musculus (Factor headings shown in green)

mb_sample_id local_sample_id Treatment Cellular fraction
SA214140AP02_41hypoxia cytosolic
SA214141AP02_42hypoxia cytosolic
SA214142AP02_43hypoxia cytosolic
SA214143AP02_44hypoxia cytosolic
SA214144AP02_27hypoxia mitochondrial
SA214145AP02_28hypoxia mitochondrial
SA214146AP02_26hypoxia mitochondrial
SA214147AP02_25hypoxia mitochondrial
SA214148AP02_11hypoxia whole cell
SA214149AP02_10hypoxia whole cell
SA214150AP02_09hypoxia whole cell
SA214151AP02_12hypoxia whole cell
SA214152AP02_36normoxia cytosolic
SA214153AP02_34normoxia cytosolic
SA214154AP02_35normoxia cytosolic
SA214155AP02_33normoxia cytosolic
SA214156AP02_19normoxia mitochondrial
SA214157AP02_18normoxia mitochondrial
SA214158AP02_20normoxia mitochondrial
SA214159AP02_17normoxia mitochondrial
SA214160AP02_02normoxia whole cell
SA214161AP02_03normoxia whole cell
SA214162AP02_04normoxia whole cell
SA214163AP02_01normoxia whole cell
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