Mouse pre-microRNA Expression Construct mir-27b
- Known as:
- Mouse pre-microRNA Expression Construct mir-27b
- Catalog number:
- mmir-27b-pa-1
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Sbi systeme bioscience
- Gene target:
- Mouse pre-microRNA Expression Construct mir-27b
Related genes to: Mouse pre-microRNA Expression Construct mir-27b
- Gene:
- MIR27B NIH gene
- Name:
- microRNA 27b
- Previous symbol:
- MIRN27B
- Synonyms:
- hsa-mir-27b, MIR-27b
- Chromosome:
- 9q22.32
- Locus Type:
- RNA, micro
- Date approved:
- 2004-04-23
- Date modifiied:
- 2019-01-24
Related products to: Mouse pre-microRNA Expression Construct mir-27b
Related articles to: Mouse pre-microRNA Expression Construct mir-27b
- Osteoarthritis (OA) is the most prevalent degenerative joint disease and a leading cause of chronic pain and disability worldwide, particularly among aging populations. It is characterized by progressive degeneration of articular cartilage, synovial inflammation, subchondral bone remodeling, and metabolic alterations in the infrapatellar fat pad, reflecting pathology across the entire joint microenvironment. The onset and progression of OA are driven by complex interactions among mechanical stress, aging, obesity, and metabolic dysregulation, which collectively disrupt joint homeostasis. Mechanical injury and cartilage damage induce the release of damage-associated molecular patterns, activating innate immune receptors on chondrocytes and synovial cells. This promotes the production of pro-inflammatory mediators, including interleukin-1β, tumor necrosis factor-α (TNF-α), interleukin-6, and interleukin-17, which contribute to extracellular matrix degradation and cartilage deterioration. MicroRNAs (miRNAs), small non-coding RNAs that regulate gene expression post-transcriptionally, have emerged as key modulators in OA pathogenesis. They regulate chondrocyte proliferation, apoptosis, extracellular matrix turnover, inflammation, and osteochondral remodeling. Notably, certain miRNAs exhibit mechanosensitive properties, responding to altered biomechanical loading and translating mechanical stimuli into gene regulatory responses. This review synthesizes current evidence on the roles of miRNAs in OA, focusing on their regulatory functions across joint tissues, including cartilage, synovium, subchondral bone, and the infrapatellar fat pad. Key miRNAs such as miR-140, miR-146a, miR-27b, miR-34a, miR-155, and mechanosensitive miR-365 are discussed, along with their interactions with major inflammatory and degenerative signaling pathways. Their potential as diagnostic biomarkers and therapeutic targets is also highlighted. - Source: PubMed
Publication date: 2026/07/21
Safiyyu Mujitapha UmarSyed Nazmul HudaAzlan MaryamZain Muhammad Rajaei Ahmad MohdNurul Asma Abdullah - Swine enteric coronaviruses (CoVs) are causes of enteric disease in pigs, characterised by acute watery diarrhoea, more severe in piglets under 7 days of age. Small non-coding RNAs (miRNAs) have been implicated in the regulation of host immune responses during viral infections; however, their involvement in the intestinal response to CoVs infection and reinfection remains poorly understood. For this purpose, 48 four-week-old, weaned piglets were allocated into four experimental groups (n = 12). Groups B, C, and D were orally inoculated with PEDV, SeCoV, or rPEDV-SeCoV strain, respectively, while group A (control) received sterile buffer. Twenty days later, all groups were challenged with rPEDV-SeCoV strain. Clinical signs, growth performance, intestinal viral load, intestinal histomorphometry, and the expression of selected miRNAs and immune-related genes were analysed in duodenum and jejunum. Primary infection was associated with higher viral load, reduced villus height, and decreased average daily gain (ADG), whereas rechallenge resulted in lower viral load, reduced intestinal damage and limited impact on growth performance. At the molecular level, miR-124, miR-146, miR-223, and miR-27b tended to increase following rechallenge, in line with their previously described immunomodulatory functions, whereas miR-15b and miR-155 were associated with IFNG induction, suggesting an association with IFNG-related antiviral responses. These miRNA patterns were accompanied by IL8 expression dynamics, highlighting their involvement in the inflammatory response. Overall, these findings provide new insights into the intestinal immune responses to CoVs infection and reinfection and highlight the involvement of miRNA-mediated regulatory networks in shaping host responses to enteric coronavirus infection in pigs. - Source: PubMed
Publication date: 2026/08/03
Álvarez-Delgado CarmenRuedas-Torres InésArgüello HéctorCarvajal AnaCarrasco LibradoŚmieszek AgnieszkaGómez-Laguna JaimePuente Héctor - Heart disease is characterized by stress-induced endoreplication preceding pathological cardiomyocyte overgrowth, yet the upstream regulatory mechanisms linking tissue hypoxia to aberrant cellular growth remain incompletely defined. Here, we identify cardiac hypoxia as a key determinant of endoreplication through activation of a hypoxia-inducible factor-1 alpha-microRNA regulatory axis that converges on mitochondrial energetic control. We show that stress-induced activation of hypoxia-inducible factor-1 alpha drives transcriptional induction of microRNA-27b-5p, which directly represses the ATP synthase subunit ATP5A1, resulting in impaired mitochondrial ATP synthesis and accumulation of intra-mitochondrial ADP. Elevated ADP serves as a rate-limiting cofactor for one-carbon metabolism, promoting formate production and de novo purine biosynthesis, thereby enabling pathological endoreplication and cardiomyocyte hypertrophic growth. Genetic gain- and loss-of-function studies targeting hypoxia-inducible factor-1 alpha, microRNA-27b, and ATP5A1 across multiple mouse models of cardiac stress, together with correlative analyses of human cardiac biopsies, establish a conserved and causal relationship between dysregulated mitochondrial energetics and pathological cardiac remodeling. Inhibition of microRNA-27b-5p attenuates established cardiac hypertrophy, improves cardiac function, and suppresses stress-induced multinucleation in vivo. Leveraging this mechanistic insight, we identify the clinically approved antifolate compound methotrexate as an effective inhibitor of stress-induced cardiac endoreplication and pathological hypertrophy in preclinical models. Collectively, these findings define a druggable hypoxia-driven metabolic pathway linking mitochondrial ATP homeostasis to pathological cardiomyocyte growth and suggest therapeutic opportunities for targeting maladaptive cardiac remodeling. - Source: PubMed
Publication date: 2026/05/14
Mirtschink PeterYuan TingBischof CorinnePham Minh DucZhu ChaonanWare AkshayMao YijieWu MeiqianRogg Eva-MariaBottermann KatharinaGonzalez-Gonoggia SuamBerthonneche CorinneGercken BettinaHagag EmanStrassburger KatrinSossalla SamuelStehr Sebastian NAbplanalp WesleyZamboni NicolaMartelli FabioPedrazzini ThierryStoffel MarkusDimmeler StefanieKrishnan Jaya - Spinal cord injury (SCI) is a debilitating neurological condition that leads to physical dependence, substantial financial burden, and psychological stress. Current for SCI, such as stem cell therapy, pharmacological interventions, and neural implants offer limited functional recovery. Among emerging strategies, exosome-based therapies in nerve damage can reduce neuroinflammation and promote neural repair by angiogenesis and neurogenesis. MicroRNAs (miRNAs) are key modulators of inflammatory and regenerative pathways in SCI. Specifically, miR-19a-3p, miR-19b-3p, and miR-27b have been implicated in regulating neuroinflammatory responses, neuronal survival, and tissue remodeling. Dysregulation of these miRNAs following SCI can exacerbate inflammation and hinder recovery. In this study, exosomes were extracted and characterized using flowcytometry for surface markers CD81 and CD9, scanning electron microscopy (SEM), dynamic light scattering (DLS), and Zeta potential analysis. Thirty-two female rats were randomly assigned into four groups: laminectomy only, contusion, contusion + PBS, and contusion + exosomes. SCI were induced using contusion model and thirty minutes after the injury, the exosome-treated group received an intravenous injection of 100 μl of exosomes via the tail vein for 7 days. Motor and behavioral functions were assessed through the open-field test, Basso, Beattie, and Bresnahan (BBB) scale and narrow beam test (NBT). Eight weeks after the SCI, real time PCR, Western blotting was utilized to assess changes in inflammatory cytokines, while histological changes were observed using hematoxylin and eosin (H&E) staining and stereology. In vivo experiments showed that the administration of exosomes significantly enhanced functional recovery and behavioral test outcomes following SCI. The treatment also resulted in a significant reduction in inflammatory cytokine levels and a marked decrease in the size of the cavity in the group treated with exosomes. Molecular analysis revealed that exosome therapy modulated the expression of miR-19a-3p, miR-19b-3p, and miR-27b, which are key regulators of neuroinflammation and neural repair. These findings suggest that exosomes hold strong therapeutic potential for treating SCI by modulating inflammation and promoting neural repair. Collectively, these findings indicate a potential mechanism through which exosomes exert their neuroprotective effects, particularly by regulating inflammatory and regenerative pathways. - Source: PubMed
Publication date: 2026/01/05
Jahanbaz ShimaMosleh Hamid RezaDarabi ShahramTaheri HadiseMirni Hooman KazemiBahrami MaryamAliaghaei AbbasKaramian AminBahar RezaHasanzadeh MaralTahmasebinia FoozhanBeirami AmirrezaAbbaszadeh Hojjat-AllahDarabi Leila - Oral lichen planus (OLP) is a chronic T-cell-mediated immune disease of unknown aetiology. MicroRNA (miRNAs) are short non-coding RNAs capable of regulating mRNA and may have roles in T-cell-related diseases. The aim of this study was to investigate the profile of miRNAs in OLP patients and its interaction with potential target genes. - Source: PubMed
Publication date: 2026/02/03
Heba Mousa AliAnastasia ResteuAndreas WernerMarco Carrozzo