Circ-KATNAL1 Knockdown Reduces Neuronal Apoptosis and Alleviates Spinal Cord Injury Through the miR-98-5p/PRDM5 Regulatory Axis.

Spinal cord injury (SCI) is a common disease of the central nervous system. circRNAs play a crucial role in neurological disease. The purpose of this study was to investigate the role of circ-KATNAL1 in SCI and its regulatory mechanism. T9-L10 spinal segment of Sprague Dawley rats was compressed or contused after T10 laminectomy to establish the SCI rat model. Then, rats were divided into SCI group, si-NC group, si-circ-KATNAL1 group, si-circ-KATNAL1 + antagomir NC group, si-circ-KATNAL1 + miR-98-5p antagomir group, si-circ-KATNAL1 + oe-NC group, and si-circ-KATNAL1 + oe-PRDM5 group, with 6 rats in each group. There was another sham operation group that received no treatment. Basso, Beattie, and Bresnahan (BBB) scores were used to evaluate the neural function of rats. In addition to that, the pathological changes of spinal cord tissue, neuronal apoptosis, and inflammatory responses were correspondingly observed and analyzed. Quantitative measurements of circ-KATNAL1, miR-98-5p, and PRDM5 levels were conducted, as well as analyses of their interrelationship. Circ-KATNAL1 was up-regulated in the spinal cord tissue of SCI rats, and circ-KATNAL1 knockdown could improve neural function, alleviate pathological changes of spinal cord tissue, and inhibit neuronal apoptosis and inflammatory responses in SCI rats. For miR-98-5p, circ-KATNAL1 was an upstream factor, while PRDM5 was a downstream actor. miR-98-5p deficiency or PRDM5 restoration impaired the remission effect of circ-KATNAL1 knockdown on SCI. Circ-KATNAL1 knockdown reduces neuronal apoptosis and alleviates SCI through miR-98-5p/PRDM5 regulatory axis.