Skip to main content


Fig. 6 | Journal of Neuroinflammation

Fig. 6

From: Long noncoding RNA MALAT1 in exosomes drives regenerative function and modulates inflammation-linked networks following traumatic brain injury

Fig. 6

Spleen regulatory networks. Gene networks altered by TBI in the spleen are depicted in this figure. On the left C vs T is the gene expression in these networks when comparing the control and TBI gene expression showing activation of inflammatory pathways TGFB1, IL19, and IL37. BCL2 is activated, likely in response to the impact of the brain injury as a compensatory process in the spleen. NUPR1 is a transcriptional cofactor involved in apoptosis and is reciprocally inhibited by TBI. In the right panel C vs TE, it is shown that exosome treatment returns NUPR1 expression back towards control levels. Also of interest is a predicted regulation of these networks by beta-estradiol activation following TBI, which is inhibited following exosome treatment. A number of genes related to this pathway are the inflammatory changes and also mir-322 which is responsive to hypoxia and oxidative stress [32]. Beta-estradiol is known to play a role in splenic response to injury by modulating macrophage and dendritic cell function

Back to article page