Effect of Glucocorticoids on lncRNA and mRNA Expression Profile of the Human Bone Microcirculatory Endothelial Cells
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ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Qingsheng Yu
PROVIDER: E-GEOD-60332 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Appropriate gene expression patterns form the basis for bone microcirculatory endothelial cells’ function and bone morphology. Although previous studies have elucidated the impact of hydrocortisone on bone microcirculatory endothelial cells’ specific gene expression, the exact differential transcriptomes and comprehensive gene expression profiles remain unknown. We have investigated the microRNA expression patterns before and after hydrocortisone administration of bone microcirculatory endothelial cells. Only 5 microRNAs were Benjamini-Hochberg characterized over 368 microRNAs candidates. Transcriptomic analysis of bone microcirculatory endothelial cells from human samples is highly informative due to their relevance to the large number of expressed genes. Our study provides a very valuable basis for investigation of genes, regulation and their co-expression network contributing to hydrocortisone induced disorders.
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Project description:Appropriate gene expression patterns form the basis for bone microcirculatory endothelial cells’ function and bone morphology. Although previous studies have elucidated the impact of hydrocortisone on bone microcirculatory endothelial cells’ specific gene expression, the exact differential transcriptomes and comprehensive gene expression profiles remain unknown. We have investigated the mRNA and lncRNA expression patterns before and after hydrocortisone administration of bone microcirculatory endothelial cells. At mRNAs level totally 518 differentially expressed genes were identified. Furthermore, we identified 73 upregulated and 166 downregulated long non-coding RNAs after administration of hydrocortisone. These RNAs appeared to be highly important to gene co-expression network. Transcriptomic analysis of bone microcirculatory endothelial cells from human samples is highly informative due to their relevance to the large number of expressed genes. Our study provides a very valuable basis for investigation of genes, regulation and their co-expression network contributing to hydrocortisone induced disorders.
2015-01-01 | GSE60332 | GEO
Project description:Many studies have demonstrated miRNAs as key regulators of inflammatory responses in endothelial cells (Ecs). However, because of the complexity of inflammatory genes and miRNAs, there would be many undiscovered miRNAs involved in inflammatory responses of ECs. Let-7e is an important member of let-7e family and plays key roles in the regulation of inflammation and endothelial cell proliferation. Furthermore, let-7e expression is significantly increased in many cardiovascular diseases including coronary heart disease. Therefore,we speculated that let-7e might play important roles in the regulation of inflammatory responses in endothelial cells by directly or indirectly targeting certain inflammatory genes. In order to reveal the action of let-7e in vascular endothelial cells, the expression profiles of mRNAs and lncRNAs induced by let-7e in human umbilical vein endothelial cells (HUVECs) were investigated using microarray technology.
2018-12-29 | E-MTAB-4971 | biostudies-arrayexpress
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2015-12-31 | E-GEOD-65263 | biostudies-arrayexpress
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Project description:Long non-coding RNAs (lncRNAs) are master regulators of gene expression and have recently emerged as potential innovative therapeutic targets. The deregulation of lncRNA expression patterns has been associated with age-related and noncommunicable diseases, including osteoporosis and bone tumors. However, the specific role of lncRNAs in physiological or pathological conditions in the bone tissue still needs to be further clarified, for their exploitation as therapeutic tools. In the present study, we evaluate the potential of the lncRNA CASC2 as a regulator of osteogenic differentiation and mineralization. Results show that CASC2 expression is decreased during osteogenic differentiation of human bone marrow-derived Mesenchymal Stem/Stromal cells (MSCs). CASC2 knockdown using small interfering RNA (siCASC2) increases the expression of the late osteogenic marker Bone Sialoprotein (BSP), but does not impact ALP staining levels, or the expression of early osteogenic transcripts including RUNX2 and OPG. Although siCASC2 does not impact hMSC proliferation nor apoptosis, it promotes the mineralization of hMSC cultured under osteogenic-inducing conditions, as shown by the increase of calcium deposits. Mass spectrometry-based proteomic analysis revealed that 89 proteins are regulated by CASC2 at late osteogenic stages, including proteins associated with bone diseases or anthropometric and musculoskeletal traits. Specifically, the Cartilage Oligomeric Matrix Protein (COMP) is highly enhanced by CASC2 knockdown at late stages of osteogenic differentiation, at either transcriptional and protein level. Inhibition of COMP impairs osteoblasts mineralization as well as the expression of BSP levels. The results indicate that lncRNA CASC2 regulates late osteogenesis and mineralization in hMSC via COMP and BSP. In conclusion, this study suggests lncRNA CASC2 as a potential new therapeutic target in bone mineralization.
2023-06-14 | PXD040463 | Pride
Project description:Rationale: Despite shortening vasopressor use in shock, hydrocortisone administration remains controversial, with potential harm on the immune system. Few studies assessed hydrocortisone impact on the transcriptional response in shock, and we are lacking data in burns. Objectives: To assess the hydrocortisone-induced transcriptional modulation in severe burn shock, particularly on the immune response. Methods: We collected whole blood samples (n= 117) during a randomized controlled trial assessing the efficacy of hydrocortisone administration on burn shock. Using whole genome microarrays, we first compared burn patients from the placebo group (n=15) to healthy volunteers (n=13) to describe the transcriptional modulation induced by burn shock over the first week. Then we compared burn patients randomized for either hydrocortisone administration (n=15) or placebo (n=15) to assess hydrocortisone-induced modulation. Measurements and Main Results: Study groups were similar in terms of severity and major outcomes, but shock duration (significantly reduced in the hydrocortisone group). Many genes (n=2250) were differentially expressed between burn patients and healthy volunteers, with 85% of them exhibiting a profound and persistent modulation over seven days. Interestingly, we showed that hydrocortisone enhanced the shock-associated repression of adaptive, but also innate immunity. Conclusions: We found that the initial host response to burn shock encompasses a wide and persistent modulation of gene expression, with profound modulation of pathways associated with metabolism and immunity. Importantly, hydrocortisone administration may worsen the immunosuppression associated with severe injury. These data should be taken into account in the risk ratio of hydrocortisone administration in patients with inflammatory shock.
2017-07-02 | GSE77791 | GEO