Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0

Determine the effects of Hdac3 deletion on H3K27ac profiles in murine chondrocytes


ABSTRACT: Histone deacetylase inhibitors are efficacious epigenetic-based therapies for some cancers and neurological disorders; however, these drugs inhibit multiple Hdacs and have detrimental effects on the pre- and post-natal skeleton. To better understand how Hdac inhibitors affect the skeleton, we focused on understanding the role of one of their targets, Hdac3, in endochondral bone formation by deleting it in immature murine chondrocyte micro masses with Adeno-Cre. Hdac3-deficient chondrocytes expressed higher levels of pro-inflammatory and matrix degrading genes (e.g., Il-6, Mmp3, Mmp13, Saa3) and lower levels of genes related to the extracellular matrix production, bone development and ossification (e.g., Acan, Col2a1, Ihh, Col10a1). Histone acetylation was increased in and around genes with elevated expression. This SuperSeries is composed of the SubSeries listed below. High Throughput RNA sequencing and Chromatin immunopreciptation sequencing experiments were performed in chondrocyte cultures. Differential analysis was conducted on ChIP-seq and RNA-seq data to identify H3K27Ac profiles for up and down-regulated genes in Hdac3-deficient murine chondrocytes. mm10 was used as reference genome. Refer to individual Series

ORGANISM(S): Mus musculus

SUBMITTER: Jennifer Jane Westendorf 

PROVIDER: E-GEOD-75552 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

altmetric image

Publications

Histone deacetylase 3 supports endochondral bone formation by controlling cytokine signaling and matrix remodeling.

Carpio Lomeli R LR   Bradley Elizabeth W EW   McGee-Lawrence Meghan E ME   Weivoda Megan M MM   Poston Daniel D DD   Dudakovic Amel A   Xu Ming M   Tchkonia Tamar T   Kirkland James L JL   van Wijnen Andre J AJ   Oursler Merry Jo MJ   Westendorf Jennifer J JJ  

Science signaling 20160809 440


Histone deacetylase (HDAC) inhibitors are efficacious epigenetic-based therapies for some cancers and neurological disorders; however, each of these drugs inhibits multiple HDACs and has detrimental effects on the skeleton. To better understand how HDAC inhibitors affect endochondral bone formation, we conditionally deleted one of their targets, Hdac3, pre- and postnatally in type II collagen α1 (Col2α1)-expressing chondrocytes. Embryonic deletion was lethal, but postnatal deletion of Hdac3 dela  ...[more]

Similar Datasets

2016-08-10 | E-GEOD-75549 | biostudies-arrayexpress
2016-08-10 | E-GEOD-75547 | biostudies-arrayexpress
2016-08-10 | GSE75549 | GEO
2016-08-10 | GSE75547 | GEO
2016-08-10 | GSE75552 | GEO
2024-06-16 | PXD046993 | Pride
2023-12-01 | GSE218830 | GEO
2024-10-22 | GSE239343 | GEO
2015-01-20 | E-GEOD-65077 | biostudies-arrayexpress
2017-06-22 | PXD005551 | Pride