Figures & data
Figure 1 The probable mechanisms of the effects produced by lncRNAs on TBI.
Notes: There are several lncRNAs that have been reported to play different roles in the process of TBI. Knocking down GAS5 would alleviate RGCs oxidative stress injury by upregulating miR-124. GAS5 could also inhibit microglia M2 polarization by suppressing transcription of TRF4. lincRNA-p21 may promote microglial activation through a p53-dependent transcriptional pathway. In addition to neuroinflammation, lncRNA MALAT1 is also related to neurodegeneration and astrocyte apoptosis via CREB signaling pathway and alternative splicing of PKC δII respectively. Astrocyte apoptosis are associated with NEAT1 and Gm4419 in which Gm4419 could play the role of sponge for miR-466l which could target TNF-α. H19 is considered to alleviate hypoxia-induced injury by downregulated miR-28 expression. SNHG1 protected secondary cerebral ischemia and hypoxia via sponging miR-338.
Abbreviations: lncRNA, long noncoding RNA; TBI, traumatic brain injury; GAS5, growth arrest-specific 5; RGC, retinal ganglion cells; MALAT1, metastasis-associated lung adenocarcinoma transcript 1; CREB, cAMP response element-binding protein; NEAT1, nuclear enriched abundant transcript 1; TNF-α, tumor necrosis factor-alpha; SNHG1, small nucleolar RNA host gene 1.
Abbreviations: lncRNA, long noncoding RNA; TBI, traumatic brain injury; GAS5, growth arrest-specific 5; RGC, retinal ganglion cells; MALAT1, metastasis-associated lung adenocarcinoma transcript 1; CREB, cAMP response element-binding protein; NEAT1, nuclear enriched abundant transcript 1; TNF-α, tumor necrosis factor-alpha; SNHG1, small nucleolar RNA host gene 1.
