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RNAseq analysis comparing siRNA knocked down FOXF2 in and MKX in human normotrophic scar dermal fibroblasts

ABSTRACT: RNAseq analysis comparing siRNA knocked down FOXF2 in and MKX in human normotrophic scar dermal fibroblasts

PROVIDER: PRJNA756550 | ENA |

REPOSITORIES: ENA

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RNAseq analysis comparing siRNA knocked down FOXF2 in and MKX in human normotrophic scar dermal fibroblasts

Project description:3mm punch biopsies were taken from a healed normotrophic scar in burn patients with a scar at least 1 year old and fibroblasts were cultured from explants. Previous transcriptomic and epigenomic work found MKX and FOXF2 genes were overexpressed and these were knocked down using siRNA. RNA was then extracted and analysed using RNAseq to determine genes and pathways affected by this knockdown

2021-08-27 | GSE182515 | GEO

siRNA profiling of human primary prostate stromal cells knocked down for FOXF2

Project description:To identify the genes and pathways regulated by FOXF2, we investigated potential FOXF2 gene targets by microarray analyses of primary prostate stromal cells (PrSC) in which FOXF2 was knocked down by siRNA. 190 differentially expressed genes were selected, of which 104 genes were more highly expressed in PrSC cells treated with FOXF2 siRNA and 86 were more highly expressed in PRSC cells treated with negative control siRNA. Experiment Overall Design: In each experiment, we compared gene expression of PrSC cells treated with FOXF2 siRNA versus PrSC cells treated with negative control siRNA, in a total of 6 affymetrix arrays. 190 differentially expressed genes were selected (ratio negative control siRNA/siRNA â¥ 2log |0.8| as average in all arrays).

2008-11-13 | E-GEOD-12444 | biostudies-arrayexpress

A methylation analysis of human normotrophic scar dermal fibroblasts

Project description:A methylation analysis of human normotrophic scar dermal fibroblasts

| PRJNA564632 | ENA

A methylation analysis of human normotrophic scar dermal fibroblasts

Project description:3mm punch biopsies were taken from a healed normotrophic scar and a contralateral matched control site in burn patients with a scar at least 1 year old. Fibroblasts were cultured from explants to passage 2 and DNA was extracted and run on methylation arrays to examine differences in scar and control fibroblast gene expression Normotrophic scar maintains its abnormal scar phenotype for the rest of the patients life, long after the injury has healed. Differences in gene expression may reaveal target genes that can be modulated to improve scar appearance

2019-09-10 | GSE137134 | GEO

Porcine dermal extracellular matrix LC-MSMS

Project description:Hitherto, microenvironments provided by dermal analogues could not avoid frequent split-thickness skin grafts (STSGs) failure and scar fibrosis. We reported a novel method assembling 3D-printed dermal analogues (PDAs) with porcine dermal extracellular matrix(dECM)'s recapitulated the latter’s compositional and topological features. These optimized PADs reduced skin wounds contraction and improved cosmetic upshots proving superior to STSGs and commercially available dermal templates. Once grafted onto wounds beds, optimized PDAs evoked a type-2-like immune response, activated type-2 macrophages (M2-Mφ), upregulated anti-inflammatory genes like Wnt11, Fgf16 and ATF3, downregulated profibrotic genes like Il13r⍺2, Itg⍺11, and IL1β, and hindered fibrosis. Thus, PDAs' beneficial effects resulted from preserved dermis-specific ECM cues (by mass spectrometry analysis we identified more than 200 unique protein species inside our dECM powder) and well-balanced physicochemical properties, which collaboratively modulated crucial endogenous signaling pathways.

2022-02-16 | PXD020956 | Pride

RNA-seq of human hypertrophic scar fibroblast cell treated with fkbp10 siRNA against untreated controls

Project description:human hypertrophic scar fibroblast cell treated with fkbp10 siRNA and control siRNA for 48 hours

2020-08-26 | E-MTAB-9471 | biostudies-arrayexpress

RNA-seq of human hypertrophic scar fibroblast cell treated with pcolce siRNA against untreated controls

Project description:human hypertrophic scar fibroblast cell treated with pcolce siRNA and control siRNA for 48 hours

2020-08-26 | E-MTAB-9472 | biostudies-arrayexpress

Expression data from control siRNA and β-catenin siRNA transfected cultured mouse dermal cells

Project description:β-catenin activity of dermal cells is crucial for hair follicle neogenesis and strongly suggest that transcriptional target genes of β-catenin pathway are essential for maintaining trichogenicity of dermal cells. We used microarrays to identify genes targeted by the β-catenin pathway that are essential for maintaining the trichogenicity of dermal cells.

2013-09-03 | GSE50525 | GEO

FOXF2-regulated genes in human primary prostate stromal cells

2008-11-01 | GSE12444 | GEO

Type V collagen in scar tissue regulates the size of scar after heart injury

Project description:The mammalian heart possesses a poor ability to regenerate after acute ischemic cardiac injury and lost cardiac muscle is replaced by scar tissue. Multiple clinical studies demonstrate that the size of scar tissue following myocardial infarction is an independent predictor of cardiovascular outcomes, yet little is known about factors that regulate the size of scar after ischemic cardiac injury. In this report, we demonstrate that collagen V, a fibrillar collagen and a minor constituent of heart scars regulates the size of heart scars after ischemic cardiac injury. Depletion of collagen V in heart scars in two independent animal models led to a significant and paradoxical increase in post infarction scar tissue size with worsening of heart function. A systems genetics approach analyzing genes versus traits across 100 in-bred strains of mice independently demonstrated that collagen V is a critical driver of post injury heart function. We show that collagen V deficiency alters the ultra-structure and mechanical properties of scar tissue that make it more vulnerable to expansion. There is altered reciprocal feedback between matrix and cells that induce expression of specific mechanosensitive integrins which drive fibroblast activation and increased ECM gene expression. Scar size increases. Administration of cilengitide, an inhibitor of specific integrins, completely rescues the phenotype of increased post injury scarring, myofibroblast formation and cardiac dysfunction in collagen V deficient mice. These observations demonstrate that collagen V, a structural constituent of heart scar tissue regulates scar size in an integrin dependent manner.

2020-06-04 | GSE151695 | GEO

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