Role of microRNA-92b in the pathophysiology of acute transverse myelitis in children / 中华实用儿科临床杂志

ABSTRACT

Objective To explore microRNAs that play key regulatory roles in the pathophysiology of acute transverse myelitis in children,and to find therapeutic targets.Methods Twelve patients with acute transverse myelitis were enrolled as ATM group and three children with normal cerebrospinal fluid as the control group.MicroRNA in cerebrospinal fluid of children with acute transverse myelitis was detected by using microarray4.0 chip.Bioinformatics was used to demonstrate microRNA,which plays a key regulatory role,and to predict target genes.Real-time quantitative polymerase chain reaction (qPCR) technique was adopted for in biology and technology duplication.Enzyme-linked immunosorbent assay (ELISA) and Western blot technique were used to detect the expression of key miRNA target protein.The key candidate microRNA was inhibited/overexpressed in dorsal root ganglion neurons,and the function was verified in vitro.Flavopiridol was used to inhibit the activity of CDKs to verify that miR-92b worked through p57-CDKs-GAP-43 pathway.Results The characteristic elevation of miR-92b in cerebrospinal fluid samples of acute transverse myelitis was significant.Bioinformatics analysis showed that p57 was the target gene of miR-92b.The expression of miR-92b was contrary to the p57 protein.In vitro experiments showed that the length of axons in miR-92bmimics group was significantly shorter than that in the blank group.The axons of neurons in antimiR-92b group were obviously prolonged.In the miR-92b mimics + Flavopiridol groups,the axons of neurons were still significantly prolonged compared with that in the blank group.Western blot showed that p57 and GAP-43 protein expression in miR-92b mimics group was lower than that in blank group.The expression of p57 and GAP-43 protein in antimiR-92b group was significantly higher than that in blank group.But in miR-92b mimics + Flavopiridol group,the expression of p57 was lower compared with that in blank group,and the expression of GAP-43 protein was higher compared with that in blank group.Conclusions Up-regulation of miR-92b in children with acute transverse myelitis leads to a down-regulation of p57.The activity of CDKs is enhanced,which inhibits the expression of GAP-43 protein and the regeneration of axons in spinal cord injury region.MiR-92b is one of the key targets in the treatment of children with acute transverse myelitis.