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This study was aimed to investigate the influence of miR-33-5p on the M1/M2 polarization of microglia and the underlying mechanism. Transcriptome sequencing was performed using microglia from miR-33-5p mimic and control groups. In total, 507 differentially expressed genes, including 314 upregulated genes and 193 downregulated genes, were identified. The subnetwork of module A, which was extracted from the protein-protein interaction networks, mainly contained the downregulated genes. ,and , the members of module-A networks with the highest degrees, possess the potential of being biomarkers of ischemic stroke due to their function in the cell cycle. NFY, a transcription factor, was predicted to have the regulatory relation with nine downregulated genes. Overall, our findings will provide a valuable foundation for genetic mechanisms and treatment studies of ischemic stroke.
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http://dx.doi.org/10.1080/21655979.2022.2061285 | DOI Listing |
Cell Mol Immunol
September 2025
Department of Infectious Diseases, Medical Research Institute, Zhongnan Hospital of Wuhan University; Frontier Science Center for Immunology; Taikang Center for Life and Medical Sciences; State Key Laboratory of Virology; Institute of Hepatobiliary Diseases of Wuhan University, Wuhan, Hubei, 430071,
Upon DNA virus infection, cGAS senses viral DNA and triggers MITA (also called STING)-dependent induction of type I interferons (IFN-Is) and other cytokines/chemokines. IFN-Is further activate STAT1/2 to induce interferon-stimulated genes (ISGs) and the innate antiviral response. How the innate antiviral response is silenced in uninfected cells and efficiently mounts upon viral infection is not fully understood.
View Article and Find Full Text PDFGenes Immun
September 2025
Department of Genetics, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.
In coeliac disease (CeD), the epithelial lining (EL) of the small intestine is severely damaged by a complex auto-inflammatory response, leading intraepithelial lymphocytes to attack epithelial cells. To understand the intestinal changes and genetic regulation in CeD, we investigated the heterogeneity in the transcriptomic profile of the duodenal EL using RNA-seq and eQTL analysis on predicted cell types. The study included duodenal biopsies from 82 patients, grouped into controls, gluten-free diet treated CeD and untreated CeD.
View Article and Find Full Text PDFJ Neurosci
September 2025
Department of Neuroscience, College of Medicine, The Ohio State University, Columbus, OH 43210, USA
The purpose of this study was to investigate how Sphingosine-1-phosphate (S1P) signaling regulates glial phenotype, neuroprotection, and reprogramming of Müller glia (MG) into neurogenic MG-derived progenitor cells (MGPCs) in the adult male and female mouse retina. We found that S1P-related genes were dynamically regulated following retinal damage. (S1P receptor 1) and (sphingosine kinase 1) are expressed at low levels by resting MG and are rapidly upregulated following acute damage.
View Article and Find Full Text PDFJ Invertebr Pathol
September 2025
Aquatic and Animal Health Group, CIIMAR, University of Porto, Matosinhos 4450-208, Portugal.
Parasites can induce gene expression changes in their hosts, either benefiting the parasite or the host. In particular, trematodes are not only one of the most ubiquitous groups of aquatic parasites, they also have huge impacts on individual hosts with significant ecological and economic repercussions. The trematode Bucephalus minimus infects Cerastoderma edule (the edible cockle), a socioeconomically and ecologically important bivalve, as its first intermediate host.
View Article and Find Full Text PDFBone
September 2025
Department of Bone and Mineral Research, Research Institute, Osaka Women's and Children's Hospital, Osaka Prefectural Hospital Organization, Izumi, Osaka, 594-1101, Japan. Electronic address:
Hypophosphatasia (HPP) is caused by inactivating variants of ALPL, the gene encoding tissue non-specific alkaline phosphatase (TNSALP). In order to deepen our understanding of the pathogenic mechanisms of HPP, we herein generated ALPL-knockout (KO) human induced pluripotent stem (iPS) cells by applying CRISPR/Cas9-mediated gene deletion to an iPS clone derived from a healthy subject. We analyzed two ALPL-KO clones, one ALPL-hetero KO clone, and a control clone isogenic except for ALPL.
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