Changes of gene expression of traumatic brain injury based on transcriptomics

Abstract

Objective To investigate the changes of gene expression after traumatic brain injury (TBI) and the neuroprotective mechanism after TBI. Methods A cell stretch injury model was induced by using a cell injury controller Ⅱ (CIC Ⅱ). Each parameter was set as pulse time 50 ms and metering valve pressure 0.165 MPa. The gas pulse pressure was 0.021±0.001 MPa. The cell RNAs were extracted by using Trizol reagent in the injury group and the control group, and then the mRNA sequencing was performed. The gene ontology of the differentially expressed genes was analyzed and the ingenuity pathway analysis (IPA) software was used to conduct signaling pathway analysis. The quantitative results were validated by qPCR. Results There were 14 310 000 and 15 510 000 reads were obtained respectively in the two samples, and 15 018 genes expressed in the two samples were identified. There were 1 424 differentially expressed genes. Compared to the control group, 1 198 genes were up-regulated and 226 genes were down-regulated in the injury group (P<0.01). Compared with the control group, HIF-1α and ZFP36 expression levels were down-regulated in the injury group and 13 differentially expressed genes after TBI were found and constituted a regulatory network with HIF-1α and ZFP36 as the center. In this network, HIF-1α was regulated by EGLN2 and ZFP36, and interacted with PER1, and regulated the expression of multiple downstream genes at the same time, such as H2AFX, ABCF2, and SLC39A7. Conclusions When the injury lasted for 12 hours, HIF-1α at the mRNA level was down regulated by ZFP36, HNRNPD, and EGLN2, respectively, and further regulated the expression of H2AFX, and then prevented the nerve cells from apoptosis, and promoted the repair of nerve cell injury. Key words: Craniocerebral trauma; Transcriptome; Gene expression; RNA sequence; Hypoxia inducible factor-1α