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Traumatic nerve injuries have become a common clinical problem, and axon regeneration is a critical process in the successful functional recovery of the injured nervous system. In this study, we found that peripheral axotomy reduces PTEN expression in adult sensory neurons; however, it did not alter the expression level of PTEN in IB4‐positive sensory neurons. Additionally, our results indicate that the artificial inhibition of PTEN markedly promotes adult sensory axon regeneration, including IB4‐positive neuronal axon growth. Thus, our results provide strong evidence that PTEN is a prominent repressor of adult sensory axon regeneration, especially in IB4‐positive neurons. [ABSTRACT FROM AUTHOR]

The inflammatory response is a critical regulator for the regeneration of axon following nervous system injury. Nuclear factor‐kappa B (NF‐κB) is characteristically known for its ubiquitous role in the inflammatory response. However, its functional role in adult mammalian axon growth remains elusive. Here, we found that the NF‐κB signaling pathway is activated in adult sensory neurons through peripheral axotomy. Furthermore, inhibition of NF‐κB in peripheral sensory neurons attenuated their axon growth in vitro and in vivo. Our results also showed that NF‐κB modulated axon growth by repressing the phosphorylation of STAT3. Furthermore, activation of STAT3 significantly promoted adult optic nerve regeneration. Taken together, the findings of our study indicated that NF‐κB/STAT3 cascade is a critical regulator of intrinsic axon growth capability in the adult nervous system. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]