Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1159121 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR30628882_1.fastq.gz | Fastqsanger.gz | |||
| SRR30628882_2.fastq.gz | Fastqsanger.gz | |||
| SRR30628883_1.fastq.gz | Fastqsanger.gz | |||
| SRR30628883_2.fastq.gz | Fastqsanger.gz | |||
| SRR30628884_1.fastq.gz | Fastqsanger.gz |
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Project description:Analysis of ex vivo isolated lymphatic endothelial cells from the dermis of patients to define type 2 diabetes-induced changes. Results preveal aberrant dermal lymphangiogenesis and provide insight into its role in the pathogenesis of persistent skin inflammation in type 2 diabetes. The ex vivo dLEC transcriptome reveals a dramatic influence of the T2D environment on multiple molecular and cellular processes, mirroring the phenotypic changes seen in T2D affected skin. The positively and negatively correlated dLEC transcripts directly cohere to prolonged inflammatory periods and reduced infectious resistance of patients´ skin. Further, lymphatic vessels might be involved in tissue remodeling processes during T2D induced skin alterations associated with impaired wound healing and altered dermal architecture. Hence, dermal lymphatic vessels might be directly associated with T2D disease promotion.
2012-06-02 | GSE38396 | GEO
Project description:Analysis of ex vivo isolated lymphatic endothelial cells from the dermis of patients to define type 2 diabetes-induced changes. Results preveal aberrant dermal lymphangiogenesis and provide insight into its role in the pathogenesis of persistent skin inflammation in type 2 diabetes. The ex vivo dLEC transcriptome reveals a dramatic influence of the T2D environment on multiple molecular and cellular processes, mirroring the phenotypic changes seen in T2D affected skin. The positively and negatively correlated dLEC transcripts directly cohere to prolonged inflammatory periods and reduced infectious resistance of patients´ skin. Further, lymphatic vessels might be involved in tissue remodeling processes during T2D induced skin alterations associated with impaired wound healing and altered dermal architecture. Hence, dermal lymphatic vessels might be directly associated with T2D disease promotion. Global gene expression profile of normal dermal lymphatic endothelial cells (ndLECs) compared to dermal lymphatic endothelial cells derived from type 2 diabetic patients (dLECs).Quadruplicate biological samples were analyzed from human lymphatic endothelial cells (4 x diabetic; 4 x non-diabetic). subsets: 1 disease state set (dLECs), 1 control set (ndLECs)
2012-06-01 | E-GEOD-38396 | biostudies-arrayexpress
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Project description:ABSTRACT: Background: Oral Submucous Fibrosis (OSF) is a chronic inflammatory disease resulting in progressive fibrosis of the oral soft tissues. Habit of chewing betel quid has been proposed as an important etiological factor in the development of this disease. But the exact mechanism of pathogenesis is still not clear. Methods: We took microarray approach to identify differentially regulated genes in 10 OSF tissues against 8 pooled normal tissues using oligonucleotide arrays. Microarray results have been confirmed by qRT-PCR. Regulation of genes in epithelial and fibroblast cells was studied after treatment with arecoline, TGF-b and LAP followed by qRT-PCR. Results: Total number of genes found to be commonly regulated in OSF (p<=0.05 and Fold change>=1.5) tissues are 5288 and among them 2884 are up-regulated and 2404 are down-regulated. Extra cellular matrix genes that have been reported in OSF such as collagens, fibronectin and cytokines ET1, CTGF and TGF-b1 are among the up regulated genes. The list of up and down regulated genes also includes RARRES1, TGM2, THBS1, CHGB, MMP3, SPP1 and ALOX12, C4orf7 respectively. Analysis of microarray data revealed TGF-? pathway as a principal gene network involved in the development of OSF. Intriguingly, there was no regulation of CTGF and THBS1 in fibroblasts by arecoline. However, TGF-b1 treatment regulated all these genes in both epithelial and fibroblast cells. Conclusion: We demonstrate over expression of novel genes in OSF and suggest that OSF development involves TGF-b pathway in an epithelial-stromal cooperation. Targeting TGF-b signaling could be an alternate strategy to treat OSF. Two-condition experiment: 10 OSF tissues against 8 pooled normal tissues
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