Abstract：Objective To investigate the association between long non-coding RNAs (lncRNAs) and brain injury in inflammation-induced preterm mice, and to provide a reference for the prevention and treatment of brain injury. Methods An intraperitoneal injection of lipopolysaccharide in pregnant mice was performed to establish a model of inflammation-induced preterm mice with brain injury (preterm group). The full-term mice delivered by normal pregnant mice were used as controls (full-term group). The lncRNA chip assay was used to screen out the lncRNAs associated with brain injury in preterm mice. Quantitative real-time PCR was used to validate the lncRNAs identified by the above method. Results The preterm and full-term groups showed significant differences in the expression of 1 978 lncRNAs (P<0.05), consisting of 786 up-regulated lncRNAs and 1 192 down-regulated lncRNAs, and 29 lncRNAs were 1.5 or more times differentially expressed between the two groups. A further analysis was performed for the 10 most differentially expressed lncRNAs, and the results showed that these lncRNAs were involved in the biological processes including transcription, signal transduction, apoptosis, cell cycle, and inflammatory response, as well as G proteincoupled receptor signaling pathway and neuropeptide signaling pathway. Real-time PCR was performed to validate the expression of two lncRNAs in brain tissue in the preterm and full-term groups, and the results were consistent with those of the chip assay. Conclusions The expression profiles of lncRNAs in brain tissue change significantly in inflammation-induced preterm mice, and the G protein-coupled receptor signaling pathway may be involved in the pathogenesis of preterm brain injury.
CHEN Ru-Juan,XI Sha,WANG Fan et al. Screening and validation of long non-coding RNAs in brain tissue of inflammationinduced preterm mice[J]. CJCP, 2016, 18(5): 435-439.
Yuan TM, Sun Y, Zhan CY, et al. Intrauterine infection/ inflammation and perinatal brain damage: role of glial cells and Toll-like receptor signaling[J]. J Neuroimmunol, 2010, 229(1-2): 16-25.
[2]
Salmaso N, Jablonska B, Scafidi J, et al. Neurobiology of premature brain injury[J]. Nat Neurosci, 2014, 17(3): 341-346.
[3]
Fancy SP, Harrington EP, Baranzini SE, et al. Parallel states of pathological Wnt signaling in neonatal brain injury and colon cancer[J]. Nat Neurosci, 2014, 17(4): 506-512.
[4]
Nagano T, Fraser P. No-nonsense functions for long noncoding RNAs[J]. Cell, 2011, 145(2): 178-181.
[5]
Ponting CP, Oliver PL, Reik W. Evolution and functions of long noncoding RNAs[J]. Cell, 2009, 136(4): 629-641.
[6]
Mercer TR, Dinger ME, Mattick JS. Long non-coding RNAs: insights into functions[J]. Nat Rev Genet, 2009, 10(3): 155-159.
[7]
Wilusz JE, Sunwoo H, Spector DL. Long noncoding RNAs: functional surprises from the RNA world[J]. Genes Dev, 2009, 23(13): 1494-1504.
[8]
Ng SY, Lin L, Soh BS, et al. Long noncoding RNAs in development and disease of the central nervous system[J]. Trends Genet, 2013, 29(8): 461-468.
[9]
Qureshi IA, Mehler MF. Emerging roles of non-coding RNAs in brain evolution, development, plasticity and disease[J]. Nat Rev Neurosci, 2012, 13(8): 528-541.
[10]
Zheng B, Liu H, Wang R, et al. Expression signatures of long non-coding RNAs in early brain injury following experimental subarachnoid hemorrhage[J]. Mol Med Rep, 2015, 12(1): 967-973.
[11]
Mehta SL, Kim T, Vemuganti R. Long noncoding RNA FosDT promotes ischemic brain injury by interacting with RESTassociated chromatin-modifying proteins[J]. J Neurosci, 2015, 35(50): 16443-16449.
[12]
Wang F, Xiao M, Lin XJ, et al. Expression of heme oxygenase 1 and leukemia inhibitory factor in maternal plasma and placental tissue in a lipopolysaccharide induced late-pregnancy preterm birth mouse model[J]. J Reprod Med, 2016, 61(1-2): 39-46.
[13]
Faghihi MA, Modarresi F, Khalil AM, et al. Expression of a noncoding RNA is elevated in Alzheimer's disease and drives rapid feed-forward regulation of beta-secretase[J]. Nat Med, 2008, 14(7): 723-730.
Hangauer MJ, Vaughn IW, McManus MT. Pervasive transcription of the human genome produces thousands of previously unidentified long intergenic noncoding RNAs[J]. PLoS Genet, 2013, 9(6): e1003569.
[16]
Giera S, Deng Y, Luo R, et al. The adhesion G proteincoupled receptor GPR56 is a cell-autonomous regulator of oligodendrocyte development[J]. Nat Commun, 2015, 6: 6121.
[17]
Bae BI, Tietjen I, Atabay KD, et al. Evolutionarily dynamic alternative splicing of GPR56 regulates regional cerebral cortical patterning[J]. Science, 2014, 343(6172): 764-768.
[18]
Singer K, Luo R, Jeong SJ, et al. GPR56 and the developing cerebral cortex: cells, matrix, and neuronal migration[J]. Mol Neurobiol, 2013, 47(1): 186-196.
