Calcium/calmodulin‐dependent protein kinase II regulates mammalian axon growth by affecting F‐actin length in growth cone

While axon regeneration is a key determinant of functional recovery of the nervous system after injury, it is often poor in the mature nervous system. Influx of extracellular calcium (Ca2+) is one of the first phenomena that occur following axonal injury, and calcium/calmodulin‐dependent protein kin...

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Bibliographic Details
Published in:Journal of cellular physiology 2019-12, Vol.234 (12), p.23053-23065
Main Authors: Xi, Feng, Xu, Ren‐Jie, Xu, Jin‐Hui, Ma, Jin‐Jin, Wang, Wei‐Hua, Wang, Feng, Ma, Yan‐Xia, Qi, Shi‐Bin, Zhang, Hong‐Cheng, Zhang, Hao‐Nan, Qin, Xu‐Zhen, Chen, Jian‐Quan, Li, Bin, Liu, Chang‐Mei, Yang, Hui‐Lin, Meng, Bin, Saijilafu
Format: Article
Language:English
Subjects:
Actin
axon growth
Axon guidance
Axotomy
Ca2+/calmodulin-dependent protein kinase II
Calcium
Calcium (extracellular)
Calcium influx
Calcium ions
Calcium-binding protein
Calmodulin
CaMKII
Central nervous system
Cytoskeleton
Dorsal root ganglia
F‐actin
Growth cones
Kinases
Mammals
Nervous system
Proteins
Recovery of function
Regeneration
Sensory neurons
Substrates
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Summary:While axon regeneration is a key determinant of functional recovery of the nervous system after injury, it is often poor in the mature nervous system. Influx of extracellular calcium (Ca2+) is one of the first phenomena that occur following axonal injury, and calcium/calmodulin‐dependent protein kinase II (CaMKII), a target substrate for calcium ions, regulates the status of cytoskeletal proteins such as F‐actin. Herein, we found that peripheral axotomy activates CaMKII in dorsal root ganglion (DRG) sensory neurons, and inhibition of CaMKII impairs axon outgrowth in both the peripheral and central nervous systems (PNS and CNS, respectively). Most importantly, we also found that the activation of CaMKII promotes PNS and CNS axon growth, and regulatory effects of CaMKII on axon growth occur via affecting the length of the F‐actin. Thus, we believe our findings provide clear evidence that CaMKII is a critical modulator of mammalian axon regeneration. We found that the activation of calcium/calmodulin‐dependent protein kinase II (CaMKII) promotes the peripheral nervous system and central nervous system axon growth, and regulatory effects of CaMKII on axon growth occur via affecting the length of the F‐actin. Thus, manipulation of the cytoskeletal protein assembly in the growth cone may be an effective strategy to promote axon regeneration of the damaged nervous system.
ISSN:0021-9541
1097-4652
DOI:10.1002/jcp.28867