Human Anatomy & Physiology (11th Edition)
11th Edition
ISBN:9780134580999
Author:Elaine N. Marieb, Katja N. Hoehn
Publisher:Elaine N. Marieb, Katja N. Hoehn
Chapter1: The Human Body: An Orientation
Section: Chapter Questions
Problem 1RQ: The correct sequence of levels forming the structural hierarchy is A. (a) organ, organ system,...
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![Autophagy has a complex signaling control system, and many studies have indicated that the PI3K/Akt/mTOR signaling pathway is closely related to autophagy. Downstream phosphorylation of Akt can activate Tuberous Sclerosis 1/2 (TSC1/2), which further promotes mTOR activation. mTOR functions by inhibiting the downstream molecular complex ULK1 to negatively regulate autophagy levels [9,10]. However, mTOR activity is inhibited in the absence of nutrients and activates autophagy; in contrast, autophagy is inhibited when mTOR is activated in the presence of excess nutrients [11,12]. Noshita N found that p-Akt expression decreased 1 h after injury in a study of traumatic brain injury (TBI) and continued to decrease for 4 h. p-Akt expression was increased after TBI in the hippocampal CA1 region, and further studies showed that p-Akt plays a protective role after TBI [13].
Mitochondria are the control centers of apoptosis and play a decisive role in the occurrence of apoptosis after the cell is affected by adverse external factors [14]. Cytochrome C is the key signaling molecule in the mitochondrial apoptosis pathway. Release of cytochrome C from the mitochondria can activate the apoptotic effector caspase-3, leading to apoptosis, while caspase-3 activation can in turn promote the release of cytochrome C from the mitochondria, leading to a vicious cycle [15,16]. The early stage of rapamycin-induced brain injury can be reduced, mainly through the enhancement of autophagy, which reduces mitochondrial cytochrome C release [17]. Current research has demonstrated that beclin-1 can function as a caspase target; the product can alter how mitochondrial membrane permeability promotes cell apoptosis, indicating a molecular link between autophagy and apoptosis [18–20]. However, the relationship between autophagy and apoptosis in spinal cord injury is unclear. In this study, we used an in vitro mechanical injury spinal cord neural cell model to evaluate the relationship between autophagy signal transduction and the mitochondrial apoptotic pathway.](/v2/_next/image?url=https%3A%2F%2Fcontent.bartleby.com%2Fqna-images%2Fquestion%2Fd9036ccd-b518-40e3-89ff-336d4c576363%2Fd3a61590-7a7f-4ff1-8d86-b1e3a34ca1ed%2Fntc6z1o_processed.jpeg&w=3840&q=75)
Transcribed Image Text:Autophagy has a complex signaling control system, and many studies have indicated that the PI3K/Akt/mTOR signaling pathway is closely related to autophagy. Downstream phosphorylation of Akt can activate Tuberous Sclerosis 1/2 (TSC1/2), which further promotes mTOR activation. mTOR functions by inhibiting the downstream molecular complex ULK1 to negatively regulate autophagy levels [9,10]. However, mTOR activity is inhibited in the absence of nutrients and activates autophagy; in contrast, autophagy is inhibited when mTOR is activated in the presence of excess nutrients [11,12]. Noshita N found that p-Akt expression decreased 1 h after injury in a study of traumatic brain injury (TBI) and continued to decrease for 4 h. p-Akt expression was increased after TBI in the hippocampal CA1 region, and further studies showed that p-Akt plays a protective role after TBI [13].
Mitochondria are the control centers of apoptosis and play a decisive role in the occurrence of apoptosis after the cell is affected by adverse external factors [14]. Cytochrome C is the key signaling molecule in the mitochondrial apoptosis pathway. Release of cytochrome C from the mitochondria can activate the apoptotic effector caspase-3, leading to apoptosis, while caspase-3 activation can in turn promote the release of cytochrome C from the mitochondria, leading to a vicious cycle [15,16]. The early stage of rapamycin-induced brain injury can be reduced, mainly through the enhancement of autophagy, which reduces mitochondrial cytochrome C release [17]. Current research has demonstrated that beclin-1 can function as a caspase target; the product can alter how mitochondrial membrane permeability promotes cell apoptosis, indicating a molecular link between autophagy and apoptosis [18–20]. However, the relationship between autophagy and apoptosis in spinal cord injury is unclear. In this study, we used an in vitro mechanical injury spinal cord neural cell model to evaluate the relationship between autophagy signal transduction and the mitochondrial apoptotic pathway.
![**1. Introduction**
Spinal cord injury is a serious neurological disorder. The secondary pathological changes induced by spinal cord injury are the greatest obstacle to repair; these changes include edema, necrosis, apoptosis, oxidative stress, inflammation, and other processes [1-3]. Therefore, the neural functions associated with spinal cord injury have become an intensely researched topic. Autophagy is a protective physiological process in eukaryotic organisms that is characterized by the formation of a bilayer membrane structure and is associated with abnormal proteins and damaged organelles in the cytoplasm [4-6]. Kanno H found that the autophagy-specific protein microtubule-associated protein 1 light chain 3 (LC3) was highly expressed in injured spinal cord neurons, which confirmed the existence of autophagy in neuronal cells [7]. By establishing an in vitro model of spinal cord injury, we found that autophagy can be induced in the early stage of injury. Further study revealed that autophagy was enhanced after injury, which could reduce the level of apoptosis and protect neurons [8].
---
* Corresponding author.
E-mail address: 13705977551@163.com (W. Liu).
¹ Joint first authors.
http://dx.doi.org/10.1016/j.neulet.2017.07.036
0304-3940/© 2017 Published by Elsevier Ireland Ltd.](/v2/_next/image?url=https%3A%2F%2Fcontent.bartleby.com%2Fqna-images%2Fquestion%2Fd9036ccd-b518-40e3-89ff-336d4c576363%2Fd3a61590-7a7f-4ff1-8d86-b1e3a34ca1ed%2Fh30fone_processed.jpeg&w=3840&q=75)
Transcribed Image Text:**1. Introduction**
Spinal cord injury is a serious neurological disorder. The secondary pathological changes induced by spinal cord injury are the greatest obstacle to repair; these changes include edema, necrosis, apoptosis, oxidative stress, inflammation, and other processes [1-3]. Therefore, the neural functions associated with spinal cord injury have become an intensely researched topic. Autophagy is a protective physiological process in eukaryotic organisms that is characterized by the formation of a bilayer membrane structure and is associated with abnormal proteins and damaged organelles in the cytoplasm [4-6]. Kanno H found that the autophagy-specific protein microtubule-associated protein 1 light chain 3 (LC3) was highly expressed in injured spinal cord neurons, which confirmed the existence of autophagy in neuronal cells [7]. By establishing an in vitro model of spinal cord injury, we found that autophagy can be induced in the early stage of injury. Further study revealed that autophagy was enhanced after injury, which could reduce the level of apoptosis and protect neurons [8].
---
* Corresponding author.
E-mail address: 13705977551@163.com (W. Liu).
¹ Joint first authors.
http://dx.doi.org/10.1016/j.neulet.2017.07.036
0304-3940/© 2017 Published by Elsevier Ireland Ltd.
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