MicroRNA (Shariqah, United Arab Emirates)最新文献

Introduction: Alzheimer's disease (AD) is a late-onset neurodegenerative disease that affects older people. Deregulations of miRNAs play essential roles in AD pathogenesis; as a re-sult, they might be potential biomarkers for AD development, diagnosis, and treatment. This case-control study aimed to assess the expression of miR-214, miR-204, miR-15a, miR-25, and inves-tigate their correlations with the expression of IL-33, plasma level of Malondialdehyde (MDA), and Mini-Mental State Examination (MMSE) score of the AD patients.

Methods: Blood samples were obtained from 125 participants, including 75 AD patients and 50 healthy controls. Plasma MDA level was assessed using the ZellBio ELISA kit. Total RNA was extracted from blood lymphocytes using RiboExTM (GeneAll), and expression levels of miRNAs and IL-33 were evaluated by qRT-PCR.

Results: Results showed that miR-15a and miR-25, and IL-33 were downregulated in the pa-tients' group, but miR-214 and miR-204 were upregulated. Besides, the plasma level of MDA was significantly higher in the AD patients. A statistically significant negative correlation was observed between miR-15a and IL-33 expression. The MDA level showed a negative correlation with MMSE and a positive correlation with IL-33. Correlations between the miRNAs and MDA or MMSE scores were all non-significant. However, ROC curve analysis revealed that expres-sions of the studied miRNAs, IL-33, and the plasma level of MDA effectively differentiate AD patients from healthy controls.

Discussion: Results showed that expression levels of miR-214, miR-204, miR-25, miR-15a, and IL-33 and MDA plasma levels are deregulated in AD patients, highlighting their potential relation with AD pathogenesis.

Conclusion: Expression levels of the studied miRNAs and IL33, and plasma level of MDA might be considered as potential biomarkers for AD development and diagnosis.

Introduction: In animal taxa and jellyfish, the same genome encodes for the dif-ferent phenotypes that characterize life stages that follow each other during ontogeny. This situation underscores the existence of profound regulation of genomic information at the epigenetic level. MicroRNAs are fundamental epigenetic regulators. The aim of this study is to evaluate the role of microRNA regulation during jellyfish metamorphosis and to explore the existence of evolutionarily conserved microRNAs.

Methods: Specimens belonging to the 4-metamorphosis stages of A. aurita (polyps, ephyra, young, and adult jellyfish) were bred and collected. The expression of 2,549 miRNAs for each stage was tested using microarray technology. The comparison of microRNA expres-sion for each phase was performed using line plot analysis and Principal Component Anal-ysis of variance (PCA), while the identification of microRNA clusters was performed via volcano plot analysis.

Results: A remarkable number of A. aurita miRNAs specifically hybridize with a human miRNA library. Each metamorphosis stage is characterized by a different level of expression of miRNAs: 1) Polyp vs. Ephyra stage: 128 upregulated, 2 downregulated; 2) Ephyra vs. Young stage: 2 upregulated, 135 downregulated; 3) Young vs. Adult stage: 69 upregulated, 6 downregulated. Specific functions inferred from known activities of corresponding miR-NAs in higher animals (PubMed database) appear to be coherent with the correlated exper-imental model.

Discussion: Present results reveal that microRNAs with human homologs undergo specific expression changes throughout Aurelia aurita metamorphosis. This observation reinforces the hypothesis of a shared evolutionary origin of certain miRNA families between Cnidaria and Bilateria. The dynamic and stage-specific regulation pattern observed suggests that miR-NAs play a key role in orchestrating the complex transitions involved in jellyfish develop-ment. These findings point to a broader conservation of epigenetic mechanisms, such as miRNA-mediated gene silencing, which may have emerged early in metazoan evolution and contributed to the regulation of cell differentiation and phenotype modulation.

Conclusion: The present study highlights the importance of Aurelia aurita as a model for investigating miRNA-driven epigenetic regulation in non-bilaterian animals. The identifica-tion of human-homologous miRNAs provides novel insights into the evolutionary stability of the epigenetic machinery and suggests conserved regulatory functions across distant taxa. Although limited by the use of a human-based microarray platform, the data presented here lay a solid foundation for future studies employing sequencing and functional assays to fur-ther explore the role of miRNAs in cnidarian development and evolution.

Difficulties in wound healing pose a considerable clinical problem and are a significant source of morbidity in the general population. Systemic disorders such as diabetes and venous insufficiency often result in chronic wounds and an impaired healing process. The healthcare cost of treating chronic wounds in the U.S. already exceeds 20 billion dollars per year and is expected to rise with an aging population and increasing incidence of diabetes. Recently, research and review articles have been used to understand the normal healing process and identify the reasons why certain wounds fail to heal, which should enable the development of more effective thera-peutic interventions. Animal models have provided valuable information; however, the healing process differs between humans and animals, and data obtained from in vitro studies can be chal-lenging to extrapolate to a clinical context. In conclusion, this study aims to summarize the current understanding of inflammation, epithelialization, and tissue repair processes, mainly through the use of data from in vitro and in vivo studies. Inflammation, re-epithelialization, granulation tissue development, and collagen remodeling are the fundamental steps in the healing process. As a result, any deviation from the normal sequence and time course of events may result in abnormal healing. Wound healing occurs to repair damaged, devitalized, or missing cells and tissues. In human beings, the result is the reestablishment of structural and functional integrity. This is a vital process that all living organisms undergo at some stage in their lives.

The revolutionary CRISPR/Cas9 gene editing technology holds immense potential for treating genetic diseases and tackling conditions like cancer. However, efficient delivery remains a significant challenge. This is where nanoparticles come into play, emerging as powerful allies in the realm of drug delivery. Nanoparticles can accommodate larger insertion sizes, enabling the incorporation of larger Cas9 enzymes and complex guide RNAs, thus opening up the possibility of editing previously inaccessible genetic regions. Their relatively straightforward and scalable production processes make them cost-effective options for wider applications. Notably, nanoparticles excel in vivo, demonstrating efficient tissue penetration and targeted delivery, which are crucial for maximizing therapeutic impact while minimizing side effects. This review aims to explore the potential of nanoparticle-based delivery systems for CRISPR/Cas9, highlighting their advantages and challenges in gene editing applications. The diverse range of nanoparticles further bolsters their potential. Polymeric nanoparticles, for instance, offer tunable properties for customization and controlled release of the CRISPR cargo. Lipid-based nanoparticles facilitate efficient cellular uptake and endosomal escape, ensuring the CRISPR components reach the target DNA. Even gold nanoparticles, known for their unique biocompatibility and photothermal properties, hold promise in light-activated editing strategies. Non-viral delivery systems, particularly those based on nanoparticles, stand out due to their inherent advantages. Collectively, the evidence paints a promising picture: nanoparticles are not merely passive carriers but active participants in the CRISPR/Cas9 delivery landscape. Their versatility, efficiency, and safety position them as key enablers of a future where gene editing can revolutionize drug development, offering personalized and targeted therapies for a wide range of diseases.

MicroRNAs (miRNAs) are molecules that regulate gene expression by targeting the 3' untranslated region (UTR) of mRNAs. They are essential in numerous biological processes like growth, metabolism, and muscle development. miRNA research has become crucial in livestock breeding, offering solutions for improving animal health and productivity. This review focuses on miRNAs' roles in equine performance, reproduction, and disease, highlighting key findings and future applications in these areas. It discusses the use of circulating miRNAs (ci-miRNA) as biomarkers for athletic performance, particularly in endurance sports, by monitoring responses to exercise-induced stress and recovery. It also examines miRNAs involved in reproductive health, such as those influencing endometritis, oocyte maturation, and embryo development. In terms of disease, miRNAs are highlighted as potential biomarkers for osteoarthritis and sarcoids, offering insights into early diagnosis and treatment. Overall, the review emphasizes the promise of miR-NAs in improving equine care through personalized diagnostics and therapeutic approaches.

In the last forty years, cancer mortality rates have risen by more than 40%, with colo-rectal cancer (CRC) ranking as the third most common kind worldwide, significantly affected by dietary factors. Restricted access to sophisticated medical treatment and insufficient comprehen-sion of colorectal cancer's biology contribute to its elevated occurrence. Researchers have recog-nized dysbiosis of the gut microbiome as a critical contributor to the development of colorectal cancer, as it influences the expression of non-coding RNAs (ncRNAs) and subsequent molecular pathways essential for tumor proliferation. Moreover, interactions between gut and skin microbi-ota can impact systemic health and ncRNA regulation, influencing CRC advancement. This study shows how important the gut-skin microbiome axis is in developing colorectal cancer. It suggests that targeting this axis may lead to new treatments, such as changing the microbiome through probiotics, prebiotics, or fecal microbiota transplantation. Nonetheless, we must address obstacles such as population heterogeneity and intricate microbiome-host interactions to facilitate the tran-sition of these medicines into clinical practice. This study seeks to elucidate the roles of dietary treatments, microbiomes, and ncRNAs in the etiology and prevention of colorectal cancer (CRC).

Colorectal Cancer (CRC) is the third most lethal cancer worldwide. Complex intercel-lular communication within the tumor microenvironment influences cancer progression, thera-peutic resistance, with Exosomes (Exos) and Circulating Extracellular Vesicles (EVs) playing a critical role in this communication. Exosomes can impact recipient cells by carrying various bio-molecules, promoting changes that support cancer progression. This review focuses specifically on exosome-derived noncoding RNAs (ncRNAs) in CRC, including microRNAs (miRNAs]), circular RNAs (circRNAs), and long noncoding RNAs (lncRNAs), as significant regulators of cancer biology. The roles of these exosomal ncRNAs in CRC are central to tumor progression, metastasis, and treatment resistance. This review delves into specific molecular mechanisms, such as exosomal lncRNA H19, which enhances CRC chemoresistance by activating the β-catenin pathway, and exo-miR-21, which is implicated in 5-FU chemoresistance. We also high-light emerging evidence on exosomal circRNAs like circ_0006174, linked to doxorubicin re-sistance through miR-1205/CCND2 axis modulation. These exo-ncRNAs have shown promise as biomarkers and potential therapeutic targets, with studies indicating their diagnostic and prog-nostic capabilities in CRC patient cohorts. By examining recent in vivo and in vitro studies, we offer a comprehensive understanding of exosomal ncRNAs' roles in CRC pathogenesis and po-tential applications in clinical trials.

MicroRNAs (miRNAs) are a class of noncoding RNAs that regulate gene expression in cancer cells and Cancer Stem Cells (CSCs), and play an indispensable role in the development of resistance to radiotherapy and chemotherapy in cancer treatment. The dysregulation of miRNAs in CSCs plays a vital role in influencing the features of CSCs and their resistance mechanisms in different forms of cancer. These miRNAs are also engaged in regulating important signaling pathways, such as Notch and Wnt, which have an impact on the behavior of CSCs and their response to treatment. The intricate network of miRNAs and their interactions with essential proteins and major pathways highlight their potential as therapeutic targets for controlling cancer stem cell behavior and improving the outcomes of cancer therapy by understanding their effects. Comprehending the complex relationship among the production of microRNA, the environment surrounding the tumor, and the processes by which cells communicate can provide vital knowledge for developing successful treatments to overcome resistance to chemotherapy and radiation in cancer therapy.

MicroRNA (miRNA) modulation has emerged as a promising strategy in cancer immunotherapy, particularly in converting "cold" tumors with limited immune cell infiltration into "hot" tumors responsive to immunotherapy. miRNAs regulate immune cell recruitment and activation within the tumor microenvironment, influencing tumor behavior targeting specific miRNAs in cold tumors aims to enhance the immune response, potentially improving therapeutic efficacy. Despite ongoing research challenges, such as tumor complexity and treatment resistance, miRNA-based therapies offer personalized approaches with potential ethical considerations. Advances in miRNA profiling may enable early cancer detection and tailored treatments, underscoring its role in future oncology. This review sheds light on the role of miRNA in cold and hot tumor microenvironments, how they modulate depending on the tumor niche and the current research challenges in implementing miRNA-based therapies include the complexity of tumors and their heterogeneity, which makes it difficult to identify the most relevant miRNAs to target. Additionally, treatment resistance can develop over time, reducing the effectiveness of miRNA modulation. Despite these challenges, ongoing research and advancements in miRNA profiling hold promise for overcoming these obstacles and improving the outcomes of cancer immunotherapy. To overcome the challenges of identifying relevant miRNAs to target, researchers can employ high-throughput sequencing techniques to comprehensively profile miRNA expression in different tumor subtypes. They can also utilize bioinformatics tools and databases to analyze the vast amount of miRNA-related data and identify potential candidate miRNAs. Furthermore, collaborations between scientists and clinicians can help validate the functional significance of identified miRNAs and their potential as therapeutic targets.

Background: Myasthenia gravis is an autoimmune disease, and 30% of patients with thymoma often have myasthenia gravis. Patients with thymoma-associated MG (TAMG) have many different clinical presentations compared to non-MG thymoma (NMG), yet their gene expression differences remain unclear.

Objective: In this study, we analyzed the Differentially Expressed Genes (DEGs) and analyzed their regulatory microRNAs (miRNAs) in TAMG, which will further clarify the possible pathogenesis of TAMG.

Methods: DEGs were calculated using the RNA-sequencing data of TAMG and NMG downloaded from The Cancer Genome Atlas (TCGA) database. R software was then used to analyze the gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways of DEGs, while STRING was applied to build the protein-protein interaction (PPI) network and Cytoscape to identify and visualize the hub genes. Immune infiltration significances of hub genes were also explored by using the TIMER database and TCGA database. Upstream microRNAs (miRNAs) of the hub genes were predicted by online software.

Results: We comparatively analyzed the gene expression differences between TAMG and NMG groups. A total of 977 DEGs were identified between the two groups (|log fold change (FC)| >2, adjusted P value <0.050), with 555 down-regulated genes and 422 up-regulated genes. Five top hub genes (CTNNB1, EGFR, SOX2, ERBB2, and EGF) were recognized in the PPI network. Analysis based on the TIMER and TCGA databases suggested that 5 hub genes were correlated with multiple immune cell infiltrations and immune checkpoint-related markers, such as PDCD1, CTLA-4, and CD274, in TAMG patients. Lastly, 5 miRNAs were identified to have the potential function of regulating the hub gene expression.

Conclusion: Our study identified 5 hub genes (CTNNB1, EGFR, SOX2, ERBB2, and EGF) and their 5 regulatory miRNAs in TAMG, and the hub genes were correlated with multiple immune cell infiltrations and immune checkpoint-related markers. Our findings could help partially clarify the pathophysiology of TAMG, which could be new potential targets for subsequent clinical immunotherapy.