Aim. This study is aimed at identifying genetic and epigenetic crosstalk molecules and their target drugs involved in the interaction between neural stem/progenitor cells (NSPCs) and endothelial cells (ECs). Materials and Methods. Datasets pertaining to reciprocal mRNA and noncoding RNA changes induced by the interaction between NSPCs and ECs were obtained from the GEO database. Differential expression analysis (DEA) was applied to identify NSPC-induced EC alterations by comparing the expression profiles between monoculture of ECs and ECs grown in EC/NSPC cocultures. DEA was also utilized to identify EC-induced NSPC alterations by comparing the expression profiles between monoculture of NSPCs and NSPCs grown in EC/NSPC cocultures. The DEGs and DEmiRNAs shared by NSPC-induced EC alterations and EC-induced NSPC alterations were then identified. Furthermore, miRNA crosstalk analysis and functional enrichment analysis were performed, and the relationship between DEmiRNAs and small molecular drug targets/environment chemical compounds was investigated. Results. One dataset (GSE29759) was included and analyzed in this study. Six genes (i.e., MMP14, TIMP3, LOXL1, CCK, SMAD6, and HSPA2), three miRNAs (i.e., miR-210, miR-230a, and miR-23b), and three pathways (i.e., Akt, ERK1/2, and BMPs) were identified as crosstalk molecules. Six small molecular drugs (i.e., deptropine, fluphenazine, lycorine, quinostatin, resveratrol, and thiamazole) and seven environmental chemical compounds (i.e., folic acid, dexamethasone, choline, doxorubicin, thalidomide, bisphenol A, and titanium dioxide) were identified to be potential target drugs of the identified DEmiRNAs. Conclusion. To conclude, three miRNAs (i.e., miR-210, miR-230a, and miR-23b) were identified to be crosstalks linking the interaction between ECs and NSPCs by implicating in both angiogenesis and neurogenesis. These crosstalk molecules might provide a basis for devising novel strategies for fabricating neurovascular models in stem cell tissue engineering.

中文翻译：

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鉴定 miRNA 作为神经干/祖细胞与内皮细胞相互作用中的串扰

瞄准。本研究旨在鉴定参与神经干/祖细胞 (NSPCs) 和内皮细胞 (ECs) 相互作用的遗传和表观遗传串扰分子及其靶向药物。材料和方法. 从 GEO 数据库获得与由 NSPC 和 EC 之间的相互作用引起的相互 mRNA 和非编码 RNA 变化有关的数据集。差异表达分析 (DEA) 用于通过比较 ECs 的单一培养物和在 EC/NSPC 共培养物中生长的 ECs 之间的表达谱来识别 NSPC 诱导的 EC 改变。DEA 还用于通过比较 NSPC 的单一培养和在 EC/NSPC 共培养中生长的 NSPC 之间的表达谱来识别 EC 诱导的 NSPC 改变。然后鉴定了由 NSPC 诱导的 EC 改变和 EC 诱导的 NSPC 改变共享的 DEG 和 DEmiRNA。此外，还进行了miRNA串扰分析和功能富集分析，并研究了DEmiRNA与小分子药物靶点/环境化合物之间的关系。结果。本研究包括并分析了一个数据集 (GSE29759)。六个基因（即 MMP14、TIMP3、LOXL1、CCK、SMAD6 和 HSPA2）、三个 miRNA（即 miR-210、miR-230a 和 miR-23b）和三个通路（即 Akt、ERK1/2、和 BMP) 被鉴定为串扰分子。六种小分子药物（即地托品、氟奋乃静、石蒜碱、喹他汀、白藜芦醇和噻唑）和七种环境化合物（即叶酸、地塞米松、胆碱、多柔比星、沙利度胺、双酚 A 和二氧化钛）被确定为已鉴定的 DEmiRNAs 的潜在靶标药物。结论. 总而言之，三种 miRNA（即 miR-210、miR-230a 和 miR-23b）被确定为串扰，通过涉及血管生成和神经发生，将 ECs 和 NSPCs 之间的相互作用联系起来。这些串扰分子可能为设计用于在干细胞组织工程中制造神经血管模型的新策略提供基础。