Homo sapiens
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PROVIDER: PRJNA294608 | ENA |
REPOSITORIES: ENA
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Project description:Human Corneal Epithelial Cells (SV40-HCEC) 6h Treatment with 100nM Vitamin D (1,25D3) vs. Vehicle Control
| PRJNA294607 | ENA
Project description:Inflammatory signals must be regulated and kept in check in order to prevent tissue damage. This is especially true in the cornea, where damage can induce loss of transparency, essential for vision. Toll-like receptors (TLRs) are present at the ocular surface and, in addition to being protective against infection, have also been implicated in the pathogenesis of dry eye syndrome, an inflammatory condition that affects millions of individuals in the United States each year. Therefore, an important area of research is the development of new anti-inflammatory therapeutics that limit aberrant ocular surface inflammation. Vitamin D has been studied for its role in suppressing inflammation in other tissues. In previous studies, we have demonstrated that vitamin D is able to decrease proinflammatory mediators induced by TLRs in human corneal epithelial cells (HCEC). Therefore, the goal of the current study was to examine this mechanism further through an evaluation of vitamin Dâs influence on gene expression in two different HCEC cell lines. Microarray comparing hTCEpi, human corneal epithelial cells, treated for 6 hours with Vitamin D (1,25D3) and control (0.1% ethanol) Two-condition arrays: hTCEpi cells were treated with either 100nM 1,25D3 or 0.1% Ethanol for 6h. Two biological replicates, one per array, with a dye swap (technical replicate).
2016-09-01 | E-GEOD-72662 | biostudies-arrayexpress
Project description:Inflammatory signals must be regulated and kept in check in order to prevent tissue damage. This is especially true in the cornea, where damage can induce loss of transparency, essential for vision. Toll-like receptors (TLRs) are present at the ocular surface and, in addition to being protective against infection, have also been implicated in the pathogenesis of dry eye syndrome, an inflammatory condition that affects millions of individuals in the United States each year.  Therefore, an important area of research is the development of new anti-inflammatory therapeutics that limit aberrant ocular surface inflammation. Vitamin D has been studied for its role in suppressing inflammation in other tissues. In previous studies, we have demonstrated that vitamin D is able to decrease proinflammatory mediators induced by TLRs in human corneal epithelial cells (HCEC). Therefore, the goal of the current study was to examine this mechanism further through an evaluation of vitamin Dâ??s influence on gene expression in two different HCEC cell lines. Microarray comparing SV40-HCEC, human corneal epithelial cells, treated for 6 hours with Vitamin D (1,25D3) and control (0.1% ethanol) Two-condition arrays: SV40-HCEC cells were treated with either 100nM 1,25D3 or 0.1% Ethanol for 6h. Two biological replicates, one per array, with a dye swap (technical replicate).
2016-09-01 | E-GEOD-72663 | biostudies-arrayexpress
Project description:Inflammatory signals must be regulated and kept in check in order to prevent tissue damage. This is especially true in the cornea, where damage can induce loss of transparency, essential for vision. Toll-like receptors (TLRs) are present at the ocular surface and, in addition to being protective against infection, have also been implicated in the pathogenesis of dry eye syndrome, an inflammatory condition that affects millions of individuals in the United States each year. Therefore, an important area of research is the development of new anti-inflammatory therapeutics that limit aberrant ocular surface inflammation. Vitamin D has been studied for its role in suppressing inflammation in other tissues. In previous studies, we have demonstrated that vitamin D is able to decrease proinflammatory mediators induced by TLRs in human corneal epithelial cells (HCEC). Therefore, the goal of the current study was to examine this mechanism further through an evaluation of vitamin D’s influence on gene expression in two different HCEC cell lines. Microarray comparing SV40-HCEC, human corneal epithelial cells, treated for 6 hours with Vitamin D (1,25D3) and control (0.1% ethanol)
2016-09-01 | GSE72663 | GEO
Project description:Inflammatory signals must be regulated and kept in check in order to prevent tissue damage. This is especially true in the cornea, where damage can induce loss of transparency, essential for vision. Toll-like receptors (TLRs) are present at the ocular surface and, in addition to being protective against infection, have also been implicated in the pathogenesis of dry eye syndrome, an inflammatory condition that affects millions of individuals in the United States each year. Therefore, an important area of research is the development of new anti-inflammatory therapeutics that limit aberrant ocular surface inflammation. Vitamin D has been studied for its role in suppressing inflammation in other tissues. In previous studies, we have demonstrated that vitamin D is able to decrease proinflammatory mediators induced by TLRs in human corneal epithelial cells (HCEC). Therefore, the goal of the current study was to examine this mechanism further through an evaluation of vitamin D’s influence on gene expression in two different HCEC cell lines. Microarray comparing hTCEpi, human corneal epithelial cells, treated for 6 hours with Vitamin D (1,25D3) and control (0.1% ethanol)
2016-09-01 | GSE72662 | GEO
Project description:LC-MS/MS based investigation of protein abundance changes, induced by DZNep treatment in A549-ACE2 cell line (0.75 uM DZNep, vehicle PBS; 6h pre-treatment, harvested 24 h.p.i. with mock/SARS-CoV/SARS-CoV-2 at MOI 3) or primary human bronchial epithelial cells (NHBEs) (1.5 uM DZNep, vehicle PBS; 6h pre-treatment, harvested 36 h.p.i. with mock/SARS-CoV/SARS-CoV-2 at MOI 3), or by Tubercidin in A549-ACE2 cell line (1 uM Tubercidin, vehicle DMSO; 3h pre-treatment, harvested 24 h.p.i. with mock/SARS-CoV at MOI 0.01/SARS-CoV-2 at MOI 0.1).
2022-06-28 | PXD034361 | Pride
Project description:We present ribosome profiling(for activaly translated RNA) and RNA-seq (for total RNA) data for human corneal epithelial cells exposed to mild osmotic stress (500 mOsm) for 1h and 6h (additionally torin1 (mTOR inhibitor) or MeAIB (SNAT2 inhibitor were added for the last hour of treatment.
2022-07-07 | GSE200097 | GEO
Project description:A role for vitamin A in host defense against Mycobacterium tuberculosis has been suggested through epidemiological and in vitro studies; however, the antimicrobial mechanism is unclear. Here, we demonstrate that vitamin A mediates host defense through regulation of cellular cholesterol content. Comparison of monocytes stimulated with all-trans retinoic acid (ATRA) or 1,25-dihydroxyvitamin D3, the biologically active forms of vitamin A and vitamin D respectively, indicates that ATRA and 1,25D3 induce mechanistically distinct antimicrobial activities. Gene expression profiling reveals that ATRA but not 1,25D3 triggers a lipid metabolism and efflux pathway, including expression of lysosomal lipid transport gene NPC2. ATRA-induced decrease in total cellular cholesterol content, subcellular lipid reorganization, lysosomal acidification and antimicrobial activity are all dependent upon expression of NPC2. Finally, the addition of HIV-protease inhibitors known to inhibit cholesterol efflux, Ritonavir and Nelfinavir, blocked both ATRA-induced cholesterol decrease as well as antimicrobial activity. Taken together, these results suggest that the vitamin A-mediated host defense mechanism against M. tuberculosis requires regulation of cellular cholesterol. Monocytes derived from four independent healthy blood donors that were stimulated with control (CTRL), ATRA or 1,25D3 at 10-8M for 18 hours.
2013-12-31 | E-GEOD-46268 | biostudies-arrayexpress
Project description:Identified a series of miRNAs transcriptionally regulated by vitamin D treatment within osteoblasts. Several miRNAs were validated in dose escalation experiments. Furthermore, downstream miRNA targets were appraised and found to regulate target message and protein levels. These findings were assessed in early and late passaged osteoblasts and found an age-dependent regulation of some miRNAs, while others were considered constituitiously expressed. Inhibitor studies of one key bone-related miRNA demonstrated the importance of this miRNA to regulate vitamin D-mediate osteoblastic differentiation during mineralizaition. Three independent sets of passage 8 primary human osteoblasts were either treated with vehicle (ethanol) or 1,25D3 (10nM) for 6 hours. Total RNA was collected using the miRNA Vana kit (ABI) and then quality assessed, and sent for miRNA array processesing.
2012-07-31 | E-GEOD-34144 | biostudies-arrayexpress
Project description:Most prostate cancers depend on androgen and androgen receptor signaling for their proliferation and development, which underpins the efficacy of antiandrogens as powerful therapeutic agents for prostate cancers. On the other hand, interaction between AR and other nuclear hormone receptors (NRs) such as glucocorticoid receptor in the prostatic cancer or between AR and ER in breast cancers depicts the close association or “crosstalk” of AR with other NRs in terms of the new approach toward the management of hormone-resistant prostate/breast cancers. Along with this line, chemopreventive and antiproliferative action of 1,25(OH)2D3 (abbreviated as 1,25D3), an active metabolite of vitamin D3, during the management of prostate and/or breast cancers has been recently rigorously argued. We found that in its physiological concentration, 25(OH)D3 (abbreviated as 25D3), the precursor metabolite of 1,25D3 and widely-recognized as an inactive vitamin D because of its much weaker binding activity to vitamin D receptor (VDR) compared to 1,25D3, has a gene transcription profile similar to 1,25D3 in some prostate cancers. In this study, we investigated whole genome target gene profiles and intracellular behaviors of VDR after administration of 25D3 or 1,25D3 in prostate cancer LNCaP cells to elucidate the hormonal activity of 25D3. First, we confirmed that LNCaP cells possessed functional 25D3-VDR as well as 1,25D3-VDR signaling systems by qRT-PCR. By immunofluorescent examination of nuclear translocation, western blotting and most importantly, knockdown of CYP27B1 and/or VDR after the introduction of the respective siRNA into these cells, we found that, just like 1,25D3, 10-7 M of 25D3, which is within its uppermost physiological concentrations in the bloodstream, induced VDR nuclear import and robustly activated its target gene such as CYP24A1 in the virtual absence of CYP27B1 expression in LNCaP cells. These results indicate that the unconverted 25D3 alone behaved similarly to 1,25D3 in activating CYP24A1 mRNA expression. Our comprehensive microarray analyses verified the bioactivity of 25D3 and we found that 25D3 target gene profiles largely matched those of 1,25D3, while the presence a small subset of 25D3-, or 1,25D3-specific target genes were not excluded. The concentration of 1,25D3 in the culture media after 25D3 treatment with or without siRNA for CYP27B1 mRNA was below the lower limit of the sensitivity measured by ultrasensitive LC/MS/MS method. These results indicated that 25D3 shares bioactivity with 1,25D3 without conversion to the latter at least in some prostate cancer cells.
2017-12-01 | GSE107438 | GEO