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Mature neurons: equipped for survival

Kole, A J, Annis, R P, Deshmukh, M·2013·Cell Death & Disease
DOI 10.1038/cddis.2013.220PMC PMC3702294
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Figure 1 Intrinsic mitochondrial pathway of apoptosis in immature developing neurons. Apoptotic stimuli (e.g., NGF deprivation) initiate a kinase cascade involving MLKs and JNK, which converge on phosphorylation of the transcription factor c-jun. Phosphorylated c-jun (Phos-c-Jun) translocates to the nucleus where it drives transcription of pro-apoptotic BH3-only genes such as Bim and Hrk. The BH3-only family of proteins either directly or indirectly via inhibition of pro-survival Bcl-2 proteins, activate pro-apoptotic Bax via oligomerization and insertion to the outer mitochondrial membrane. Upon mitochondrial permeabilization, cytochrome c (cyt c) is released from the mitochondrial intermembrane space. The presence of cytosolic cytochrome c initiates the formation of the apoptosome complex, which activates caspase-9 (casp-9) and caspase-3 (casp-3), and ultimately causes cell death
Figure 1 Intrinsic mitochondrial pathway of apoptosis in immature developing neurons. Apoptotic stimuli (e.g., NGF deprivation) initiate a kinase cascade involving MLKs and JNK, which converge on phosphorylation of the transcription factor c-jun. Phosphorylated c-jun (Phos-c-Jun) translocates to the nucleus where it drives transcription of pro-apoptotic BH3-only genes such as Bim and Hrk. The BH3-only family of proteins either directly or indirectly via inhibition of pro-survival Bcl-2 proteins, activate pro-apoptotic Bax via oligomerization and insertion to the outer mitochondrial membrane. Upon mitochondrial permeabilization, cytochrome c (cyt c) is released from the mitochondrial intermembrane space. The presence of cytosolic cytochrome c initiates the formation of the apoptosome complex, which activates caspase-9 (casp-9) and caspase-3 (casp-3), and ultimately causes cell deathCC BY-NC-ND · PubMed Central
Figure 2 Specific mechanisms utilized by mature neurons to inhibit apoptosis. The apoptotic pathway has been found to be inhibited at distinct points in mature neurons. First, multiple neuronal types upregulate the transcription of a microRNA (miR-29), which can target and repress the induction of BH3-only proteins. Second, Bax remains cytosolic in mature neurons and does not translocate to mitochondria, although it is unclear if this is independent of the activity of miR-29 on BH3-only proteins. Third, Apaf-1 expression is repressed via chromatin restriction. Fourth, motor neurons exhibit an increase in the XIAP/XAF ratio, which enables XIAP to more efficiently inhibit both caspase-9 and caspases-3. Fifth, mature neurons of the CNS have markedly decreased levels of caspases-3. Additional information regarding the specific neuronal types that exhibit these brakes can be found in Table 1
Figure 2 Specific mechanisms utilized by mature neurons to inhibit apoptosis. The apoptotic pathway has been found to be inhibited at distinct points in mature neurons. First, multiple neuronal types upregulate the transcription of a microRNA (miR-29), which can target and repress the induction of BH3-only proteins. Second, Bax remains cytosolic in mature neurons and does not translocate to mitochondria, although it is unclear if this is independent of the activity of miR-29 on BH3-only proteins. Third, Apaf-1 expression is repressed via chromatin restriction. Fourth, motor neurons exhibit an increase in the XIAP/XAF ratio, which enables XIAP to more efficiently inhibit both caspase-9 and caspases-3. Fifth, mature neurons of the CNS have markedly decreased levels of caspases-3. Additional information regarding the specific neuronal types that exhibit these brakes can be found in Table 1CC BY-NC-ND · PubMed Central
Figure 3 Changes in apoptotic thresholds during neuronal development and neurodegeneration. Schematic shows that developing neurons undergo programmed cell death, a necessary phenomenon for proper nervous system development. Following the developmental period, neurons mature and restrict the apoptotic pathway to permit long-term survival. Under circumstances of neurodegeneration or neuronal injury, the loss of mechanisms to restrict apoptosis causes mature neurons to resemble their immature phenotype
Figure 3 Changes in apoptotic thresholds during neuronal development and neurodegeneration. Schematic shows that developing neurons undergo programmed cell death, a necessary phenomenon for proper nervous system development. Following the developmental period, neurons mature and restrict the apoptotic pathway to permit long-term survival. Under circumstances of neurodegeneration or neuronal injury, the loss of mechanisms to restrict apoptosis causes mature neurons to resemble their immature phenotypeCC BY-NC-ND · PubMed Central

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Authors
Kole, A. J., Annis, R. P., & Deshmukh, M.
Venue
Cell Death & Disease
Publisher
Springer Science and Business Media LLC
Published
2013-06-27
Volume
4
Issue
6
Pages
e689-e689
ISSN
2041-4889
DOI
10.1038/cddis.2013.220
PMC
PMC3702294
Cited by
170
References
4
Language
en
Licence
www.springer.com/tdm (unspecified)

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