Xiaoxi Xi1, Yihong Ma2, Yuzhen Xu3, Anthony Chukwunonso Ogbuehi4, Xiangqiong Liu5, Yupei Deng5, Junming Xi1, Haitong Pan6, Qian Lin7, Bo Li8, Wanchen Ning9, Xiao Jiang10, Hanluo Li11, Simin Li10, Xianda Hu5. 1. Department of Stomatology, Northeast Petroleum University Affiliated Hospital, Fazhan Road, High Tech District, 163000 Daqing City, Heilongjiang Province, China. 2. Department of Neurology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto 860-0811, Japan. 3. Department of Neurology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, No. 301 Middle Yanchang Road, Shanghai, China. 4. Department of Physics, University of Münster, Wilhelm-Klemm-Str. 9, 48149 Münster, Germany. 5. Laboratory of Molecular Cell Biology, Beijing Tibetan Hospital, China Tibetology Research Center, 218 Anwaixiaoguanbeili Street, Chaoyang, Beijing 100029, China. 6. Department of Stomatology, Daqing Oilfield General Hospital, Zhongkang Street No. 9, Saertu District, 163000 Daqing City, Heilongjiang Province, China. 7. Department of Prosthetics, School of Stomatology, Second Affiliated Dental Hospital of Jiamusi University, Hongqi Street No. 522, Jiamusi City, Heilongjiang Province, China. 8. Department of Stomatology, South District Hospital, Daqing Oilfield General Hospital Group, Tuqiang Fourth Street No. 14, Hong Gang District, Daqing City, Heilongjiang Province, China. 9. Department of Conservative Dentistry and Periodontology, Ludwig-Maximilians-University of Munich, Goethestrasse 70, 80336 Munich, Germany. 10. Stomatological Hospital, Southern Medical University, 510280 Guangzhou, China. 11. Department of Cranio Maxillofacial Surgery, University Clinic Leipzig, Liebigstr. 12, 04103 Leipzig, Germany.
Abstract
AIM: To identify the critical genetic and epigenetic biomarkers by constructing the long noncoding RNA- (lncRNA-) related competing endogenous RNA (ceRNA) network involved in irreversible pulp neural inflammation (pulpitis). MATERIALS AND METHODS: The public datasets regarding irreversible pulpitis were downloaded from the gene expression omnibus (GEO) database. The differential expression analysis was performed to identify the differentially expressed genes (DEGs) and DElncRNAs. Functional enrichment analysis was performed to explore the biological processes and signaling pathways enriched by DEGs. By performing a weighted gene coexpression network analysis (WGCNA), the significant gene modules in each dataset were identified. Most importantly, DElncRNA-DEmRNA regulatory network and DElncRNA-associated ceRNA network were constructed. A transcription factor- (TF-) DEmRNA network was built to identify the critical TFs involved in pulpitis. RESULT: Two datasets (GSE92681 and GSE77459) were selected for analysis. DEGs involved in pulpitis were significantly enriched in seven signaling pathways (i.e., NOD-like receptor (NLR), Toll-like receptor (TLR), NF-kappa B, tumor necrosis factor (TNF), cell adhesion molecules (CAMs), chemokine, and cytokine-cytokine receptor interaction pathways). The ceRNA regulatory relationships were established consisting of three genes (i.e., LCP1, EZH2, and NR4A1), five miRNAs (i.e., miR-340-5p, miR-4731-5p, miR-27a-3p, miR-34a-5p, and miR-766-5p), and three lncRNAs (i.e., XIST, MIR155HG, and LINC00630). Six transcription factors (i.e., GATA2, ETS1, FOXP3, STAT1, FOS, and JUN) were identified to play pivotal roles in pulpitis. CONCLUSION: This paper demonstrates the genetic and epigenetic mechanisms of irreversible pulpitis by revealing the ceRNA network. The biomarkers identified could provide research direction for the application of genetically modified stem cells in endodontic regeneration.
AIM: To identify the critical genetic and epigenetic biomarkers by constructing the long noncoding RNA- (lncRNA-) related competing endogenous RNA (ceRNA) network involved in irreversible pulp neural inflammation (pulpitis). MATERIALS AND METHODS: The public datasets regarding irreversible pulpitis were downloaded from the gene expression omnibus (GEO) database. The differential expression analysis was performed to identify the differentially expressed genes (DEGs) and DElncRNAs. Functional enrichment analysis was performed to explore the biological processes and signaling pathways enriched by DEGs. By performing a weighted gene coexpression network analysis (WGCNA), the significant gene modules in each dataset were identified. Most importantly, DElncRNA-DEmRNA regulatory network and DElncRNA-associated ceRNA network were constructed. A transcription factor- (TF-) DEmRNA network was built to identify the critical TFs involved in pulpitis. RESULT: Two datasets (GSE92681 and GSE77459) were selected for analysis. DEGs involved in pulpitis were significantly enriched in seven signaling pathways (i.e., NOD-like receptor (NLR), Toll-like receptor (TLR), NF-kappa B, tumor necrosis factor (TNF), cell adhesion molecules (CAMs), chemokine, and cytokine-cytokine receptor interaction pathways). The ceRNA regulatory relationships were established consisting of three genes (i.e., LCP1, EZH2, and NR4A1), five miRNAs (i.e., miR-340-5p, miR-4731-5p, miR-27a-3p, miR-34a-5p, and miR-766-5p), and three lncRNAs (i.e., XIST, MIR155HG, and LINC00630). Six transcription factors (i.e., GATA2, ETS1, FOXP3, STAT1, FOS, and JUN) were identified to play pivotal roles in pulpitis. CONCLUSION: This paper demonstrates the genetic and epigenetic mechanisms of irreversible pulpitis by revealing the ceRNA network. The biomarkers identified could provide research direction for the application of genetically modified stem cells in endodontic regeneration.
Authors: Baris E Dayanc; Sanjay Bansal; Ali Osmay Gure; Sandra O Gollnick; Elizabeth A Repasky Journal: Int J Hyperthermia Date: 2013-08 Impact factor: 3.914