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Molecular neurobiology

Vimentin regulates neuroplasticity in transected spinal cord rats associated with micRNA138.


PMID 24874717

Abstract

Spinal cord injury (SCI) often results in motor disability concomitant with limit neuroplasticity; the underlying mechanism, however, is still unclear. This study established spinal cord transection rats model (T10), then performed cDNA microarray analysis and found that vimentin located in astrocytes was increased significantly in scar tissues after transection. To understand the role of vimentin and it's mechanism of regulation, RNA interference and luciferase assay were used. Vimentin knockdown in the scar tissues showed a significant improvement on locomotor function in hindlimbs, while vimentin overexpression exhibited an opposite effect. In vitro, vimentin downregulation or overexpression can effectively inhibit or increase astrogliosis, respectively. Moreover, by using biological informatics technology, we predicted that vimentin may be as the target of micRNA138 (miR-138), and confirmed that miR-138 could regulate vimentin by luciferase activity assay. The present results not only validated the exact role of vimentin in transected spinal cord, but also exhibited a novel regulation mechanism, in which miR-138 may regulate vimentin to promote neuroplasticity. It, therefore, provides a novel target for gene drug discovery based on miRNA-138 or vimentin for the treatment of SCI in the future clinic trial.