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Gene-expression profiles of HepG2.2.15 cells induced by overexpression of Complement 2

ABSTRACT: Gene-expression profiles of HepG2.2.15 cells induced by overexpression of Complement 2

PROVIDER: PRJNA601970 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10908764_1.fastq.gz	Fastqsanger.gz
	SRR10908764_2.fastq.gz	Fastqsanger.gz
	SRR10908765_1.fastq.gz	Fastqsanger.gz
	SRR10908765_2.fastq.gz	Fastqsanger.gz
	SRR10908766_1.fastq.gz	Fastqsanger.gz

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Gene-expression profiles of HepG2.2.15 cells induced by overexpression of Complement 2

Project description:To explore the effect of overexpression of complement component 2 (C2) on HepG2.2.15 cells, we established HepG2.2.15-mock cells and C2-overexpressing HepG2.2.15 cells (HepG2.2.15-shC2) to identify differentially expressed genes and then performed GO and KEGG analysis to identified the altered pathways caused by over-expression of C2.

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Project description:Complement proteins are deposited in the muscles of patients with myositis. However, the local expression and regulation of complement genes within myositis muscle have not been well characterized. In this study, bulk RNA sequencing (RNAseq) analyses of muscle biopsy specimens revealed that complement genes are locally overexpressed and correlate with markers of myositis disease activity, including the expression of interferon-gamma (IFN )-induced genes. Single cell and single nuclei RNAseq analyses showed that most local expression of complement genes occurs in macrophages, fibroblasts, and satellite cells, with each cell type expressing different sets of complement genes. Biopsies from immune-mediated necrotizing myopathy patients, who have the lowest levels of IFN -induced genes, also had the lowest complement gene expression levels. Furthermore, data from cultured human cells showed that IFN upregulates complement expression in macrophages, fibroblasts, and muscle cells. Taken together, our results suggest that in myositis muscle, IFN coordinates the local overexpression of complement genes that occurs in several cell types.

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Coordinated local overexpression of complement induced by interferon gamma in myositis

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Gene expression profiles associated with ITGBL1 overexpression

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Genome-wide Transcriptome Analysis of CD36 Overexpression in HepG2.2.15 Cells to Explore Its Regulation Role of Metabolism and HBV Life Cycle

Project description:To understand the molecular basis underlying the response to increasing CD36 overexpression in HepG2.2.15 cell, we performed genome-wide sequencing of the mRNAs from HepG2.2.15-CD36OE cell and HepG2.2.15-vector cell using the RNA-seq technology to detect its differential transcriptomic profile.

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Project description:Rhabdomyolysis is a severe condition caused by skeletal muscle damage, leading to acute kidney injury (AKI). We demonstrate that complement has a direct pathogenic role in rhabdomyolysis-induced AKI. Deposition of C3d in the tubules of patients and mice correlated with rhabdomyolysis-induced AKI. Moreover, C3-defiient mice with rhabdomyolysis had preserved renal function. Mechanistically, C3-deficiency attenuated strongly inflammatory and apoptotic components of the renal transcriptome, perturbed by rhabdomyolysis. Complement was activated intrarenal by the lectin pathway via collectin-11. It proceeded in a C4-bypass manner and was amplified by heme-activated alternative pathway. Therefore, complement and heme are promising therapeutic targets for rhabdomyolysis-induced AKI.

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