Project description:Comparison of longitudinal transcriptomic profiles of activated human primary hepatic stellate cells to activated human primary hepatic stellate cells that are treated with anti-fibrotic inhibitor reveals inflammatory signaling as a key pathway that is modulated during pro-fibrotic activation and repressed during attenuation of fibrotic response.
Project description:This SuperSeries is composed of the following subset Series: GSE19354: Expression data for rno-miR-146a overexpressing cell line HSC-2 GSE19462: microRNA profiling in vitro activated primary hepatic stellate cells Refer to individual Series
Project description:The molecular determinants of a healthy human liver cell phenotype remain largely uncharacterized. In addition, the gene expression changes associated with activation of primary human hepatic stellate cells, a key event during fibrogenesis, remain poorly characterized. Here, we provide the transriptomic profile underpinning the healthy phenotype of human hepatocytes, liver sinusoidal endothelial cells (LSECs) and quiescent hepatic stellate cells (qHSCs) as well as activated HSCs (aHSCs) We assess the transcriptome for purified, non-cultured human hepatocytes, liver sinusoidal cells (LSECs) and quiescent hepatic stellate cells (qHSCs) as well as culture-activated HSCs (aHSCs).
Project description:The molecular determinants of a healthy human liver cell phenotype remain largely uncharacterized. In addition, the gene expression changes associated with activation of primary human hepatic stellate cells, a key event during fibrogenesis, remain poorly characterized. Here, we provide the transriptomic profile underpinning the healthy phenotype of human hepatocytes, liver sinusoidal endothelial cells (LSECs) and quiescent hepatic stellate cells (qHSCs) as well as activated HSCs (aHSCs) We assess the transcriptome for purified, non-cultured human hepatocytes, liver sinusoidal cells (LSECs) and quiescent hepatic stellate cells (qHSCs) as well as culture-activated HSCs (aHSCs). Hepatocytes (n=2 donors), LSECs (n=3), qHSCs (n=3) and in vitro activated HSCs (n=3; from the same donors as the qHSCs and LSECs) were used for this study.
Project description:ZnO nanoparticles can elicit a range of perturbed cell responses in vitro. The liver is a target for ZnO nanoparticle-, or Zn2+ released from ZnO nanoparticles-induced accumulation and/or impact in vitro and in vivo. The response of human hepatic stellate cells to ZnO nanoparticles has not yet been assessed. We aimed to determine whether the presence of surface coatings could protect human hepatic stellate cells from ZnO nanoparticle-induced cytotoxicity. Primary human hepatic stellate cells were treated with one of two types of uncoated ZnO nanoparticles (Z-COTE or Nanosun), two types of coated ZnO nanoparticles (HP1, MAX), a mass equivalent of ZnSO4, or were left untreated. After 24 h, RNA was isolated and processed for whole genome transcriptional profiling, comparing the expresson profiles of treated cells to the untreated controls. Each treatment was prepared in duplicate.
