The miR-22-5p/Clec4e axis has diagnostic potential in fructose-induced nonalcoholic fatty liver disease
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1098750 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28618100.fastq.gz | Fastqsanger.gz | |||
| SRR28618101.fastq.gz | Fastqsanger.gz | |||
| SRR28618102.fastq.gz | Fastqsanger.gz | |||
| SRR28618103.fastq.gz | Fastqsanger.gz | |||
| SRR28618104.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 8 |
Similar Datasets
Project description:Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease.MicroRNAs play roles in the onset and progression of the disease. This study aimed to screen microRNA profiles and potential RNA networks for the diagnosis and treatment of NAFLD. Mice were high-fructose diet (HFrD) fed to induce NAFLD. MicroRNA expression profiles of the livers in HFrD mice and chow-diet fed mice were analyzed by RNA-seq. We successfully constructed high fructose induced NAFLD. There are 13 differentially expressed (DE) miRNAs in the livers of NAFLD mice. In summary, this study furthered our understanding of the genome mechanisms and the development of potential biomarkers for the treatment of fructose-induced NAFLD.
2024-11-15 | GSE263701 | GEO
Project description:The incidence rate of nonalcoholic steatohepatitis (NASH) is on the rise with no effective clinical treatment available to date. Understanding the key molecular mechanism underlying the process of NASH can provide theoretical support for the development of safe and effective therapeutic drugs. Sonic hedgehog (SHH) and heat shock protein 90β (HSP90β) have been implicated in NASH but their molecular mechanisms of action remain elusive. HSP90β was found to be a key SHH downstream molecule that promoted NASH processes In hepatocytes, SHH reduced HSP90β ubiquitylation through deubiquitylase USP31, thus preventing HSP90β degradation and promoting hepatic lipid synthesis. As an important component protein in the formation of exosomes, HSP90β is high in high fructose, high fat, and high cholesterol (HFFC) diet-induced NASH mouse model, leading to secretion of exosomes enriched with miR-28-5p. miR-28-5p directly targets and decreases Rap1b levels, which in turn promote NF-κB transcriptional activity in macrophages and stimulate the expression of inflammatory factors. Genetic deletion, pharmacological inhibition of the SHH-HSP90β axis, or delivery of miR-28-5p to macrophages in the liver, impaired NASH symptomatic development. Importantly, analysis of NASH patient sera revealed a markedly higher abundance of miR-28-5p compared to healthy donors. Taken together, the SHH-HSP90β-miR-28-5p axis offers promising therapeutic targets against NASH, and serum miR-28-5p may serve as a novel NASH diagnostic biomarker.
2024-01-10 | GSE232759 | GEO
Project description:The incidence rate of nonalcoholic steatohepatitis (NASH) is on the rise with no effective clinical treatment available to date. Understanding the key molecular mechanism underlying the process of NASH can provide theoretical support for the development of safe and effective therapeutic drugs. Sonic hedgehog (SHH) and heat shock protein 90β (HSP90β) have been implicated in NASH but their molecular mechanisms of action remain elusive. HSP90β was found to be a key SHH downstream molecule that promoted NASH processes In hepatocytes, SHH reduced HSP90β ubiquitylation through deubiquitylase USP31, thus preventing HSP90β degradation and promoting hepatic lipid synthesis. As an important component protein in the formation of exosomes, HSP90β is high in high fructose, high fat, and high cholesterol (HFFC) diet-induced NASH mouse model, leading to secretion of exosomes enriched with miR-28-5p. miR-28-5p directly targets and decreases Rap1b levels, which in turn promote NF-κB transcriptional activity in macrophages and stimulate the expression of inflammatory factors. Genetic deletion, pharmacological inhibition of the SHH-HSP90β axis, or delivery of miR-28-5p to macrophages in the liver, impaired NASH symptomatic development. Importantly, analysis of NASH patient sera revealed a markedly higher abundance of miR-28-5p compared to healthy donors. Taken together, the SHH-HSP90β-miR-28-5p axis offers promising therapeutic targets against NASH, and serum miR-28-5p may serve as a novel NASH diagnostic biomarker.
2024-01-10 | GSE232758 | GEO
Project description:Ovarian cancer is a malignant gynecologic disease rarely diagnosed in the early stages. Among ovarian cancers, clear cell carcinoma has a poor prognosis due to its malignant potential. MicroRNAs (miRNAs) regulate gene expression in cells by suppressing the translation of the target gene or by degrading the target mRNA. They are also secreted from the cells in the blood, binding to the proteins or lipids and assisting in cell-cell communication. Hence, serum miRNAs can also be diagnostic biomarkers for ovarian cancer. This study investigated and identified specific miRNAs for ovarian clear cell carcinoma and compared them to those of ovarian endometrioma in healthy patients. CA125, an ovarian tumor marker, did not differ between patients with ovarian clear cell carcinoma, endometriosis, or healthy controls. Four miRNAs (miR-146a-5p, miR-191-5p, miR-484, and miR-574-3p) were analyzed. The miR-146a-5p and miR-191-5p expression levels were significantly increased in the serum samples from the patients with ovarian clear cell carcinoma compared to the healthy controls but not in the patients with endometriosis (P < 0.05). Furthermore, the bioinformatics analysis showed that CCND2 and NOTCH2 were the candidate target genes of miR 146a-5p and miR-191-5p. In conclusion, our results showed that miR 146a-5p and miR-191-5p might be useful as early and non-invasive diagnostic tools in ovarian clear cell carcinoma. These miRNAs can help in distinguishing between ovarian clear cell carcinoma and ovarian endometrioma. To the best of our knowledge, no studies have screened any candidates specifically for clear cell carcinoma.
2023-10-06 | GSE239685 | GEO
Project description:High-throughput profiling of miRNA expression in the livers of vervet monkeys fed a high fructose or chow diet. Analysis of differentially expressed miRNAs revealed miR-148a-3p, miR-181a-5p, miR-342-5p and miR-574-5p may have regulatory roles in coordinating changes in hepatic gene expression in response to a high fructose diet.
2021-12-15 | GSE178269 | GEO
Project description:To study and correlate modulations of miRNome with modifications of transcriptome in human stress-induced senescent fibroblasts, Agilent microarrays data were compared by bioinformatics analysis with a focus on ECM components. We identified two unreported direct interactions since we highlighted a reduction in the expression of both miR-22-5p and -199a-5p in senescent fibroblasts, correlated to an increase of MMP1 expression.
2022-01-09 | GSE77406 | GEO
Project description:To study and correlate modulations of miRNome with modifications of transcriptome in human stress-induced senescent fibroblasts, Agilent microarrays data were compared by bioinformatics analysis with a focus on ECM components. We identified two unreported direct interactions since we highlighted a reduction in the expression of both miR-22-5p and -199a-5p in senescent fibroblasts, correlated to an increase of MMP1 expression.
2022-01-09 | GSE77074 | GEO
Project description:Diagnostic value of circulating miR-146b-5p and miR-222-5p in patients with acute myocardial infarction
| PRJNA1001022 | ENA
Project description:MiR-146a-5p and miR-191-5p as novel diagnostic marker candidates for ovarian clear cell carcinoma
| PRJNA1000564 | ENA
Project description:The crucial role of nutrition for cerebral health and the impact of dietary habits on brain structure and function have been long far recognized. To date a major health concern is associated with the increased consumption of fructose as added sugar in many types of drinks and processed foods, especially among young people. High-fructose intake has been pointed out as the possible culprit for the raised incidence of chronic diseases, such as obesity, cardiovascular disease, nonalcoholic fatty liver disease, and type 2 diabete. Further, it has been reported that high-fructose intake is associated with the over-activation of its cerebral metabolism, which was proposed to negatively impact on whole brain physiology and cognitive function. Notably, we previously reported that short-term fructose-rich diet induces mitochondrial dysfunction, oxidative stress, and neuroinflammation in hippocampus of young rats, as well as the imbalance of redox homeostasis, autophagic mechanisms and representation of synaptic markers in frontal cortex of both adult and young rats. Animal studies have also revealed the damaging effect of high-fructose diets on hippocampal functions during periods of neurocognitive development, such as childhood and adolescence. Hypothalamus plays a crucial role in maintaining whole body homeostasis. Long-term fructose overfeeding was reported to alter hypothalamic-pituitary-adrenal axis, leading to elevations in glucocorticoids in peri-adolescent rats [22]. Further, fructose overconsumption was associated with impairment of hypothalamic insulin signalling, oxidative stress and inflammation , and it was proposed that fructose-driven perturbations of hypothalamic function may compromise the potential for satiety, thereby increasing the prospect of developing obesity. Data currently available on hypothalamic dysfunctions related to a high-fructose diet essentially refer to the effects of long-term sugar feeding, while information on corresponding alterations associated with a short-term dietary treatment, particularly in the critical period of adolescence, is still lacking. Due to complexity and multiplicity of hypothalamic functions, there is also the need for a holistic characterization aimed at unveiling the general picture of hypothalamic dysfunctions associated with a high-fructose diet. To fill this gap, we investigated adolescent rats fed a fructose-rich or control diet, for 3 weeks. To verify whether the fructose-driven changes are rescued after the switch to a control diet, half of the rats from both animal groups were then fed a control diet for additional 3 weeks until young adulthood phase. Quantitative proteomics on hypothalamic extracts of all animal groups was used to identify molecular alterations triggered by fructose-rich diet and to obtain insights into the relationship between sugar feeding and possible dysfunctions of hypothalamus.
2023-03-11 | PXD038834 | Pride