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RISS 인기검색어
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- 저자 : Die Zhou (검색결과 3 건)
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Zhou Zuolin,Zhi Chunchun,Chen Die,Cai Zhaowei,Jiang Xiaoling 한국유전학회 2023 Genes & Genomics Vol.45 No.10
Background Down syndrome (DS), the most frequently occurring human chromosomal disorder, is caused by trisomy 21. The exact molecular effects of trisomy on certain cell populations in the brain remain poorly understood. Objective The purpose of this study was to investigate the effects of trisomy on the transcriptomes of various types of neurons and nonneuronal cells in the hippocampus. Methods A total of 8993 nuclei from the WT and 6445 nuclei from the Dp16 hippocampus were analyzed by single-nucleus RNA sequencing (snRNA-seq). Cell clustering was achieved by the Seurat program. Results Hippocampal cells were grouped into multiple neuronal and nonneuronal populations. Only a limited number of trisomic genes were upregulated (q < 0.001) over 1.25-fold in a specific type of hippocampal cell. Specifically, deregulation of genes associated with synaptic signaling and organization was observed in multiple cell populations, including excitatory neurons, oligodendrocytes, and microglia. This observation suggests the potential importance of synapse deficits in DS. Interestingly, GO annotation of the upregulated genes suggested potential activation of the immune system by hippocampal excitatory neurons. Fewer trisomic genes were altered in nonneuronal cells than in neurons. Notably, microglial transcriptome analysis revealed significantly (q < 0.001) increased expression of C1qb and C1qc, which suggested potential involvement of complement-mediated synapse loss mediated by microglia in DS. Conclusion The trisomy-related hippocampal deficits should be driven by a small amount, not all, of the trisomic genes in a specific type of cell. Our work may help to narrow down both the molecular and cellular targets for future gene therapies in DS.
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Bo Bi,Liping Shan,Die Zhou 대한정신약물학회 2018 CLINICAL PSYCHOPHARMACOLOGY AND NEUROSCIENCE Vol.16 No.1
Patients with urologic chronic pelvic pain syndromes (UCPPS) report interstitial cystitis/bladder pain syndrome and/or chronic prostatitis/chronic pelvic pain syndrome. The pathogenesis of these syndromes remains unclear and there is currently no standard treatment. UCPPS is, therefore, often misdiagnosed and its management is complex. The present case report involves a 62-year-old male patient with UCPPS whose main presentation is painful bladder filling and painful urgency refractory to conventional treatment with medication, which was successfully treated with the combined use of duloxetine and olanzapine. The combined use of duloxetine and olanzapine may become a new therapeutic option in the management of UCPPS.
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Gen-Xia Liu,Shu Ma,Yao Li,Yan Yu,Yi-Xiang Zhou,Ya-Die Lu,Lin Jin,Zi-Lu Wang,Jin-Hua Yu 생화학분자생물학회 2018 Experimental and molecular medicine Vol.50 No.-
The putative tumor suppressor microRNA let-7c is extensively associated with the biological properties of cancer cells. However, the potential involvement of let-7c in the differentiation of mesenchymal stem cells has not been fully explored. In this study, we investigated the influence of hsa-let-7c (let-7c) on the proliferation and differentiation of human dental pulp-derived mesenchymal stem cells (DPMSCs) treated with insulin-like growth factor 1 (IGF-1) via flow cytometry, CCK-8 assays, alizarin red staining, real-time RT-PCR, and western blotting. In general, the proliferative capabilities and cell viability of DPMSCs were not significantly affected by the overexpression or deletion of let-7c. However, overexpression of let-7c significantly inhibited the expression of IGF-1 receptor (IGF-1R) and downregulated the osteo/odontogenic differentiation of DPMSCs, as indicated by decreased levels of several osteo/odontogenic markers (osteocalcin, osterix, runt-related transcription factor 2, dentin sialophosphoprotein, dentin sialoprotein, alkaline phosphatase, type 1 collagen, and dentin matrix protein 1) in IGF-1-treated DPMSCs. Inversely, deletion of let- 7c resulted in increased IGF-1R levels and enhanced osteo/odontogenic differentiation. Furthermore, the ERK, JNK, and P38 MAPK pathways were significantly inhibited following the overexpression of let-7c in DPMSCs. Deletion of let-7c promoted the activation of the JNK and P38 MAPK pathways. Our cumulative findings indicate that Let-7c can inhibit the osteo/odontogenic differentiation of IGF-1-treated DPMSCs by targeting IGF-1R via the JNK/P38 MAPK signaling pathways.
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