Project description:Safrole oxide (SFO) at 50 μg/ml could most effectively induce EndoMT within 12 h. Transcriptional profiling of control and SFO-treated Human umbilical vascular endothelial cells was analyzed to understand the underlying molecular mechanism
Project description:Safrole oxide (SFO) at 50 M-NM-<g/ml could most effectively induce EndoMT within 12 h. Transcriptional profiling of control and SFO-treated Human umbilical vascular endothelial cells was analyzed to understand the underlying molecular mechanism Two groups were used. One is control group, the other is SFO treatment group. 6 dishes of cells in each group were used for microarray analysis.
Project description:Effect of TNF-alpha on microRNAs levels in Human Umbilical Endothelial Cells (HUVECs). HUVEC that were treated or not for 2 or 24 hours with TNF (10 ng/ml). Duplicate samples (1 or 2) of two different isolations of HUVEC (A or B)
Project description:Transcriptional profiling of Homo sapiens inflammatory skin diseases (whole skin biospies): Psoriasis (Pso), vs Atopic Dermatitis (AD) vs Lichen planus (Li), vs Contact Eczema (KE), vs Healthy control (KO) In recent years, different genes and proteins have been highlighted as potential biomarkers for psoriasis, one of the most common inflammatory skin diseases worldwide. However, most of these markers are not psoriasis-specific but also found in other inflammatory disorders. We performed an unsupervised cluster analysis of gene expression profiles in 150 psoriasis patients and other inflammatory skin diseases (atopic dermatitis, lichen planus, contact eczema, and healthy controls). We identified a cluster of IL-17/TNFα-associated genes specifically expressed in psoriasis, among which IL-36γ was the most outstanding marker. In subsequent immunohistological analyses IL-36γ was confirmed to be expressed in psoriasis lesions only. IL-36γ peripheral blood serum levels were found to be closely associated with disease activity, and they decreased after anti-TNFα-treatment. Furthermore, IL-36γ immunohistochemistry was found to be a helpful marker in the histological differential diagnosis between psoriasis and eczema in diagnostically challenging cases. These features highlight IL-36γ as a valuable biomarker in psoriasis patients, both for diagnostic purposes and measurement of disease activity during the clinical course. Furthermore, IL-36γ might also provide a future drug target, due to its potential amplifier role in TNFα- and IL-17 pathways in psoriatic skin inflammation. In recent years, different genes and proteins have been highlighted as potential biomarkers for psoriasis, one of the most common inflammatory skin diseases worldwide. However, most of these markers are not psoriasis-specific but also found in other inflammatory disorders. We performed an unsupervised cluster analysis of gene expression profiles in 150 psoriasis patients and other inflammatory skin diseases (atopic dermatitis, lichen planus, contact eczema, and healthy controls). We identified a cluster of IL-17/TNFα-associated genes specifically expressed in psoriasis, among which IL-36γ was the most outstanding marker. In subsequent immunohistological analyses IL-36γ was confirmed to be expressed in psoriasis lesions only. IL-36γ peripheral blood serum levels were found to be closely associated with disease activity, and they decreased after anti-TNFα-treatment. Furthermore, IL-36γ immunohistochemistry was found to be a helpful marker in the histological differential diagnosis between psoriasis and eczema in diagnostically challenging cases. These features highlight IL-36γ as a valuable biomarker in psoriasis patients, both for diagnostic purposes and measurement of disease activity during the clinical course. Furthermore, IL-36γ might also provide a future drug target, due to its potential amplifier role in TNFα- and IL-17 pathways in psoriatic skin inflammation.
Project description:Gene expression profiling of Human Umbilical Vein Endothelial Cells (HUVEC) after treatment with Erg or control antisense (GeneBloc)
Project description:<p>This document focuses on exploring the specific impact of MYH9 on the metabolic processes of vascular endothelial cells. To achieve this, a well-designed experimental approach was adopted: human umbilical vein endothelial cells (HUVECs) were subjected to different treatments using adenoviruses, including MYH9 knockdown (MYH9_KD), knockdown control (MYH9_KDC), overexpression (MYH9_OE), and overexpression control (MYH9_OEC).</p><p>Subsequently, untargeted metabolomics analysis based on ultra-performance liquid chromatography-mass spectrometry (UPLC-MS) was employed to systematically profile the metabolic changes in these treated cells. Through this comprehensive analysis, a total of 152 differential metabolites were identified, which exhibit distinct expression patterns across the different treatment groups. These differential metabolites are closely associated with several key metabolic pathways, with sulfur metabolism and glycerophospholipid metabolism being particularly prominent.</p><p>To further validate the reliability of the findings, seven core metabolites were selected for verification in the overexpression model, and their expression changes were confirmed, strengthening the credibility of the results. Overall, this study not only identifies potential biomarkers that may be related to MYH9-mediated vascular endothelial cell metabolism but also provides a solid mechanistic basis for understanding the role of MYH9 in the pathogenesis of vascular diseases, which is of great significance for the development of novel diagnostic and therapeutic strategies for MYH9-related vascular disorders.</p>