Spinal cord ischemia-
reperfusion injury(SCII)affects nerve function through many mechanisms, which are complex and not fully understood. Recently, accumulating evidence has indicated that long noncoding RNAs (lncRNAs) play an increasingly important role in SCII. We investigated the role of
lncRNA growth arrest-specific 5(Gas5) in a rat SCII model, and its effects on apoptosis and
inflammation possibly by modulating MMP-7, cleaved
caspase-3 and IL-1β.
LncRNA Gas5 and MMP-7 were knocked down by intrathecal
siRNA injection. Neurological assessment and TUNEL assay were performed. The
RNA and
protein expression levels of
lncRNA Gas5, MMP-7, cleaved
caspase-3 and IL-1β were determined by PCR and Western blotting, respectively. MMP-7 localization was visualized by double-immunofluorescence. SCII induced functional impairment in the hind limb, and the expression of
lncRNA Gas5 was highest at 24 h after SCII.
LncRNA Gas5 downregulation inhibited the
RNA and
protein expression of MMP-7, as well as the
protein expression of cleaved
caspase-3 and IL-1β.
LncRNA Gas5 downregulation reduced the number of TUNEL-positive and MMP-7-positive double-labeled cells. Therefore,
lncRNA Gas5 downregulation alleviated hind limb functional impairment and improved neuronal apoptosis after SCII. MMP-7 downregulation also inhibited apoptosis and
inflammation and alleviated damage. Pretreatment with
intrathecal injection of si-
lncRNA Gas5 and si-MMP-7 reduced the expression levels of cleaved
caspase-3 and IL-1β, protecting nerve function after SCII. These results show that
lncRNA Gas5 plays an important role in SCII, perhaps by inhibiting MMP-7, cleaved
caspase-3 and IL-1β.
LncRNA Gas5 downregulation could be a promising therapeutic approach in the SCII treatment.