AI Article Synopsis
- This study looked at a special molecule called H19 to see how it behaves in people with a disease called systemic lupus erythematosus (SLE).
- The researchers found that H19 levels were higher in SLE patients, while another molecule called miR-19b had lower levels in their blood.
- They discovered that H19 might make certain immune cells unhealthy by causing them to die and react more, which could help understand why SLE happens.
Article Abstract
Aim: This study aimed to investigate the expression of H19 and its possible molecular mechanism in systemic lupus erythematosus (SLE).
Methods: The expression of H19 and miR-19b in serum and peripheral blood mononuclear cells (PBMCs) were detected by reverse transcription quantitative polymerase chain reaction (RT-qPCR). Receiver operator characteristic (ROC) curve was constructed to evaluate the diagnostic value of serum H19 in SLE. Pearson correlation coefficient was used to analyze the correlation between serum levels of H19 and miR-19b. Flow cytometry and Cell counting kit-8 (CCK-8) assay were performed to detect cell apoptosis and viability. The levels of pro-inflammatory and anti-inflammatory factors were measured by enzyme-linked immunosorbent assay (ELISA). Luciferase reporter gene assay was conducted to verify the interaction between H19 and miR-19b.
Results: The expression of H19 and miR-19b in SLE group were up-regulated and down-regulated, respectively. Serum H19 has certain clinical diagnostic value in SLE. In in vitro studies, overexpression of H19 can significantly inhibit the viability of PBMCs and promote apoptosis and inflammatory response of PBMCs by interacting with miR-19b.
Conclusions: The expression of H19 is upregulated in patients with SLE and plays a role in cell function and inflammation by targeting miR-19b in PBMCs, which may be one of the pathological mechanisms of SLE.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1177/09612033241243175 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
The Association of Cell-Free LncH19 and miR-29b Expression with the PI3K/AKT/HIF-1/VEGF Pathway in Patients with Diabetic Nephropathy: In Silico Prediction and Clinical Validation.
Curr Issues Mol Biol
December 2024
Medical Biochemistry and Molecular Biology Department, Faculty of Medicine, Suez Canal University, Ismailia 41522, Egypt.
Diabetic nephropathy (DN) affects about one-third of patients with diabetes and can lead to end-stage renal disease despite numerous trials aimed at improving diabetic management. Non-coding RNAs (ncRNAs) represent a new frontier in DN research, as increasing evidence suggests their involvement in the occurrence and progression of DN. A growing body of evidence suggests that long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) in DN signaling pathways might serve as novel biomarkers or therapeutic targets, although this remains to be fully explored.
View Article and Find Full Text PDFGeneration of live mice from haploid ESCs with germline-DMR deletions or switch.
Cell Discov
January 2025
Key Laboratory of Multi-Cell Systems, Shanghai Key Laboratory of Molecular Andrology, CAS Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, China.
Genomic imprinting is required for sexual reproduction and embryonic development of mammals, in which, differentially methylated regions (DMRs) regulate the parent-specific monoallelic expression of imprinted genes. Numerous studies on imprinted genes have highlighted their critical roles in development. However, what imprinting network is essential for development is still unclear.
View Article and Find Full Text PDFCracking the code: lncRNA-miRNA-mRNA integrated network analysis unveiling lncRNAs as promising non-invasive NAFLD biomarkers toward precision diagnosis.
Comput Biol Chem
January 2025
Institute of Global Health and Human Ecology (IGHHE), School of Sciences and Engineering, The American University in Cairo, New Cairo 11835, Egypt. Electronic address:
Background: Non-alcoholic fatty liver disease (NAFLD) involves abnormal fat accumulation in the liver, mainly as triglycerides. It ranges from steatosis to non-alcoholic steatohepatitis (NASH), which can lead to inflammation, cellular damage, liver fibrosis, cirrhosis, or hepatocellular carcinoma (HCC). Long non-coding RNAs (lncRNAs) are crucial for regulating gene expression across various conditions.
View Article and Find Full Text PDFMir-483-5p-mediated activating of IGF2/H19 enhancer up-regulates IGF2/H19 expression via chromatin loops to promote the malignant progression of hepatocellular carcinoma.
Mol Cancer
January 2025
Department of Gastroenterology, The First Affiliated Hospital, Jinan University, Guangzhou, Guangdong, 510630, P. R. China.
Article Synopsis
- The study focuses on the role of miR-483-5p in regulating the overexpression of IGF2 and H19, which are linked to hepatocellular carcinoma (HCC).
- miR-483-5p enhances IGF2 and H19 expression by binding to their enhancer, activating transcription, and promoting new interactions between the enhancer and gene promoters through chromatin loops.
- The research highlights that MED1 is crucial in this process, influencing both chromatin structure and the aggressive behavior of HCC cells, indicating potential targets for therapeutic interventions.
A Novel Competing Endogenous RNA Network Reveals Potential Mechanisms and Biomarkers of Chemoresistance in Lung Adenocarcinoma.
J Cancer
January 2025
Department of Biostatistics, School of Public Health, Harbin Medical University, Harbin 150081, China.
Platinum resistance is a common cause of chemotherapy failure in lung adenocarcinoma (LUAD). Competing endogenous RNAs (ceRNAs), which function by competitively binding to miRNAs, can influence drug response. However, the regulatory mechanisms of ceRNAs underlying chemoresistance in LUAD remain largely unknown.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!