Mouse pre-microRNA Expression Construct mir-130a
- Known as:
- Mouse pre-microRNA Expression Construct mir-130a
- Catalog number:
- mmir-130a-pa-1
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Sbi systeme bioscience
- Gene target:
- Mouse pre-microRNA Expression Construct mir-130a
Related genes to: Mouse pre-microRNA Expression Construct mir-130a
- Gene:
- MIR130A NIH gene
- Name:
- microRNA 130a
- Previous symbol:
- MIRN130A
- Synonyms:
- hsa-mir-130a
- Chromosome:
- 11q12.1
- Locus Type:
- RNA, micro
- Date approved:
- 2004-04-23
- Date modifiied:
- 2019-01-30
Related products to: Mouse pre-microRNA Expression Construct mir-130a
Related articles to: Mouse pre-microRNA Expression Construct mir-130a
- Cadmium (Cd), as a common environmental pollutant, spreads in the ecosystem through nutrient transfer, posing potential hazards to livestock health and indirectly harming humans through the food chain. Cd can impair the immune function. Interestingly, Cd can also cause lung damage through apoptosis, but the mechanism of its lung toxicity remains unclear. MicroRNAs (miRNAs) are key post-transcriptional regulators implicated in various pathological processes, including inflammation and apoptosis. In this experiment, a pig model of Cd poisoning was established by administering 20 mg/kg CdCl₂ to the diet over a 40-day period. The actual Cd accumulation in pig lung tissue was confirmed by ICP-MS. Results showed that Cd exposure downregulated miR-130a and upregulated miR-532 in pig lung tissue. Bioinformatics prediction and experimental verification confirmed that miR-130a directly targets the Th1 marker tumor necrosis factor-α (TNF-α), while miR-532 targets the Th2 marker chemokine receptor 4 (CCR4). Downregulation of miR-130a relieved its inhibitory effect on TNF-α, and upregulation of miR-532 inhibited on CCR4, leading to a shift in the Th1/Th2 balance toward Th1. Furthermore, the Th1/Th2 imbalance induced by Cd activated the endoplasmic reticulum stress (ERS) pathway. The activated ERS pathway subsequently induced apoptosis. Collectively, our findings demonstrate that Cd exposure regulates the miR-130a/TNF-α and miR-532/CCR4 axes to induce Th1/Th2 imbalance, which further triggers ERS-mediated apoptosis in pig lung tissue. These observational results provide a reference solution for the pathogenesis of Cd-induced lung diseases in pigs, and lay a research foundation for the prevention and treatment intervention of Cd-related diseases in the livestock industry. - Source: PubMed
Publication date: 2026/08/25
Zhang YimingZhang ZiyiJing FeifeiZhao ZhirongZhao BingLi JichangLi Shu - Repeated blood donations deplete 200-250 mg of iron per donation. While biochemical consequences on iron stores are well documented, the role of circulating microRNAs (miRNAs) in maintaining iron homeostasis remains poorly characterized. This study investigated whether repeated blood donation alters iron metabolism-related miRNA expression. - Source: PubMed
Publication date: 2026/08/10
Karaca AzizÇitli ŞenolArpa MedeniSönmez Kübra - Arrhythmogenic cardiomyopathy (ACM/ARVC) is an inherited myocardial disease characterized by progressive fibro-fatty replacement, ventricular arrhythmias, and an increased risk of sudden cardiac death. In addition to mutations in desmosomal genes, growing evidence suggests that microRNAs (miRNAs) actively contribute to disease pathogenesis by regulating key processes such as fibrosis, cell adhesion, and cardiac remodeling. This systematic review analyzed the main miRNAs identified in studies of human cardiac tissue and animal models of ARVC. - Source: PubMed
Publication date: 2026/06/22
Napoletano GabrieleGhamlouch AlessandroRacciatti MauraSonnini ElenaTreves BiancamariaDe Angelis GaiaMontalto Filippo AlessandroMaiese AnielloLa Russa RaffaeleFrati PaolaDe Matteis Alessandra - Regular physical activity is a powerful non-pharmacological strategy for preventing and managing cardiovascular diseases (CVDs), including heart failure, by promoting cardioprotective adaptations through molecular mechanisms that remain incompletely elucidated. This review explores the central role of non-coding RNAs (ncRNAs), particularly microRNAs (miRNAs), in exercise-induced cardioprotection, highlighting their interactions within miRNA-lncRNA and miRNA-circRNA axes, as well as the function of exosomal miRNAs as key exerkines facilitating inter-organ crosstalk. Synthesizing current literature, we examine ncRNA biogenesis, canonical functions, and exercise-responsive profiles, focusing on pivotal miRNAs such as miR-1, miR-133, miR-21, miR-126, miR-29, miR-208a, and miR-499; lncRNA-miRNA networks including MALAT1/miR-150-5p, H19/miR-139, and GAS5/miR-217; circRNA-miRNA interactions like circUtrn/miR-132/212; and exosomal miRNAs derived from skeletal muscle (e.g., miR-130a, miR-1), brown adipose tissue (e.g., miR-17-3p), endothelium (e.g., miR-126), and cardiomyocytes (e.g., miR-21-3p). These elements are evaluated in models of physiological cardiac remodeling, myocardial infarction, ischemia-reperfusion injury, diabetic cardiomyopathy, and heart failure, with consideration of influencing factors such as sex, age, and training modality. Exercise-modulated miRNAs differentiate benign "athlete's heart" from pathological hypertrophy by governing angiogenesis, fibrosis, metabolic shifts, and arrhythmia risk, while lncRNA-miRNA and circRNA-miRNA axes regulate apoptosis, inflammation, mitochondrial dynamics, and extracellular matrix remodeling in CVD contexts. Exosomal miRNAs enable remote protection by activating survival, angiogenic, and anti-fibrotic pathways via signaling cascades like PI3K/AKT and NF-κB. Responses exhibit variability based on demographic and exercise variables, underscoring ncRNAs' promise as diagnostic biomarkers, therapeutic targets, or mimics of exercise benefits for heart failure management. - Source: PubMed
Publication date: 2026/03/25
Li YangWang JunminMa DeHe Jinpeng - Exposure to immune stress or lipopolysaccharide (LPS) during critical developmental stages like puberty may lead to gut microbiome dysbiosis and epigenetic dysregulation in mammary glands, affecting gene expression and potentially elevating breast cancer susceptibility in adulthood. Although LPS's adverse impacts on intestinal and brain functions are well-documented, its effects on mammary glands remain underexplored. Using an immunocompetent BALB/c mouse model, we administered an acute LPS dose (1.5 mg/kg body weight) during puberty. The study evaluated the long-term consequences of LPS exposure alone and combined with AHCC (Lentinula edodes cultured extract, 2 g/kg body weight/day) on DNA methylation patterns, cytokine profiles, and microRNA expression in mammary glands at 9 weeks of age. Analyses included DNA methylation sequencing, multiplex immunoassays, quantitative PCR, and image processing. Pubertal LPS exposure produced persistent molecular dysregulation in mammary glands, including differential DNA methylation (> 5% change vs. control; FDR-adjusted p < 0.05), elevated inflammatory mediators, and altered microRNA expression. Differentially methylated regions were enriched in regulatory features, with decreased methylation at transcription start sites, promoters, and 5' UTRs of genes implicated in mammary development and oncogenic signaling (including Vav3, Pdgfa, Pdgfc, Jag2, Hras, Ksr1, Il2rb, Il17b, and Il17rb) in the LPS group, whereas the AHCC + LPS group exhibited a shift toward hypermethylation at these loci (approximately 5%-10% decrease). Inflammatory profiling showed increased IL-17A/F (∼2-fold vs. control; p < 0.05), while microRNA analyses indicated reduced let-7a/c (∼30% vs. control; p < 0.05). Notably, miR-130a and miR-34a increased ∼1.5-fold across all treatment groups relative to control. Pubertal LPS exposure induces enduring epigenetic and inflammatory changes in mammary glands that may heighten breast cancer risk. AHCC's mitigating role indicates potential for dietary interventions to counteract these effects. - Source: PubMed
Yasavoli-Sharahi HamedShahbazi RoghayehAlsadi NawalSahebi Nasim BondarCuenin CyrilleCahais VincentChung Felicia Fei-LeiHerceg ZdenkoMatar Chantal