hsa_mir_10a pre_miRNA Construct in pMIF_cGFP_Zeo
- Known as:
- hsa_mir_10a pre_miRNA Construct pMIF_cGFP_Zeo
- Catalog number:
- MIFCZ337PA-1
- Product Quantity:
- 10 ug
- Category:
- -
- Supplier:
- SBI
- Gene target:
- hsa_mir_10a pre_miRNA Construct pMIF_cGFP_Zeo
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Related articles to: hsa_mir_10a pre_miRNA Construct in pMIF_cGFP_Zeo
- Morphine and other synthetic opioids are widely prescribed to treat pain. Prolonged morphine exposure can paradoxically enhance pain sensitivity in humans and nociceptive behavior in rodents. To better understand the molecular mechanisms underlying opioid-induced hyperalgesia, we investigated changes in microRNA (miRNA) composition of small extracellular vesicles (sEVs) from the serum of mice after a morphine treatment paradigm that induces hyperalgesia. We observed significant differential expression of 18 miRNAs in sEVs from morphine-treated mice of both sexes compared with controls. Several of these miRNAs were bioinformatically predicted to regulate cyclic AMP response element binding protein (CREB), a well characterized transcription factor implicated in pain and drug addiction. We confirmed the binding and repression of Creb mRNA by miR-155 and miR-10a. We tested if serum-derived sEVs from morphine-treated mice could elicit nociceptive behavior in naïve recipient mice. Intrathecal injection of 1 μg sEVs did not significantly impact basal mechanical and thermal thresholds in naïve recipient mice. However, prophylactic 1 μg sEV administration in recipient mice resulted in faster resolution of complete Freund's adjuvant-induced mechanical and thermal inflammatory hypersensitivity. Other behaviors assayed following administration of these sEVs were not impacted, including sEV-conditioned place preference and locomotor sensitization. These results indicate that morphine regulation of serum sEV composition can contribute to analgesia and suggest a potential for sEVs to be a nonopioid therapeutic intervention strategy to treat pain. SIGNIFICANCE STATEMENT: A mouse model of opioid-induced hyperalgesia was used to show that chronic morphine treatment causes differential microRNA packaging into small extracellular vesicles (sEVs) present in the serum of mice. Two of these sEV microRNAs can downregulate CREB expression, and administration of these sEVs attenuates pain hypersensitivity in recipient mice. These studies position sEVs as a potential pain therapeutic and highlight changes underlying opioid-induced hyperalgesia, shedding light on a phenomenon with unclear pathophysiology. - Source: PubMed
Publication date: 2025/02/06
Reddy DeepaLin ZhuchengRamanathan SujayLuo XuanPande RichaTian YuzhenSide Christine MBarker Jacqueline MSacan AhmetBlendy Julie AAjit Seena K - Splenic masses are common in dogs and vary dramatically in their clinical behavior. Clinically, and even with histology, it can be challenging to differentiate between benign and malignant splenic masses. Hemangiosarcoma (HSA), the most common malignancy of the spleen, is a very aggressive tumor with a poor prognosis. We hypothesize that microRNAs (miRNAs) in mass tissue and serum can differentiate between HSA and other splenic masses. Fifty-nine miRNAs were investigated by reverse-transcription followed by real-time quantitative polymerase chain reaction (RT-qPCR) in serum and/or tissue from dogs with HSAs (serum = 24 and tissue = 17; postsplenectomy serum = 11), lymphomas (serum = 8 and tissue = 11), nonangiomatous nonlymphomatous sarcomas (serum = 6 and tissue = 10), histiocytic sarcomas (tissue = 4), benign splenic masses (myelolipomas, nodular hyperplasia, and hematomas; total serum = 21 and total tissue = 35), and normal dogs (serum = 14 and tissue = 7). Numerous miRNAs were differentially expressed in serum and tissue of HSA cases compared to those with other splenic masses or normal spleens. In serum, our 5-miRNA model (miR-135a-5p, miR-10a, miR-450b, miR-152-3p, and miR-126-5p) accurately classified 100% (24/24) of dogs with HSA from normal dogs and those with a benign splenic mass (recall = 1 for HSA). The overall accuracy of the model was 86%. In HSA and benign splenic mass tissues, our 3-miRNA model (miR-126-5p, miR-502-3p, and miR-452-5p) accurately classified 96% of the cases. This study demonstrates the utility of miRNA models in serum and tissue for screening and diagnosis of HSA in dogs. Future studies include the evaluation of prospective and prediagnosis serum samples. - Source: PubMed
Publication date: 2025/02/19
Ludwig LatashaTreleaven HeatherKhachadoorian ArleneDegasperi BrigitteWalter IngridStuart DeirdreFoster Robert AWood Robert DarrenAli R AyeshaWood Geoffrey A - The homeobox (HOX) genes especially for HOXA cluster play crucial roles in leukemogenesis. HOXA overexpression caused by genetic alterations, such as KMT2A rearrangements, NUP98- fusions and FLT3-ITD mutations, is frequently identified in AML. However, very few studies determined the DNA methylation-mediated epigenetic regulation of the HOXA cluster genes in AML. - Source: PubMed
Publication date: 2025/02/07
Xie FeiZhang Ting-JuanZhang Xin-LongXu Zi-JunQiao LiangWang YunZhao Yang-JingQian JunZhou Jing-Dong - The fat content of yak meat is significantly correlated with the meat quality, and an appropriate fat content helps to improve the texture of the meat. The involvement of miR-10a in regulating the differentiation and proliferation of various cell types has been reported. Therefore, in this study, the effects of miR-10a on lipid droplet accumulation were investigated by transfection of yak adipocyte precursors with an miR-10a inhibitor, followed by Oil Red O, BODIPY, EdU staining, and cell cycle analysis of the transfected and control cells. The relative expression of lipogenic marker genes was determined by RT-qPCR to clarify the effect of miR-10a on the differentiation and proliferation of yak adipocyte precursors. Mature adipocytes were collected for transcriptome analysis to identify differentially expressed target genes and the association of these genes with adipogenic pathways was investigated by GO and KEGG enrichment analyses. In addition, the phylogeny and expression profiles of miR-10a were analyzed in various yak tissues. The results showed that miR-10a could inhibit the differentiation and promote the proliferation of yak adipocyte precursors. Analysis of the RNA-Seq results showed that miR-10a inhibitor and inhibitor NC had six differentially expressed genes: FABP4, AKR1B7, IGF2, ROCK1, IFNB1, and PLA2G3. These genes were found to be involved in the regulation of adipogenesis, with IGF2 and IFNB1 being upregulated in the PI3K-Akt signaling pathway, which is activated upon stimulation by IGF2 and IFNB1 and inhibits the differentiation and promotes the proliferation of yak adipocytes precursor, which in turn affected adipogenesis. Moreover, phylogenetic analysis indicated that miR-10a evolved relatively recently in yak and sheep, while tissue expression profiles showed that miR-10a was highly expressed in yak lung tissues. - Source: PubMed
Publication date: 2024/12/24
Su QuyangangmaoGao ZhanhongZhang FengshuoWu ZhenlingJi QiurongZhu KainaGui Linsheng - Acute myeloid leukemia (AML) is characterized by impaired differentiation of myeloid cells leading to hematopoietic failure. Despite advances, the molecular mechanisms driving AML remain incompletely understood, limiting the identification and targeting of critical vulnerabilities in leukemic cells. Homeobox (HOX) genes, encoding transcription factors essential for myeloid and lymphoid differentiation, are distributed across four clusters: HOXA (chromosome 7), HOXB (chromosome 17), HOXC (chromosome 12), and HOXD (chromosome 2). In addition to protein-coding sequences, HOX clusters encode non-coding RNAs (ncRNAs), which are functional as transcripts and do not translate into proteins. This is the first study wherein we comprehensively reviewed the literature for HOX-embedded ncRNAs, encompassing long non-coding RNAs (lncRNAs), microRNAs, circular RNAs (circRNAs), and piwiRNAs with a role in AML. To date, there is no evidence of circular RNAs and piwi RNAs encoded from the HOX gene clusters. Our review focuses on how leukemic cells harness the regulatory mechanisms of HOX-cluster-derived ncRNAs, (predominantly HOXA and HOXB) to modulate expression of HOX transcription factors facilitating leukemogenesis. HOX ncRNAs either regulate genes on the same chromosome (e.g., lncRNA HOTTIP) or influence expression of genes on different chromosomes (e.g., HOTAIR, HOX10-AS, miR-196b, and miR-10a). We discuss how specific HOX ncRNA networks are leveraged by leukemic cells, presenting an opportunity to explore targeted therapies and address the molecular heterogeneity of AML. Additionally, the aberrant expression of HOX ncRNAs such as HOXB derived ncRNAs in NPM1 mutated AML suggests their potential utility as improved biomarkers and for prognostication of patients with specific molecular aberrations. - Source: PubMed
Publication date: 2024/11/30
Wilson ChristineSwaroop PriyankaKumar SachinChopra AnitaSharawat Surender K