Microarray combined with multiple bioinformatics for identifying hub hematopietic genes during recovery phase of irradiation injury
10.3724/SP.J.1008.2012.001293
- Author:
Yue YANG
1
Author Information
1. Group of Neuropharmacology, School of Pharmacy, Shanghai Jiaotong University
- Publication Type:Journal Article
- Keywords:
Bone marrow;
Computational biology;
Experimental radiation injuries;
Hematopoietic stem cells;
Microarray analysis
- From:
Academic Journal of Second Military Medical University
2012;33(12):1293-1300
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the changes of global gene expression during bone marrow recovery period following sublethal ionizing radiation (IR) in mice. Methods The mice were exposed to 4 Gy of 60Co γ irradiation, and RNA samples were extracted from bone marrow cells at day 0, 3, 7, 11 and 21 after irradiation and were subjected to microarray analysis for identifying differentially expressed genes. Multiple bioinformatics analyses, including clustering analysis, gene ontology (GO) analysis, and dynamic gene network analysis, were conducted to identify key hub genes, pathways and biological processes during bone marrow recovery phase. Analysis was also made for the protein of the identified hub genes. Results Compared with non-IR stimulation group, 1 302 differential genes were identified by global gene expression profiling of the irradiation-damaged bone marrow. Clustering and GO analyses revealed that the immune response (especially hematopoiesis) associated genes played a critical role in the body function recovery after IR injury. Twenty-five of the differential genes were defined as the hub genes participating in two pathways including immune response and transcription/nucleosome assembly. Key node CCL3 improved the proliferation of hematopoietic stem cells (HSCs) by spontaneous down-regulation and increased degradation by CtsG. Conclusion The 25 genes identified by microarray analysis and bioinformatics analyses may play critical roles in recovery phase after IR. Key node CCL3 may increase the proliferation of HSCs by spontaneous down-regulation and increase of protein hydrolyzation.
