Mouse pre-microRNA Expression Construct mir-200a
- Known as:
- Mouse pre-microRNA Expression Construct mir-200a
- Catalog number:
- mmir-200a-pa-1
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Sbi systeme bioscience
- Gene target:
- Mouse pre-microRNA Expression Construct mir-200a
Related genes to: Mouse pre-microRNA Expression Construct mir-200a
- Gene:
- MIR200A NIH gene
- Name:
- microRNA 200a
- Previous symbol:
- MIRN200A
- Synonyms:
- hsa-mir-200a
- Chromosome:
- 1p36.33
- Locus Type:
- RNA, micro
- Date approved:
- 2004-04-23
- Date modifiied:
- 2019-01-24
Related products to: Mouse pre-microRNA Expression Construct mir-200a
Related articles to: Mouse pre-microRNA Expression Construct mir-200a
- Doxorubicin-induced cardiotoxicity (DIC) remains a major limitation of anthracycline-based chemotherapy, characterized by progressive myocardial dysfunction and heart failure. Increasing evidence implicates microRNAs (miRNAs) as critical post-transcriptional regulators of cardiomyocyte survival; however, their pharmacological relevance is often inferred from expression profiling rather than functional validation. This systematic review synthesizes evidence from preclinical studies (2015-2025) employing transfection-based approaches, including miRNA mimics and inhibitors, with downstream validation by qRT-PCR, Western blotting, and luciferase assays. A total of 24 studies were included, identifying key miRNAs that modulate DIC through distinct yet convergent molecular pathways. Protective miRNAs such as miR-200a, miR-21, and miR-29b attenuated oxidative stress and apoptosis primarily via activation of the Keap1/Nrf2 axis and suppression of Bax-dependent mitochondrial pathways. In contrast, miR-140-5p, miR-128-3p, and miR-34a-5p exacerbated cardiotoxicity by inhibiting antioxidant signaling, disrupting PPAR-γ and Sirt3 pathways, and promoting ferroptotic and pyroptotic cell death. Emerging evidence also implicates miRNA-mediated regulation of endoplasmic reticulum stress and autophagy, although inflammatory and fibrotic signaling pathways remain underexplored. Collectively, these findings position miRNAs as mechanistically relevant modulators of doxorubicin cardiotoxicity and potential pharmacological targets. However, the predominance of non-human models, limited pathway integration, and lack of clinically translatable delivery strategies constrain therapeutic advancement. Future studies should prioritize human-relevant systems, multi-omics integration, and targeted delivery platforms to enable the translation of miRNA-based interventions into cardioprotective therapies. - Source: PubMed
Publication date: 2026/09/18
Dhami Inderjit SinghKaur SatinderBhatti Gurjit KaurMastana Sarabjit SinghBhatti Jasvinder Singh - Chronic hepatitis B virus (CHB) infection remains a major cause of hepatocellular carcinoma (HCC), yet the premalignant microenvironment that links to HBV-associated HCC (HBV-HCC) is still poorly defined. This review synthesizes evidence that HBV-infected hepatocytes function as signaling hubs that, through microRNA (miRNA)-regulated crosstalk with Kupffer cells, liver sinusoidal endothelial cells, hepatic stellate cells and cancer-associated fibroblasts (CAFs), progressively remodel the liver from an antiviral tissue into a premalignant and early tumor microenvironment. Across the HBV-HCC continuum, a core set of dysregulated miRNAs, including miR-21, miR-29a/b, miR-122, miR-146a, miR-155, miR-200a, miR-126, miR-210 and the miR-130/301 family, coordinates transition from innate antiviral responses to HSC activation, extracellular matrix deposition, mechanotransduction, angiogenesis, chronic inflammation and cancer-associated CAF programing. By mapping these stage-specific miRNA networks onto acute infection, CHB, early fibrogenesis, advanced fibrosis and CAF-rich dysplastic states, the review reframes HBV-HCC pathogenesis as a sequence of miRNA-guided hepatocyte-stromal states rather than a purely hepatocyte-intrinsic process. This perspective suggests that composite, cell-type-resolved miRNA signatures in serum or liver tissue could serve as biomarkers for identifying CHB patients who are entering a premalignant microenvironment before conventional surveillance markers become abnormal. It further highlights miRNA hubs that couple antiviral, fibrogenic, angiogenic and CAF-associated signaling as potential therapeutic targets for reprograming the HBV-driven premalignant microenvironment, with the long-term goal of intercepting HBV-HCC development at earlier, microenvironmentally defined stages. - Source: PubMed
Publication date: 2026/08/24
Sartorius KurtKramvis AnnaChuturgoon Anil - Assessment of antemortem liver condition is often challenging in forensic autopsy, particularly when macroscopic findings are inconclusive and conventional postmortem biochemical markers are unreliable. MicroRNAs (miRNAs) are relatively resistant to degradation and may remain detectable in postmortem samples. Bile, a hepatocyte-derived biological fluid, represents an attractive but underexplored matrix for postmortem molecular analysis. In this study, bile samples were collected during forensic autopsy from cases with normal liver, fatty liver, and liver cirrhosis. MicroRNA expression profiles were first explored using next-generation sequencing, followed by differential expression analysis with TCC-GUI. Based on these exploratory results, selected miRNAs were quantitatively validated using quantitative real-time PCR. Distinct bile miRNA expression patterns were observed among the three histopathological groups. Quantitative PCR analysis demonstrated significantly reduced expression levels of miR-17, miR-29a, miR-29c, miR-194, and miR-200a in fatty liver and liver cirrhosis compared with normal liver, and miR-126 expression was significantly lower in liver cirrhosis cases. These findings indicate that bile miRNA expression profiles vary according to liver histopathological status in forensic autopsy cases. The present data support a preliminary, group-level association and suggest that bile miRNAs may provide supplementary information on morphological liver pathology, although controlled postmortem stability studies and larger age-matched cohorts are required before diagnostic or cause-of-death applications can be established. - Source: PubMed
Publication date: 2026/09/01
Kohyama TakanoriShinba YorikoAbe YukiYamashita HiromiTakei SellaMurase TakehikoIkematsu Kazuya - : Cystinuria is an inherited disorder characterized by impaired proximal tubular reabsorption of cystine, resulting in recurrent cystine stone formation. Mutations in the and genes are the main genetic causes of the disease, while variants in have also been associated with cystinuria in specific populations. Despite advances in understanding its molecular basis, cystinuria remains clinically heterogeneous, making disease progression and prognosis difficult to predict. This study aimed to investigate circulating microRNAs (miRNAs) as potential molecular biomarkers, characterize their expression profile in patients with cystinuria, and evaluate their association with clinical indicators of disease severity. : The study group included 16 patients with a clinically established diagnosis of cystinuria, while the control group consisted of 11 healthy individuals without a history of nephrolithiasis. Candidate miRNAs were selected based on their predicted regulatory interactions with genes implicated in cystinuria pathogenesis. Eight microRNAs (miR-29a-3p, miR-29b-3p, miR-29c-3p, miR-1207-3p, miR-10a-3p, miR-3658, miR-141-3p, and miR-200a-3p) were analyzed by quantitative real-time PCR (qPCR). Among the eight miRNAs evaluated, miR-10a, miR-141, miR-200a, and miR-3658 were significantly downregulated in patients with cystinuria compared with healthy controls. Higher expression levels of miR-10a, miR-141, and miR-200a were significantly associated with a greater number of previous surgical procedures ( < 0.05). Additionally, increased miR-10a expression was associated with impaired renal function, defined as serum creatinine levels above 1.2 mg/dL. miR-10a, miR-141, miR-200a, and miR-3658 were significantly downregulated in patients with cystinuria compared with healthy controls. Within the cystinuria cohort, higher expression of miR-10a was associated with impaired renal function, whereas increased expression of miR-10a, miR-141, and miR-200a correlated with a greater number of surgical interventions, suggesting a potential relationship with disease severity. Further studies in larger, genetically characterized cohorts are warranted to clarify the biological role and clinical utility of these miRNAs as biomarkers of cystinuria. - Source: PubMed
Publication date: 2026/07/28
Ayres Daniel CernachPimenta RuanDos Santos Gabriel ArantesCandido PatríciaAntunes MilenaDip Junior Nelson GasparMarchini Giovanni STorricelli Fábio CVicentini Fábio CDanilovic AlexandreBatagello Carlos ALeite Kátia R MNahas William CReis Sabrina TMazzucchi Eduardo - Type 2 diabetes mellitus (T2DM) is strongly associated with oxidative stress and inflammation. Harmaline (HAR), an alkaloid with antioxidant and anti-inflammatory properties, has been suggested to possess antidiabetic potential. This study investigated the effects of HAR in experimental T2DM and its association with changes in the nuclear factor erythroid 2-related factor 2 (Nrf2) and nuclear factor kappa-B (NF-κB) pathways. - Source: PubMed
Malekinia FarimaAhangarpour AkramHoseinynejad KhojastehMard Seyyed AliRadan MaryamNejaddehbashi Fereshteh