Project description:Steroid-induced avascular necrosis of the femoral head (SANFH) is closely associated with the imbalance between adipogenic and osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs). Additionally, epigenetic regulation plays a critical role in this process. Our previous research found that during BMSC adipogenic differentiation, C/EBPα enhances the histone H3K27 acetylation modification at the PPARγ promoter, promoting sustained adipogenic differentiation of BMSCs, suggesting that Histone deacetylases (HDACs) may play an important role in BMSC adipogenic differentiation. However, identifying specific HDAC target genes requires further investigation. This study combines cell experiments with clinical specimen experiments to screen specific HDAC genes involved in BMSC adipogenic differentiation and explore their preliminary functions. Our findings indicate that HDAC10 influences the progression of steroid-induced avascular necrosis of the femoral head by regulating BMSC adipogenic differentiation, possibly through its association with PPARγ histone acetylation. These discoveries provide promising directions for the treatment of steroid-induced avascular necrosis of the femoral head.
Project description:The rat pancreatic cell line AR42J is relatively undifferentiated under normal culture conditions. When the glucocorticoid dexamethasone is added to the medium the cells display a dramatic decrease in proliferative rate and are induced to a more exocrine phenotype that includes increased expression of exocrine pancreas products (digestive enzymes) and more developed regulated secretion. We used microarray to determine changes in gene expression comparing control (without dexamethasone) vs induced (plus dexamethasone).
Project description:The rat pancreatic cell line AR42J is relatively undifferentiated under normal culture conditions. When the glucocorticoid dexamethasone is added to the medium the cells display a dramatic decrease in proliferative rate and are induced to a more exocrine phenotype that includes increased expression of exocrine pancreas products (digestive enzymes) and more developed regulated secretion. We used microarray to determine changes in gene expression comparing control (without dexamethasone) vs induced (plus dexamethasone). Three independent pairs of control and dexamethasone-induced cultures were prepared followed by total RNA extraction and microarray analysis using the Affymetrix Rat 230A chip.
Project description:Whole genome gene expression data (baseline and following GR-stimulation with 1.5 mg dexamethasone p.o.) were analysed to identify glucocorticoid receptor (GR)-mediated changes in gene expression. A Dexamethasone Suppression Test was performed in 297 subjects. Baseline and stimulated (3 hours after 1.5 mg dexamethasone p.o.) whole blood samples were analyzed using Illumina Human HT-12 v3 and v4 arrays.
Project description:We report chromatin organization changes in DND41 cells upon USP7 inhibitor with or without dexamethasone. DND41 cells were treated with USP7 inhibitor with or without dexamethasone. ATAC-seq were performed to detect chromatin organization change
Project description:We report chromatin accessibility changes in DND41 cells upon USP7 inhibitor with or without dexamethasone. DND41 cells were treated with USP7 inhibitor with or without dexamethasone. ATAC-seq were performed to detect chromatin accessibility change
Project description:We report chromatin accessibility changes in DND41 cells upon USP7 inhibitor with or without dexamethasone. DND41 cells were treated with USP7 inhibitor with or without dexamethasone. ATAC-seq were performed to detect chromatin accessibility change
Project description:The osteonecrotic area of steroid-induced avascular necrosis of the femoral head (SANFH) is a hypoxic microenvironment that leads to apoptosis of transplanted bone marrow mesenchymal stem cells (BMSCs). However, the underlying mechanism remains unclear. Here, we explore the mechanism of hypoxic-induced apoptosis of BMSCs, and use the mechanism to improve the transplantation efficacy of BMSCs. We analyzed LncRNA/mRNA expression profile of BMSCs under hypoxia conditions, and successfully screened the key long non-coding RNA AABR07053481 (LncAABR07053481) which mediated hypoxic apoptosis of BMSCs, we further determined its regulatory mechanism. Importantly, overexpression of LncAABR07053481 can improve the survival rate and repair efficacy of BMSCs under hypoxia conditions.
Project description:While dexamethasone impairs bone growth and adds to the development of osteoporosis, lithium enhances cell renewal. The aim of this project was to explore the genes and pathways affected by adding dexamethasone, lithium or both to the medium in which fetal rat metatarsal bones were cultivated. RNA sequencing and differential gene expression analysis were implemented to describe the transcriptome of the metatarsals. We identified significant opposite as well as independent effects of the substances on several cellular pathways. This may open up to identify the mechanisms of dexamethasone induced bone growth and structure impairment and possible preventive measures.