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Links from GEO DataSets

Items: 14

1.

Tricyclic Antidepressants Induce Inactivation of Hepatic Stellate Cell (HSC) Myofibroblasts

(Submitter supplied) Hepatic stellate cells (HSCs) are the primary cell type responsible for liver fibrosis, the final common pathway leading to cirrhosis and liver failure for nearly every cause of chronic liver disease. Activation of HSCs in response to injury represents the key step in hepatic fibrogenesis, and is characterized by a phenotypic change from a non-fibrogenic, quiescent HSC to a fibrogenic HSC myofibroblast that secretes extracellular matrix proteins responsible for the fibrotic scar. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL11154 GPL20301
12 Samples
Download data: BW, TXT
2.

Depletion of ABHD17B mRNA in primary human hepatic stellate cells

(Submitter supplied) ABHD17B mRNA was depleted in primary human hepatic stellate cells to evaulate effect on gene expression.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
9 Samples
Download data: TXT
Series
Accession:
GSE240123
ID:
200240123
3.

Nanchangmycin exerts antifibrotic activity by inhibiting collagen production, migration, and proliferation of hepatic stellate cells

(Submitter supplied) We report the RNA sequencing results of human primary hepatic stellate cells (HSCs) treated with DMSO or 1 µM nanchangmycin (NCMC) for 48 hours. We find that multiple HSC activity and liver fibrosis related gene signatures, including ECM-related gene signatures, are negatively enriched in nanchangmycin treated HSCs.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
5 Samples
Download data: TXT
4.

Genome wide mapping of long noncoding (lnc) RNAs in hepatic stellate cells

(Submitter supplied) Hepatic stellate cells are the primary cell type responsible for development of fibrosis in chronic liver disease. We used directional RNA sequencing (RNA-seq) and chromatin immunoprecipitation and sequencing (ChIP-seq) to identify the lncRNAs expressed in human HSCs. We also identified the lncRNAs that change in expression with differentiation of nonfibrotic quiescent HSCs into fibrotic HSC myofibroblasts and those that are regulated by TGF-beta signaling. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing; Non-coding RNA profiling by high throughput sequencing
Platforms:
GPL11154 GPL20301
22 Samples
Download data: BW
5.

Conserved long noncoding RNA TILAM promotes liver fibrosis in humans and mice.

(Submitter supplied) Fibrosis is the common endpoint for all forms of chronic liver injury, and progression of fibrosis is responsible for the development of end stage liver disease and liver failure. The activation of hepatic stellate cells (HSCs) and their transition to HSC myofibroblasts is a key step in the disease process, as these cells are the primary source of the extracellular matrix (ECM) proteins, which form the fibrotic scar. more...
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL20301 GPL17021
18 Samples
Download data: RESULTS
Series
Accession:
GSE238159
ID:
200238159
6.

Deactivation of Hepatic Stellate Cells during Liver Fibrosis Resolution in Mice

(Submitter supplied) Gene expression of mouse hepatic stellate cells was characterized under the following conditions: Quiescent (isolated from normal mouse liver) and reverted (isolated from mouse liver treated with 4 injections of carbontetrachloride followed by 45 day rest period) Affymetrix Mouse 1.0ST gene expression measurements were used to characterize the transcriptomic basis in quiescent hepatic stellate cells, isolated from normal liver, and reverted hepatic stellate cells, isolated from liver treated with 4 injections of CCl4 followed by a 45 day rest period.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
8 Samples
Download data: CEL
Series
Accession:
GSE38648
ID:
200038648
7.

Single Cell RNA Sequencing Identifies Subsets of Hepatic Stellate Cells and Myofibroblasts in Liver Fibrosis

(Submitter supplied) Hepatic stellate cells and activated myofibroblasts display a high heterogeneity in healthy and fibrotic liver characterized by differential expression of collagens and chemokines.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
10 Samples
Download data: CSV
Series
Accession:
GSE132662
ID:
200132662
8.

ZNF469 is a novel pro-fibrotic regulator of extracellular matrix in hepatic stellate cells

(Submitter supplied) Activation of quiescent hepatic stellate cells (HSCs) into proliferative myofibroblasts drives extracellular cellular matrix (ECM) accumulation and liver fibrosis; nevertheless, transcriptional network that promotes such the process remains elusive. ZNF469, a putative C2H2 zinc finger protein, is found to be upregulated upon HSC activation; however, the molecular function of ZNF469 is completely unknown. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
6 Samples
Download data: TXT
Series
Accession:
GSE252958
ID:
200252958
9.

Gene Expression Analysis of the response to ACC inhibition

(Submitter supplied) BACKGROUND & AIMS: Nonalcoholic steatohepatitis (NASH) is a chronic liver disease characterized by hepatic lipid accumulation, inflammation, and progressive fibrosis. Acetyl-CoA carboxylase (ACC) catalyzes the rate-limiting step of de novo lipogenesis and regulates fatty-acid beta-oxidation in hepatocytes. ACC inhibition reduces hepatic fat content and markers of liver injury in NASH patients; however, the effect of ACC inhibition on liver fibrosis has not been reported. more...
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL24014 GPL17021
74 Samples
Download data: TXT
Series
Accession:
GSE148849
ID:
200148849
10.

Multi-Modal Comparison of human Hepatic Stellate Cells identifies novel therapeutic targets for Metabolic Dysfunction-Associated Steatotic Liver Disease

(Submitter supplied) Background and aims: Metabolic dysfunction-associated steatotic liver disease (MASLD) progresses from steatosis (Metabolic dysfunction-associated steatotic liver, MASL) to Metabolic dysfunction-associated steatohepatitis (MASH) with fibrosis. Activation of Hepatic Stellate Cells (HSCs) into fibrogenic myofibroblasts plays a critical role in the pathogenesis of MASH liver fibrosis. Here we compared gene expression and chromatin accessibility profiles of human HSCs in NORMAL, MASL, and MASH livers at single cell resolution. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL18573 GPL24676
36 Samples
Download data: BED
Series
Accession:
GSE244832
ID:
200244832
11.

TGFβ blockade in pancreatic cancer enhances sensitivity to combination chemotherapy

(Submitter supplied) We evaluated the TGFβ blocking antibody NIS793 in combination with either gemcitabine/n(ab)-paclitaxel or FOLFIRINOX chemotherapy in orthotopic pancreatic cancer. Blockade of TGFβ with chemotherapy reduced tumor burden in poorly immunogenic pancreatic cancer, without affecting the metastatic rate of cancer cells. TGFβ blockade decreased total aSMA+ fibroblasts but had minimal effect on fibroblast heterogeneity.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
6 Samples
Download data: TAR
Series
Accession:
GSE224688
ID:
200224688
12.

Foxd1 expression identifies a distinct subset of hepatic stellate cells involved in liver fibrosis

(Submitter supplied) Hepatic stellate cells (HSCs) are pericytes of the liver and are responsible for liver fibrosis and cirrhosis, which are end stages of chronic liver diseases. TFG-β activates HSCs leading to differentiation of myofibroblasts in the process of liver fibrosis. While heterogeneity of HSCs is appreciated in the fibrotic liver, it remains elusive which HSC subsets mainly contribute to fibrosis. We here show that expression of pericyte marker, Foxd1, specifically marked a subset of HSCs in the Foxd1-fate tracer mice. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21273
12 Samples
Download data: TXT
Series
Accession:
GSE270404
ID:
200270404
13.

Inhibitory effect of a human microRNA, miR-6133-5p, on the fibrotic activity of hepatic stellate cells in culture

(Submitter supplied) Purpose: We recently identified 39 human microRNAs, which effectively suppress hepatitis B virus (HBV) replication in hepatocytes. Because chronic HBV infection often results in active, hepatitis-related liver fibrosis, we assessed whether any of these microRNAs have anti-fibrotic potential and predicted that miR-6133-5p may target several fibrosis-related genes. Methods: The hepatic stellate cell line LX-2 was transfected with miR-6133-5p mimic and subsequently treated with TGF-β. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
4 Samples
Download data: TXT
14.

Hedgehog and metabolism

(Submitter supplied) Deregulated accumulation of myofibroblasts (MF) is central to liver fibrosis pathogenesis, but the mechanisms controlling myofibroblast fate remain poorly understood. Here we investigated whether Hedgehog (Hh) signaling regulates MF fate by modulating MF metabolism. We performed microarrays to screen hepatic stellate cells (HSC) for transition-associated changes in metabolism. To capture early and late events in their MF transition process, we compared gene expression in freshly isolated primary HSC with gene expression in the same cells after 7 days in culture.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
6 Samples
Download data: CEL
Series
Accession:
GSE34949
ID:
200034949
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