A transcriptomic study of selenium against liver injury by RNA-seq
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ABSTRACT:
PROVIDER: PRJNA503871 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8159220_1.fastq.gz | Fastqsanger.gz | |||
| SRR8159220_2.fastq.gz | Fastqsanger.gz | |||
| SRR8159230_1.fastq.gz | Fastqsanger.gz | |||
| SRR8159230_2.fastq.gz | Fastqsanger.gz | |||
| SRR8159221_1.fastq.gz | Fastqsanger.gz |
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Project description:Evidence from biochemical indicators suggested that selenium could effectively repair the liver injury caused by beta-cypermethrin (β-CYP). However, the molecular mechanisms of selenium against liver injury induced by β-CYP remains unclear. In the present study, dynamic changes in gene expression profiles before and after the treatment of Na2SeO3 in liver injury mice were analyzed by using RNA sequencing. As a result, several essential genes and pathways were identified to be significantly associated with this process.
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Project description:Methanococcus maripaludis utilizes selenocysteine-(Sec-) containing proteins (selenoproteins), mostly active in the organism’s primary energy metabolism, methanogenesis. Under selenium depletion, M. maripaludis employs a set of enzymes containing cysteine (Cys) instead of Sec. The genes coding for these Sec-/Cys-containing isoforms are the only genes known expression of which is influenced by the selenium status of the cell. Using quantitative proteomics and transcriptomics approx. 7% and 12%, respectively, of all genes/proteins were differentially expressed/synthesized in response to the selenium supply. Some of the genes identified involve methanogenesis, nitrogenase functions, and putative transporters. An increase of transcript abundance for putative transporters under selenium-depleted conditions indicated the organism’s effort to tap into alternative sources of selenium. Selenium sources M. maripaludis is known to utilize are selenite and dimethylselenide. To expand this list, a selenium responsive reporter strain was assessed with nine other, environmentally relevant selenium species. While some had a similar biological window as selenite, others were effectively utilized at lower concentrations. Conversely, selenate and seleno-amino acids were only utilized at unphysiologically high concentrations and two compounds were not utilized at all. To address the role of the selenium-regulated putative transporters in selenium transport, M. maripaludis mutant strains lacking one or two of the putative transporters were tested for the capability to utilize the different selenium species. Of the five putative transporters analyzed by loss-of-function mutagenesis, none appeared to be absolutely required for utilizing any of the selenium species tested, indicating they have redundant and/or overlapping specificities, or are not dedicated selenium transporters.
2024-03-27 | PXD047095 | Pride
Project description:We used selenium as a photodynamic anti-tumor synergist of phycocyanin to explore its inhibitory effect on lung cancer and its molecular mechanism in vitro. First of all, we used LLC-luc mouse lung cancer cells to establish a tumor-bearing model. Selenium-enriched phycocyanin was injected next to the tumor. When it was absorbed by the tumor tissue, the tumor site was irradiated by a 620nm wavelength laser. The changes in tumor size were monitored in real-time and the physiological indexes of mice were measured. It was found that selenium phycocyanin photodynamic therapy could enhance the inhibitory effect of tumors and improve the level of antioxidation in tumor-bearing mice. In addition, the pathological section observation and electron microscope microstructure analysis of the tumor tissue showed that the effect of the selenium-enriched phycocyanin photodynamic treatment group was more significant. At the same time, the tumor tissue transcriptional group sequencing analysis and qRT-PCR verification analysis showed that selenium-enriched phycocyanin photodynamic treatment group could reduce the expression of Mmp13, Serpine1, Vegfa, and Ppbp genes inhibit tumor cell metastasis and proliferation, up-regulate the expression of Ccl2, Ccl3, Cxcl2 and down-regulate the expression of Ccl24 chemokine, and promote tumor local immunity. Our results show that selenium phycocyanin photodynamic therapy plays an anti-tumor effect by promoting tumor cell apoptosis, reducing inflammation, and promoting tumor immunity.
2023-01-01 | GSE192635 | GEO
Project description:Acute liver failure is a serious clinical manifestation resulting from sudden liver injury, which can be triggered by various factors. Early studies have shown that PGE2 significantly alleviated acute liver failure induced by galactosamine/lipopolysaccharide(Dgaln/lps), APAP, and carbon tetrachloride. However, the precise mechanism by which PGE2 alleviates Dgaln/lps-induced acute liver failure remains unclear. The aim of this study is to investigate the mechanisms underlying the protective effects of PGE2 against Dgaln/lps-induced hepatocyte injury.
2023-09-01 | GSE241513 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE26695: Transcriptomic response of murine liver to severe injury and hemorrhagic shock: Affymetrix portion of dual platform GSE26696: Transcriptomic response of murine liver to severe injury and hemorrhagic shock: CodeLink portion of dual platform Refer to individual Series
2011-01-24 | E-GEOD-26697 | biostudies-arrayexpress
Project description:<p>The National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) has established the Drug-Induced Liver Injury Network (DILIN) to collect and analyze cases of severe liver injury caused by prescription drugs, over-the-counter drugs, and alternative medicines, such as herbal products and supplements.</p>
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Project description:BACKGROUND & AIMS: c-Jun N-terminal kinase (JNK)1 and JNK2 are expressed in hepatocytes and have overlapping and distinct functions. JNK proteins are activated, via phosphorylation, in response to acetaminophen- or CCl4-induced liver damage; the level of activation correlates with the degree of injury. SP600125, a JNK inhibitor, has been reported to block acetaminophen-induced liver injury. We investigated the role of JNK in drug-induced liver injury (DILI) in liver tissues from patients and in mice with genetic deletion of JNK in hepatocytes. METHODS: We studied liver sections from patients with DILI (due to acetaminophen, phenprocoumon, non-steroidal anti-inflammatory drugs or autoimmune hepatitis), or patients without acute liver failure (controls), collected from a DILI Biobank in Germany. Levels of total and activated (phosphorylated) JNK were measured by immunohistochemistry and western blotting. Mice with hepatocyte-specific deletion of Jnk1 (Jnk1Îhepa) or combination of Jnk1 and Jnk2 (JnkÎhepa), as well as Jnk1-floxed C57BL/6 (control) mice, were given injections of CCl4 (to induce fibrosis) or acetaminophen (to induce toxic liver injury). We performed gene expression microarray, and phosphoproteomic analyses to determine mechanisms of JNK activity in hepatocytes. RESULTS: Liver samples from DILI patients contained more activated JNK, predominantly in nuclei of hepatocytes and in immune cells, than healthy tissue. Administration of acetaminophen to JnkÎhepa mice produced a greater level of liver injury than that observed in Jnk1Îhepa or control mice, based on levels of serum markers and microscopic and histologic analysis of liver tissues. Administration of CCl4 also induced stronger hepatic injury in JnkÎhepa mice, based on increased inflammation, cell proliferation, and fibrosis progression, compared to Jnk1Îhepa or control mice. Hepatocytes from JnkÎhepa mice given acetaminophen had an increased oxidative stress response, leading to decreased activation of AMPK, total protein AMPK levels, and pJunD and subsequent necrosis. Administration of SP600125 before or with acetaminophen protected JnkÎhepa and control mice from liver injury. CONCLUSIONS: In hepatocytes, JNK1 and JNK2 appear to have combined effects in protecting mice from CCl4- and acetaminophen-induced liver injury. It is important to study the tissue-specific functions of both proteins, rather than just JNK1, in the onset of toxic liver injury. JNK inhibition with SP600125 shows off-target effects. Livers and primary hepatocytes were isolated from wild type and JNKÎhepa (Jnk1Îhepa/global Jnk2-/-) double-knockout mice and subjected to gene expression profiling.
2016-01-04 | E-GEOD-59602 | biostudies-arrayexpress
Project description:In this study, juvenile rainbow trout were exposed four dietary doses of organic selenium (7.1, 10.7 19.5 and 31.8 mg/kg Selenium) over 60 days. The RNA was exctracted from liver tissue and used for further gene expression analysis.
2015-06-30 | GSE67599 | GEO
Project description:In this study, juvenile rainbow trout were exposed four dietary doses of organic selenium (7.1, 10.7 19.5 and 31.8 mg/kg Selenium) over 60 days. The RNA was exctracted from liver tissue and used for further gene expression analysis. There were 39 samples analyzed (8) control liver tissues (8) 7.1 mg/kg Se dosed fish liver tissues (7) 10.7 mg/kg Se dosed fish liver tissues (8) 19.5 mg/kg Se dosed fish liver tissues (9) 31.8 mg/kg Se dosed fish liver tissues. There was a total of 39 microarrays processed.
2015-06-30 | E-GEOD-67599 | biostudies-arrayexpress
Project description:Acute liver failure is a serious clinical manifestation resulting from sudden liver injury, which can be triggered by various factors. One of the most frequent causes of acute liver failure is excessive ingestion of acetaminophen (APAP), which is known to damage hepatocytes directly by reducing glutathione levels in cells, ultimately leading to hepatocyte death.PGE2 can play a dual role in inflammation, either promoting or inhibiting the inflammatory response, depending on the cell type, local concentration, receptor type, and tissue microenvironment. Early studies have shown that PGE2 significantly alleviated acute liver failure induced by galactosamine/lipopolysaccharide, APAP, and carbon tetrachloride. However, the precise mechanism by which PGE2 alleviates APAP-induced acute liver failure remains unclear. The aim of this study is to investigate the mechanisms underlying the protective effects of PGE2 against APAP-induced hepatocyte injury.
2023-09-01 | GSE241511 | GEO