Biology 2e
2nd Edition
ISBN:9781947172517
Author:Matthew Douglas, Jung Choi, Mary Ann Clark
Publisher:Matthew Douglas, Jung Choi, Mary Ann Clark
Chapter4: Cell Structure
Section: Chapter Questions
Problem 17RQ: Which of the following sequences correctly lists in order the steps involved in the incorporation of...
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![Autophagy has a complex signaling control system, and many
studies have indicated that the PI3K/Akt/mTOR signaling path-
way is closely related to autophagy. Downstream phosphorylation
of Akt can activate Tuberous Sclerosis 1/2 (TSC1/2), which fur-
ther 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 expres-
sion decreased 1h after injury in a study of traumatic brain
injury (TBI) and continued to decrease for 4h. p-Akt expression
was increased after TBI in the hippocampal CA1 region, and fur-
ther 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 mitochon-
drial cytochrome Crelease [17]. Current research has demonstrated
that beclin-1 can function as a caspase target; the product can alter
how mitochondrial membrane permeability promotes cell apopto-
sis, indicating a molecular link between autophagy and apoptosis
[18–20]. However, the relationship between autophagy and apo-
ptosis 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 path-
way is closely related to autophagy. Downstream phosphorylation
of Akt can activate Tuberous Sclerosis 1/2 (TSC1/2), which fur-
ther 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 expres-
sion decreased 1h after injury in a study of traumatic brain
injury (TBI) and continued to decrease for 4h. p-Akt expression
was increased after TBI in the hippocampal CA1 region, and fur-
ther 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 mitochon-
drial cytochrome Crelease [17]. Current research has demonstrated
that beclin-1 can function as a caspase target; the product can alter
how mitochondrial membrane permeability promotes cell apopto-
sis, indicating a molecular link between autophagy and apoptosis
[18–20]. However, the relationship between autophagy and apo-
ptosis 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
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].
Spinal cord injury is a serious neurological disorder. The sec-
ondary pathological changes induced by spinal cord injury are the
greatest obstacle to repair; these changes include edema, necro-
sis, apoptosis, oxidative stress, inflammation and other processes
[1-3]. Therefore, the neural functions associated with spinal cord
* 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
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].
Spinal cord injury is a serious neurological disorder. The sec-
ondary pathological changes induced by spinal cord injury are the
greatest obstacle to repair; these changes include edema, necro-
sis, apoptosis, oxidative stress, inflammation and other processes
[1-3]. Therefore, the neural functions associated with spinal cord
* 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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