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Many studies have indicated that autophagy and apoptosis play an important role in the pathogenesis of spinal cord injury. In recent years, research on autophagy-related signal transduction pathways has demonstrated that the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (MTOR) signaling pathway is closely associated with the initiation of autophagy. How- ever, the mechanism of the pathological relationship between this signaling pathway and apoptosis in spinal cord injury is unclear. In this study, we used an in vitro model of spinal cord injury to observe the mechanism of the PI3K/Akt/mTOR signaling pathway and the apoptosis of neurons via the mito- chondrial pathway. Mitochondrial pathway apoptosis-related proteins were detected by western blot. Akt and mTOR phosphorylation levels peaked 4h after mechanical damage and then decreased. Fol- lowing administration of the PI3K-specific inhibitor LY294002, the phosphorylation levels of Akt and mTOR decreased, and the ratio of autophagy-specific protein microtubule-associated protein 1 light chain (LC3)II/I was higher in the inhibitor-treated injury group than in the simple-injury group. TUNEL stain- ing was used to detect apoptosis, and apoptosis was significantly reduced after the inhibition of the PI3K/Akt/MTOR signaling pathway. In summary, the PI3K/Akt/MTOR signaling pathway is involved in the apoptosis of neurons after mechanical injury and can induce apoptosis through the mitochondrial pathway.

Many studies have indicated that autophagy and apoptosis play an important role in the pathogenesis of spinal cord injury. In recent years, research on autophagy-related signal transduction pathways has demonstrated that the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (MTOR) signaling pathway is closely associated with the initiation of autophagy. How- ever, the mechanism of the pathological relationship between this signaling pathway and apoptosis in spinal cord injury is unclear. In this study, we used an in vitro model of spinal cord injury to observe the mechanism of the PI3K/Akt/mTOR signaling pathway and the apoptosis of neurons via the mito- chondrial pathway. Mitochondrial pathway apoptosis-related proteins were detected by western blot. Akt and mTOR phosphorylation levels peaked 4h after mechanical damage and then decreased. Fol- lowing administration of the PI3K-specific inhibitor LY294002, the phosphorylation levels of Akt and mTOR decreased, and the ratio of autophagy-specific protein microtubule-associated protein 1 light chain (LC3)II/I was higher in the inhibitor-treated injury group than in the simple-injury group. TUNEL stain- ing was used to detect apoptosis, and apoptosis was significantly reduced after the inhibition of the PI3K/Akt/MTOR signaling pathway. In summary, the PI3K/Akt/MTOR signaling pathway is involved in the apoptosis of neurons after mechanical injury and can induce apoptosis through the mitochondrial pathway.

Biology 2e
Biology 2e
2nd Edition
ISBN:9781947172517
Author:Matthew Douglas, Jung Choi, Mary Ann Clark
Publisher:Matthew Douglas, Jung Choi, Mary Ann Clark
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A B S T R A C T Many studies have indicated that autophagy and apoptosis play an important role in the pathogenesis of spinal cord injury. In recent years, research on autophagy-related signal transduction pathways has demonstrated that the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling pathway is closely associated with the initiation of autophagy. How- ever, the mechanism of the pathological relationship between this signaling pathway and apoptosis in spinal cord injury is unclear. In this study, we used an in vitro model of spinal cord injury to observe the mechanism of the PI3K/Akt/mTOR signaling pathway and the apoptosis of neurons via the mito- chondrial pathway. Mitochondrial pathway apoptosis-related proteins were detected by western blot. Akt and mTOR phosphorylation levels peaked 4h after mechanical damage and then decreased. Fol- lowing administration of the PI3K-specific inhibitor LY294002, the phosphorylation levels of Akt and MTOR decreased, and the ratio of autophagy-specific protein microtubule-associated protein 1 light chain (LC3)II/I was higher in the inhibitor-treated injury group than in the simple-injury group. TUNEL stain- ing was used to detect apoptosis, and apoptosis was significantly reduced after the inhibition of the PI3K/Akt/mTOR signaling pathway. In summary, the PI3K/Akt/mTOR signaling pathway is involved in the apoptosis of neurons after mechanical injury and can induce apoptosis through the mitochondrial pathway.
Transcribed Image Text:A B S T R A C T Many studies have indicated that autophagy and apoptosis play an important role in the pathogenesis of spinal cord injury. In recent years, research on autophagy-related signal transduction pathways has demonstrated that the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling pathway is closely associated with the initiation of autophagy. How- ever, the mechanism of the pathological relationship between this signaling pathway and apoptosis in spinal cord injury is unclear. In this study, we used an in vitro model of spinal cord injury to observe the mechanism of the PI3K/Akt/mTOR signaling pathway and the apoptosis of neurons via the mito- chondrial pathway. Mitochondrial pathway apoptosis-related proteins were detected by western blot. Akt and mTOR phosphorylation levels peaked 4h after mechanical damage and then decreased. Fol- lowing administration of the PI3K-specific inhibitor LY294002, the phosphorylation levels of Akt and MTOR decreased, and the ratio of autophagy-specific protein microtubule-associated protein 1 light chain (LC3)II/I was higher in the inhibitor-treated injury group than in the simple-injury group. TUNEL stain- ing was used to detect apoptosis, and apoptosis was significantly reduced after the inhibition of the PI3K/Akt/mTOR signaling pathway. In summary, the PI3K/Akt/mTOR signaling pathway is involved in the apoptosis of neurons after mechanical injury and can induce apoptosis through the mitochondrial pathway.
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