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Next generation sequencing of transcriptomic change in NTCP-reconstituted HepG2 cells after hepatocyte maintanace medium treatment

ABSTRACT: Next generation sequencing of transcriptomic change in NTCP-reconstituted HepG2 cells after hepatocyte maintanace medium treatment

PROVIDER: PRJNA726192 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14360171_1.fastq.gz	Fastqsanger.gz
	SRR14360171_2.fastq.gz	Fastqsanger.gz
	SRR14360172_1.fastq.gz	Fastqsanger.gz
	SRR14360172_2.fastq.gz	Fastqsanger.gz
	SRR14360173_1.fastq.gz	Fastqsanger.gz

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Next generation sequencing of transcriptomic change in NTCP-reconstituted HepG2 cells after hepatocyte maintanace medium treatment

Project description:In order to profile the transcriptomic change in NTCP-reconstituted HepG2 cells after the treatment with hepatocyte maintanace medium. HMM-pretreated HepG2/NTCP cells turned to be more susceptible to hepatitis B virus infection.

2021-07-09 | GSE173576 | GEO

Elevated NTCP expression by an iPSC-derived human hepatocyte maintenance medium enhances HBV infection in NTCP-reconstituted HepG2 cells.

Project description:BackgroundThe sodium taurocholate cotransporting polypeptide (NTCP) is a functional receptor for hepatitis B virus (HBV). NTCP-reconstituted human hepatoma cells support HBV infection, but the infection is suboptimal and no apparent HBV spread has been observed in this system.ResultsWe found that NTCP-reconstituted HepG2 cells were highly susceptible to HBV infection after cells were cultured in a commercial human inducible pluripotent stem cell (iPSC)-derived hepatocyte maintenance medium (HMM). The enhanced HBV infection coincided with increased NTCP expression, and was observed in six different clones of HepG2-NTCP cells. Promoter assays indicated that HMM activated the cytomegalovirus immediate-early (IE) promoter that drives the NTCP expression in the HepG2-NTCP cells. RNA-Seq analysis revealed that HMM upregulated multiple metabolic pathways. Despite highly upregulated NTCP expression by HMM, no obvious HBV spread was observed even in the presence of PEG 8000.ConclusionsOur data suggest that this particular medium could be used to enhance HBV infection in NTCP-reconstituted hepatocytes in vitro.

| S-EPMC8256212 | biostudies-literature

Transcriptomic alteration after miR-6126 tranfection into HepG2-NTCP

Project description:Aim: Hepatitis B virus (HBV) infection is one of the most serious global health problems. Our previous study revealed that an increase in the miR-6126 serum level over one year of pegylated interferon therapy predicted a decrease in hepatitis B surface (HBs) antigens. We aimed to clarify whether miR-6126 downregulated the expression level of sodium taurocholate cotransporting polypeptide (NTCP), a host cell receptor required for HBV entry. Methods: HepG2-NTCP and PXB cells were utilized to evaluate the expression level of NTCP after transfection with miR-6126. The protein expression level of NTCP was evaluated using Western blot analysis and immunostaining. The expression profile of messenger RNAs was evaluated using next-generation sequencing to search for direct targets of miR-6126.

2021-12-28 | GSE192617 | GEO

RNA-seq analysis of HBV-infected HepG2-NTCP cells treated by Interferon subtypes

Project description:Examination of interferon stimulated genes treated with different kind of interferon subtypes in HBV-infected HepG2-NTCP cells.

2020-04-20 | GSE138567 | GEO

Transcriptomic alteration after miR-6126 tranfection into HepG2-NTCP

Project description:Transcriptomic alteration after miR-6126 tranfection into HepG2-NTCP

| PRJNA792405 | ENA

Expression data from HepG2-NTCP and Huh-106 cell lines

Project description:Microarray data to compare the gene expression in HepG2-NTCP and Huh-106 cell lines Knowledge of HBV virus-host interactions is still limited. Here, we performed a genome-wide gain-of-function screen using weakly permissive Huh-106 cells to uncover novel HBV host factors.

2020-04-21 | GSE132638 | GEO

Expression data from HepG2-NTCP and Huh-106 cell lines

Project description:Expression data from HepG2-NTCP and Huh-106 cell lines

| PRJNA548561 | ENA

Transcriptome profiles of Huh7.5.1-NTCP cells treated with HBV preS1 peptide

Project description:Chronic hepatitis B, C and D virus (HBV, HCV, HDV) infections are leading causes of liver disease and cancer worldwide. Although these viruses differ markedly in their life cycle and genomic organization, they exclusively infect hepatocytes. Recently, the sodium taurocholate cotransporting polypeptide (NTCP) was identified as the first functional receptor for HBV and HDV. Here, we report that NTCP also facilitates HCV entry into human hepatocytes, by augmenting the bile acid-mediated repression of IFN-stimulated genes (ISGs), including IFITM2 and IFITM3, to increase the susceptibility of cells to HCV entry. Furthermore, an HBV-derived preS1 peptide, known to bind NTCP and to inhibit bile acid uptake and HBV infection, inhibits HCV entry by enhancing the expression of ISGs. Our study highlights NTCP as a novel player linking bile acid metabolism to the interferon response in hepatocytes and establishes a role for NTCP in the entry process of multiple hepatotropic viruses, via distinct mechanisms. Collectively, these findings enhance our understanding of hepatitis virus-host interactions and suggest NTCP as an attractive antiviral target for HBV/HCV co-infection. Transcriptome profiling by DNA microarray of Huh7.5.1 cells transduced to express NTCP.

2016-10-25 | E-GEOD-79089 | biostudies-arrayexpress

Calnexin depletion by ER-stress during cholestasis inhibits the Na+-taurocholate Cotransporting Polypeptide (NTCP)

Project description:Impaired bile flow (cholestasis) leads to transcriptional downregulation of the bile acid importer Na+-taurocholate co-transporting protein (NTCP) and to ER-stress in the liver. Here, we show that ER-stress induction strongly reduces NTCP protein expression, plasma membrane abundance and NTCP-mediated bile acid uptake. This is not controlled via a single specific UPR-pathway but mainly depends on the interaction of NTCP with calnexin, an ER chaperone involved in folding of N-glycosylated proteins. In mice, expression of both Ntcp and calnexin was reduced by thapsigargin-induced ER-stress. Calnexin downregulation in HepG2 and U2OS cells results in a decreased NTCP expression and a reduced bile acid uptake. Calreticulin shows partial functional redundancy with calnexin as it also interacts with NTCP, and is downregulated upon ER-stress, but specifically in calnexin-depleted cells. In conclusion, ER stress-induced downregulation of calnexin provides an additional mechanism to dampen NTCP-mediated bile acid uptake during cholestasis.

2019-01-07 | PXD007948 | Pride

microRNA-6126 downregulates NTCP expression through decreasing stability of its messenger RNA in hepatocyte

Project description:miR-6126 downregulated expression level of sodium taurocholate cotransporting polypeptide (NTCP), a host cell receptor required for hepatitis B virus (HBV) entry.

2022-08-01 | GSE180543 | GEO

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