Mouse pre-microRNA Expression Construct mir-181c
- Known as:
- Mouse pre-microRNA Expression Construct mir-181c
- Catalog number:
- mmir-181c-pa-1
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Sbi systeme bioscience
- Gene target:
- Mouse pre-microRNA Expression Construct mir-181c
Related genes to: Mouse pre-microRNA Expression Construct mir-181c
- Gene:
- MIR181C NIH gene
- Name:
- microRNA 181c
- Previous symbol:
- MIRN181C
- Synonyms:
- hsa-mir-181c
- Chromosome:
- 19p13.12
- Locus Type:
- RNA, micro
- Date approved:
- 2004-04-23
- Date modifiied:
- 2019-01-18
Related products to: Mouse pre-microRNA Expression Construct mir-181c
Related articles to: Mouse pre-microRNA Expression Construct mir-181c
- In regenerative settings, robust differentiation of human mesenchymal stromal cells (hMSCs) requires precise coupling between post-transcriptional regulation and kinase-driven pathways to achieve optimal therapeutic efficacy. miRNA-mediated regulation is widely implicated in stem cell fate control, yet its mechanistic contribution to lineage commitment remains incompletely defined. - Source: PubMed
Publication date: 2026/09/23
Gao JingyiLiu AnhaoKaung Myint Ye YintHatasa MasahiroSrithanyarat Supreda SuphanantachatIwata Takanori - An altered T-cell repertoire with aberrant immune activation is central to the pathogenesis of acquired aplastic anemia (aAA), and miRNAs are known to orchestrate T-cell activation; their relationship is, however, incompletely explored in aAA. The study aimed to validate specific miRNA-mRNA pairs involved in aberrant T-cell activation, differentiation, and cytokine levels in aAA. - Source: PubMed
Publication date: 2026/08/16
Sabereen GhazalaGupta RuchiSingh Manish KumarGupta KusumRahman KhaliqurChaturvedi Chandra PrakashChandra DineshKashyap Rajesh - Alzheimer's disease (AD) is characterized by amyloid-β (Aβ) peptide plaques and neurofibrillary tangles from hyperphosphorylated tau, though factors linking amyloid and tau pathology remain unclear. We investigated whether microRNA-181d-5p (miR-181d) associates with AD-related brain changes and regulates neprilysin and tau. Modeling miR-181d across individuals with no cognitive impairment, mild cognitive impairment, and AD revealed region- and sex-specific associations. Higher miR-181d levels associated with greater AD probability in the temporal lobe and cerebellum, and lower probability in the posterior cingulate cortex of males; miR-181c attenuated these probabilities. SNPs near MIR181 associated with altered entorhinal cortical thickness. In cellular models, miR-181 reduced neprilysin 3'-UTR activity, mRNA, protein, and enzymatic activity, while increasing tau mRNA and protein. Neprilysin diminution impairs Aβ clearance and elevates tau, contributing to AD. RNA sequencing identified miR-181d-responsive neurodegenerative pathways. These findings identify miR-181 as a regulator of AD-relevant amyloid and tau pathways, providing novel targets. - Source: PubMed
Publication date: 2026/06/16
Wang RuizhiMaloney BryanNho KwangsikBeck John SCounts Scott ELahiri Debomoy K - Thermal injuries represent a significant global health burden, often complicated by hypertrophic scarring, chronic inflammation, and delayed re-epithelialization. While Mesenchymal Stem Cell (MSC) transplantation has shown promise, its clinical translation is hindered by risks of tumorigenicity and immunological concerns. This study evaluates the efficacy of cell-free Extracellular Vesicle (EV) therapy-derived from both mammalian MSCs and plant sources (PDNVs)-as standardized, off-the-shelf alternatives. This study synthesizes evidence focusing on re-epithelialization velocity, angiogenic activity, and anti-fibrotic outcomes, while assessing the impact of second-generation delivery scaffolds on therapeutic durability. Conducted in accordance with PRISMA 2020 guidelines and registered in PROSPERO (CRD420261305379), this review interrogated PubMed, Scopus, Embase, and Web of Science for studies published between 2015 and 2026. Eligible studies included in vivo animal models of thermal injury using purified vesicles from mammalian MSC sources or plant-derived nanovesicles compared with placebo, standard care, or untreated controls. Data were synthesized narratively; methodological quality was appraised using the SYRCLE risk of bias tool and compliance with MISEV guidelines. Synthesis of 50 studies revealed that vesicle-based interventions consistently accelerate wound closure and improve histological healing. Mammalian ADSC-derived vesicles demonstrated superior anti-fibrotic effects via the miR-192-5p and miR-125b-5p axes, while hUC-MSC vesicles attenuated systemic inflammatory signaling via miR-181c. Plant-derived nanovesicles (PDNVs) showed potent antioxidant and re-epithelialization effects, with emerging potential as engineered genetic carriers. Crucially, advanced delivery systems, including bioactive hydrogels and microneedle patches, were repeatedly associated with improved local retention and more durable effects than bolus injections. Vesicle-based therapies show consistent pro-healing signals in preclinical models, suggesting source-dependent profiles: MSC-derived vesicles excel in immunomodulation and anti-fibrotic remodeling, while PDNVs provide a scalable, low-immunogenicity platform. As a cell-free strategy, these therapies circumvent the safety risks of live cell transplantation. This review identifies a critical shift toward second-generation delivery scaffolds to overcome the clearance crisis of topical applications, emphasizing the need for harmonized MISEV-aligned characterization in future clinical translation. - Source: PubMed
Publication date: 2026/05/05
Amarandei Alexandru HristoAvadanei-Luca StefanaBulgaru-Iliescu Andra-IrinaMoraru Dan CristianSolovastru Dragos Florin GheucaConstantinescu Mihai-CodrinTatar RalucaPoroch VladimirGheuca Solovastru LauraPertea Mihaela - Chronic kidney disease (CKD) is a major global health burden leading to a loss of kidney function via podocyte damage, a non-regenerative renal cell type. Early detection of podocyte injury is crucial but remains limited, highlighting the need for non-invasive biomarkers. Therefore, we analysed urinary exosomal microRNAs (miRNAs) in relation to podocyte morphology in biopsies from 65 CKD patients, including focal segmental glomerulosclerosis (FSGS), minimal change disease (MCD) and healthy controls. Global profiling distinguished CKD patients from controls, with miR-606 consistently upregulated and miR-431 downregulated. In podocytopathies, MCD displayed a predominantly suppressed miRNA profile, with miR-141, miR-429, and miR-660 as key candidates, whereas FSGS exhibited elevated miR-181c, miR-3610, miR-663b, miR-4651, and miR-429. Super-resolution morphometry revealed diffuse foot process effacement in MCD and heterogeneous, focally disrupted architecture in FSGS, providing a structural context for the molecular findings. Regression analyses linked these miRNAs to filtration slit density and length, proteinuria, and 25-Hydroxy-vitamin-D3 levels, integrating molecular, structural, and clinical readouts. These results define a coherent miRNA signature of podocyte injury that distinguishes CKD entities and correlates molecular changes with disease severity. Combining urinary exosomal miRNAs with morphometric analysis facilitates early, non-invasive identification of podocyte damage, enabling earlier therapeutic intervention in podocytopathies. - Source: PubMed
Publication date: 2026/03/26
Lange TimMaron LuziaSimm StefanRibback SilviaDunkel Heikovon Rheinbaben SabrinaSchmidt TilmanSiegerist FlorianNauck MatthiasAmeling SabineFranzenburg SörenScheer ChristianDrenic VedranEndlich TimHoppstock GregorZimmermann UweVölker UweStracke SylviaMertens Peter REndlich Nicole