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Calcium/calmodulin‐dependent protein kinase II regulates mammalian axon growth by affecting F‐actin length in growth cone
Author(s) -
Xi Feng,
Xu RenJie,
Xu JinHui,
Ma JinJin,
Wang WeiHua,
Wang Feng,
Ma YanXia,
Qi ShiBin,
Zhang HongCheng,
Zhang HaoNan,
Qin XuZhen,
Chen JianQuan,
Li Bin,
Liu ChangMei,
Yang HuiLin,
Meng Bin
Publication year - 2019
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.28867
Subject(s) - axotomy , axon , microbiology and biotechnology , growth cone , dorsal root ganglion , biology , nervous system , axon guidance , calmodulin , calcium , peripheral nervous system , neuroscience , regeneration (biology) , central nervous system , chemistry , sensory system , organic chemistry
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 (Ca 2+ ) 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.