Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24894306_1.fastq.gz | Fastqsanger.gz | |||
| SRR24894306_2.fastq.gz | Fastqsanger.gz | |||
| SRR24894307_1.fastq.gz | Fastqsanger.gz | |||
| SRR24894307_2.fastq.gz | Fastqsanger.gz | |||
| SRR24894308_1.fastq.gz | Fastqsanger.gz |
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Project description:Our study represents the first detailed analysis of aneurysmal tissues with or without our targeted nanotherapy, generated by RNA-seq technology. The optimized data analysis workflows reported here should provide a framework for comparative investigations of expression profiles.
2025-07-12 | GSE208025 | GEO
Project description:Non-alcoholic fatty liver disease (NAFLD) is characterized by a series of pathological changes that can progress from simple fatty liver disease to non-alcoholic steatohepatitis (NASH). The objective of this study is to describe changes in global gene expression associated with the progression of NAFLD. This study is focused on the expression levels of genes responsible for the absorption, distribution, metabolism and excretion (ADME) of drugs. Differential gene expression between three clinically defined pathological groups; normal, steatosis and NASH was analyzed. The samples were diagnosed as normal, steatotic, NASH with fatty liver (NASH fatty) and NASH without fatty liver (NASH NF). Genome-wide mRNA levels in samples of human liver tissue were assayed with Affymetrix GeneChipM-. Human 1.0ST arrays
2011-07-12 | E-MEXP-3291 | biostudies-arrayexpress
Project description:Non-alcoholic fatty liver disease/steatohepatitis (NAFLD/NASH) is a significant risk factor for hepatocellular carcinoma (HCC). However, a preclinical model of progressive NAFLD/NASH is largely lacking. Here, we report that mice with hepatocyte-specific deletion of Tid1, encoding a mitochondrial cochaperone, tended to develop NASH-dependent HCC. Mice with hepatic Tid1 deficiency showed impairing mitochondrial function and causing fatty acid metabolic dysregulation; meanwhile, sequentially developed fatty liver, NASH, and cirrhosis/HCC in a diethylnitrosamine (DEN) induced oxidative environment. The pathological signatures of human NASH, including cholesterol accumulation and activation of inflammatory and apoptotic signaling pathways, are also present in these mice. Clinically, low Tid1 expression was associated with unfavorable prognosis in patients with HCC. Empirically, hepatic Tid1 deficiency directly disrupts entire mitochondria that play a key role in the NASH-dependent HCC development. Overall, we established a new mouse model that develops NASH-dependent HCC and provides a promising approach to improve the treatment.
2022-06-02 | E-MTAB-9973 | biostudies-arrayexpress
Project description:We investigated the hepatic transcriptome of 58 biopsy-proven NAFLD patients at multiple stages of the disease (NAFL, NASH with mild fibrosis, NASH with advanced fibrosis) with the aim of describing the pathophysiological events driving the development and progression of NASH.
2021-04-14 | E-MTAB-9815 | biostudies-arrayexpress
Project description:Non-alcoholic fatty liver disease (NAFLD) encompasses a spectrum of disease that ranges from simple steatosis, to inflammatory form non-alcoholic steatohepatitis (NASH), cirrhosis, and up to hepatocellular carcinoma. While NASH usually takes decades to develop at a rate of one stage per seven years, in the case of post-trasplant NASH (pt-NASH) develops fibrosis much more rapidly, with almost 50% of liver transplant recipients presenting stage 3 fibrosis by 5 years post-transplant. Archived fresh-frozen transplanted liver biopsy samples from four liver biopsy samples with evidence of NASH (2 recurrent and 2 de novo), two with simple steatosis (both de novo), and five with normal histology as controls had their transcriptome sequenced in two batches for deeper coverage.
2022-05-09 | E-MTAB-11688 | biostudies-arrayexpress
Project description:Metabolic activation of CD8+ and NKT-cells causes NASH and HCC through cross-talk with hepatocytes. Mice that devloped HCC or NASH were compared to work out genomic differences of the two diseases. In order to characterise the importance of CCR2 (activation of monocytes) in the development of NASH and HCC CCR2 double-mutant mice were compared to CCR2 wildtype mice.
2014-06-01 | E-MTAB-2469 | biostudies-arrayexpress
Project description:BACKGROUND & AIMS: Recent studies revealed that hemoglobin is expressed in some non-erythrocytes and it suppresses oxidative stress when overexpressed. Oxidative stress plays a critical role in the pathogenesis of non-alcoholic steatohepatitis (NASH). This study was to investigate whether hemoglobin is expressed in hepatocytes and how it is related to oxidative stress in NASH patients. METHODS: Microarray was performed to identify differentially expressed genes in NASH. Quantitative real time PCR (qRT-PCR) was used to examine gene expression levels. Western blotting and immunofluorescence staining were employed to examine hemoglobin proteins. Flow cytometry was used to measure intracellular oxidative stress. RESULTS: Analysis of microarray gene expression data has revealed a significant increase in the expression of hemoglobin alpha (HBA1) and beta (HBB) in liver biopspies from NASH patients. Increased hemoglobin expression in NASH was validated by qRT-PCR. However, the expression of erythrocyte specific marker genes such as SPTA, SPTB, GYPA, GATA1, and ALAS2 did not change, indicating that increased hemoglobin expression in NASH was not from erythropoiesis, but could result from increased expression in hepatocytes. Immunofluorescence staining demonstrated positive HBA1 and HBB expression in the hepatocytes of NASH livers. Hemoglobin expression was also observed in human hepatocellular carcinoma HepG2 cell line. Furthermore, treatment with hydrogen peroxide, a known oxidative stress inducer, induced a dose dependent increase in HBA1 expression in HepG2 cells. Intriguingly, forced hemoglobin expression suppressed oxidative stress. CONCLUSIONS: Oxidative stress upregulates hemoglobin expression in hepatocytes. Suppression of oxidative stress by hemoglobin could be a mechanism to protect hepatocytes from oxidative damage. These findings suggest that hemoglobin is an inducible antioxidant in hepatocytes in response to increased oxidative stress as found in NASH livers. Twelve biopsy diagnosed NASH patients were included in this study. For control groups, total RNA from 5 different subjects were purchased from ADMET. These subjects are free from liver disease.
2010-10-20 | E-GEOD-24807 | biostudies-arrayexpress
Project description:Pancreatic ductal adenocarcinoma (PDAC) is characterized by an immunosuppressive stroma rich in tumor-associated macrophages (TAMs) that limit the therapeutic efficacy. We introduce a TAM-targeted nanotherapy platform that selectively delivers either a CSF1R inhibitor or the STING agonist cGAMP to immunosuppressive TAMs. While CSF1R inhibitor–loaded nanoparticles efficiently depleted TAMs and produced moderate antitumor effects, TAM-targeted cGAMP nanoparticles reprogrammed TAMs into immune-stimulating effectors. This reprogramming normalized aberrant vasculature, alleviated desmoplasia, and enhanced infiltration and activation of cytotoxic immune cells. In combination with gemcitabine, PD-1 checkpoint blockade, or CAR-NK cell therapy, TAM-targeted STING activation provided an in situ immunostimulatory signal that markedly improved antitumor efficacy in preclinical PDAC models. Ex vivo efficacy in human PDAC tissues and a favorable safety profile show the translational potential of this TAM-targeted nanotherapy to overcome the immune desert of PDAC.
2025-12-18 | GSE313718 | GEO
Project description:Pancreatic ductal adenocarcinoma (PDAC) is characterized by an immunosuppressive stroma rich in tumor-associated macrophages (TAMs) that limit the therapeutic efficacy. We introduce a TAM-targeted nanotherapy platform that selectively delivers either a CSF1R inhibitor or the STING agonist cGAMP to immunosuppressive TAMs. While CSF1R inhibitor–loaded nanoparticles efficiently depleted TAMs and produced moderate antitumor effects, TAM-targeted cGAMP nanoparticles reprogrammed TAMs into immune-stimulating effectors. This reprogramming normalized aberrant vasculature, alleviated desmoplasia, and enhanced infiltration and activation of cytotoxic immune cells. In combination with gemcitabine, PD-1 checkpoint blockade, or CAR-NK cell therapy, TAM-targeted STING activation provided an in situ immunostimulatory signal that markedly improved antitumor efficacy in preclinical PDAC models. Ex vivo efficacy in human PDAC tissues and a favorable safety profile show the translational potential of this TAM-targeted nanotherapy to overcome the immune desert of PDAC.
2025-12-01 | GSE310136 | GEO