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Transcriptional dynamics of hepatic sinusoid-associated cells after liver injury [scRNA-seq]

ABSTRACT: Here we profile the transcripts of app. 35.000 single cells isolated from livers of healthy and diseased mice. We show the transcriptomic change associated with fibrosis induction in the non-parenchymal cell types (hepatic stellate cells, liver endothelial cells and macrophages). We reveal a hitherto unknown feature of the HSCs otherwise functionally attributed to the LECs.

ORGANISM(S): Mus musculus

PROVIDER: GSE145086 | GEO | 2020/08/25

REPOSITORIES: GEO

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Transcriptional Dynamics of Hepatic Sinusoid-Associated Cells After Liver Injury [bulk RNA-seq]

Project description:Here we profile the transcripts of app. 35.000 single cells isolated from livers of healthy and diseased mice. We show the transcriptomic change associated with fibrosis induction in the non-parenchymal cell types (hepatic stellate cells, liver endothelial cells and macrophages). We reveal a hitherto unknown feature of the HSCs otherwise functionally attributed to the LECs.

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Project description:Hepatic stellate cells (HSCs) experience phenotypic transformation, from the quiescent phenotype to the activated one, after different etiologies of liver injury. Liver fibrosis is then occurred upon the activation of HSCs. miR-16 deficiency is identified to be an important characteristic of HSCs activation. We used Affymetrix rat 230 2.0 arrays (Affymetrix, Santa Clara, U.S.A.) to uncover the global alternations of transcriptome under miR-16 restoration. We isolated quiescent hepatic stellate cells (HSCs) from adult male SD rats (normal control group) by in situ perfusion and density-gradient centrifugation. Activated HSCs were separated from rats of fibrosis model group, which were treated by 40% carbon tetrachloride (CCl4) for 8 weeks, by means of liver section, digestion and sequential centrifugation. Quiescent and activated HSCs were then divided into 4 groups at random, namely quiescent HSCs, activated HSCs, pLV-miR-16-treated HSCs and pLV-GFP-treated HSCs. The pLV-miR-16-treated group, pLV-GFP-treated group were infected with pLV-miR-16 and pLV-GFP, respectively.

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