Xin Wang1, Simin Li2, Yihong Ma3, Yuzhen Xu4, Anthony Chukwunonso Ogbuehi5, Xianda Hu6, Aneesha Acharya7, Rainer Haak2, Dirk Ziebolz2, Gerhard Schmalz2, Hanluo Li8, Sebastian Gaus8, Bernd Lethaus8, Vuk Savkovic8, Zhiqiang Su1. 1. Department of Neurology, First Affiliated Hospital of Harbin Medical University, Harbin 150001, China. 2. Department of Cariology, Endodontology and Periodontology, University Leipzig, Liebigstr. 12, 04103 Leipzig, Germany. 3. Department of Neurology, Graduate School of Medical Sciences, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan. 4. Department of Neurology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, No. 301 Middle Yanchang Road, Shanghai, China. 5. Faculty of Physics, University of Münster, Wilhelm-Klemm-Straße 9, 48149 Münster, Germany. 6. Laboratory of Molecular Cell Biology, Beijing Tibetan Hospital, China Tibetology Research Center, 218 Anwaixiaoguanbeili Street, Chaoyang, Beijing 100029, China. 7. Faculty of Dentistry, University of Hong Kong, Hong Kong, China. 8. Department of Cranio Maxillofacial Surgery, University Clinic Leipzig, Liebigstr. 12, 04103 Leipzig, Germany.
Abstract
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.
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.
Authors: Geerten P van Nieuw Amerongen; Pieter Koolwijk; Amanda Versteilen; Victor W M van Hinsbergh Journal: Arterioscler Thromb Vasc Biol Date: 2003-02-01 Impact factor: 8.311