scholarly journals Arachidonic Acid Derivatives and Their Role in Peripheral Nerve Degeneration and Regeneration

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Carlos Rodrigo Camara-Lemarroy ◽  
Emmanuel Irineo Gonzalez-Moreno ◽  
Francisco Javier Guzman-de la Garza ◽  
Nancy Esthela Fernandez-Garza

After peripheral nerve injury, a process of axonal degradation, debris clearance, and subsequent regeneration is initiated by complex local signaling, called Wallerian degeneration (WD). This process is in part mediated by neuroglia as well as infiltrating inflammatory cells and regulated by inflammatory mediators such as cytokines, chemokines, and the activation of transcription factors also related to the inflammatory response. Part of this neuroimmune signaling is mediated by the innate immune system, including arachidonic acid (AA) derivatives such as prostaglandins and leukotrienes. The enzymes responsible for their production, cyclooxygenases and lipooxygenases, also participate in nerve degeneration and regeneration. The interactions between signals for nerve regeneration and neuroinflammation go all the way down to the molecular level. In this paper, we discuss the role that AA derivatives might play during WD and nerve regeneration, and the therapeutic possibilities that arise.

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Junyang Jung ◽  
Hyun Woo Jo ◽  
Hyunseob Kwon ◽  
Na Young Jeong

Studies have shown that lysosomal activation increases in Schwann cells after nerve injury. Lysosomal activation is thought to promote the engulfment of myelin debris or fragments of injured axons in Schwann cells during Wallerian degeneration. However, a recent interpretation of lysosomal activation proposes a different view of the phenomenon. During Wallerian degeneration, lysosomes become secretory vesicles and are activated for lysosomal exocytosis. The lysosomal exocytosis triggers adenosine 5′-triphosphate (ATP) release from peripheral neurons and Schwann cells during Wallerian degeneration. Exocytosis is involved in demyelination and axonal degradation, which facilitate nerve regeneration following nerve degeneration. At this time, released ATP may affect the communication between cells in peripheral nerves. In this review, our description of the relationship between lysosomal exocytosis and Wallerian degeneration has implications for the understanding of peripheral nerve degenerative diseases and peripheral neuropathies, such as Charcot-Marie-Tooth disease or Guillain-Barré syndrome.


2017 ◽  
Vol 2017 ◽  
pp. 1-7 ◽  
Author(s):  
Lingyan Xing ◽  
Qiong Cheng ◽  
Guangbin Zha ◽  
Sheng Yi

After peripheral nerve injury, immune/inflammatory responses are triggered, which are critical for nerve regeneration. Despite their importance, the underlying molecular changes in immune/inflammatory responses remain largely unknown. In this study, we systematically analyzed differentially expressed genes in immune/inflammatory-related pathways at high temporal resolution and experimentally validated gene expression changes with RT-PCR following sciatic nerve crush in rats. We found that immune/inflammatory reactions not only occur in the acute injury but also remained activated over two weeks after injury. Detailed bioinformatic studies suggested that multiple immune/inflammatory pathways, including agranulocyte adhesion and diapedesis, granulocyte adhesion and diapedesis, IL-6 signaling, and IL-10 signaling, were sustained activated during nerve degeneration and regeneration. Our current study expands our understanding of the molecular basis of altered immune/inflammatory-related pathways following injury and thus might offer the possibility of targeting related molecules as therapeutic intervention for peripheral nerve regeneration.


2017 ◽  
Author(s):  
M. Karagyaur ◽  
P. Makarevich ◽  
E. Shevchenko ◽  
D. Stambolsky ◽  
N. Kalinina ◽  
...  

2005 ◽  
Vol 6 (4) ◽  
pp. 385-394 ◽  
Author(s):  
Hidenori Horie ◽  
Toshihiko Kadoya ◽  
Kazunori Sango ◽  
Mitsuhiro Hasegawa

BIO-PROTOCOL ◽  
2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Hyukmin Kim ◽  
Harun Noristani ◽  
Seung Han ◽  
Young-Jin Son

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Shih-Tien Hsu ◽  
Chun-Hsu Yao ◽  
Yuan-Man Hsu ◽  
Jia-Horng Lin ◽  
Yung-Hsiang Chen ◽  
...  

Abstract Recent studies describe taxol as a candidate treatment for promoting central nerve regeneration. However, taxol has serious side effects including peripheral neurotoxicity, and little information is known about the effect of taxol on peripheral nerve regeneration. We investigated the effects of taxol on regeneration in a rat sciatic nerve transection model. Rats were divided into four groups (n = 10): normal saline (i.p.) as the control, Cremophor EL vehicle, and 2 or 6 mg/kg of taxol in the Cremophor EL solution (four times in day-2, 4, 6, and 8), respectively. We evaluated neuronal electrophysiology, animal behaviour, neuronal connectivity, macrophage infiltration, location and expression levels of calcitonin gene-related peptide (CGRP), and expression levels of both nerve growth factors and immunoregulatory factors. In the high-dose taxol group (6 mg/kg), neuronal electrophysiological function was significantly impaired. Licking latencies were significantly changed while motor coordination was unaffected. Neuronal connectivity, macrophage density, and expression levels of CGRP was dramatically reduced. Expression levels of nerve growth factors and immunoregulatory factors was also reduced, while it was increased in the low-dose taxol group (2 mg/kg). These results indicate that taxol can modulate local inflammatory conditions, impair nerve regeneration, and impede recovery of a severe peripheral nerve injury.


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