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RNA-seq analyses of human periodontal ligament fibroblasts (PDLF) transfected with siRNA for PPARg

ABSTRACT: Purpose : This study was performed to investigate the effects of knockdown of PPARg for osteo/cementogenic differentiation of PDLF through RNA sequencing. Method : PDLF were transfected wtih either control siRNA or siRNA for PPARg and then cultured in mineralization inducing medium for 6 days. Total RNAs were collected before and after the culture. Result : Gene ontology analyses of RNA-seq data revealed the genes functionally related with ECM such as collagen synthesis and trimerization, proteoglycans, and fibers were selectively increased by 6-day culture and suppressed biological processes by si-PPARg compared with si-control at day 6 exhibited 5 of 7 upper ranked biological processes were related with ECM organization and metabolism. Moreover, the upper rank of suppressed pathways by si-PPARg compared with si-control at day 6 showed `Endochondral Ossification` was ranked 1st. Conclusions:These results suggested that knockdown of PPARg was sufficient to eliminate osteo/cementogenic and ECM organizing potentials by comprehensive transcriptional dysregulation in PDLF.

ORGANISM(S): Homo sapiens

PROVIDER: GSE178606 | GEO | 2021/08/31

REPOSITORIES: GEO

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Project description:Enforced enhancement of H3K4me3 and H3K27ac, active chromatin marks, by inhibiting histone demethylases and deacetylases is positively linked with hard tissue formation by inducing matrix synthesis and osteo/odontogenic differentiation. However, the key endogenous epigenetic modifier of odontoblasts to regulate the expression of the genes coding dentin extracellular matrix (ECM) proteins has not been identified yet. We herein focused on IκBζ, which was originally identified as transcriptional regulator for NF-B and recently regarded as the local epigenetic modifier by independently on NF-B, and demonstrated that the IκBζ null mice exhibited thicker dentin width and narrower pulp chamber with aged mice having more drastic phenotypes. At 6 months old, dentin fluorescent labeling exhibited that dentin synthesis was significantly accelerated in the incisors of IκBζ null mice. In molars of IκBζ null mice, aggressive reactionary dentin adjacent to pulp horn was exhibited. Mechanistically, COL1A2 and COL1A1 collagen genes were increased in the odontoblasts rich fraction of IκBζ null mice than that of wild type in vivo and human odontoblasts-like cells transfected with siRNA for IκBζ than the control siRNA transfected cells in vitro. Further, the direct binding of IκBζ to COL1A2 promoter suppressed COL1A2 expression and the local active chromatin status marked with H3K4me3. By whole-genomic identification of H3K4me3 enrichments revealed that ECM and ECM organization-related gene loci were selectively activated by the knockdown of IκBζ, which consistently resulted in the up-regulation of these genes. Collectively, these results indicated that IκBζ is the key negative regulator of dentin formation in odontoblasts since the deletion of IκBζ expression enhanced dentin formation by inducing dentin ECM and ECM organization-related gene expression via altering the local chromatin status marked by H3K4me3. Therefore, IκBζ is a potential target for improving the clinical outcomes of dentin regeneration therapies such as pulp capping and pulp revitalization procedures.

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RNA-seq analyses of human periodontal ligament fibroblasts (PDLF) transfected with siRNA for PPARg

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