The Role of NLRP3 in Repairing Sciatic Nerve Injury

The Role of NLRP3 in Repairing Sciatic Nerve Injury

Loading document ...
Page
of
Loading page ...

Author(s)

Author(s): Jia Yao, Zhu Yuzhen, High Xiao, Xuan Yang, Jianzhao Deng, Bei Zhang

Download Full PDF Read Complete Article

DOI: 10.18483/ijSci.1925 23 73 124-129 Volume 8 - Feb 2019

Abstract

NLRP3 is a member of the NOD-like family of adaptive immune responses that recognize both exogenous damage-associated molecular patterns and endogenous damage-related molecular patterns. NLRP3 recognizes that PAMPS/DAMPS is activated, binds to ASC and Caspase-1 to form NLRP3 inflammatory vesicles, and exerts immunity in pathogenic infectious diseases and autoimmune diseases by controlling the release of IL-1β and IL-18, but The role of peripheral nerve injury is not clear. The objective of this study is to investigate the effect of NLRP3 on repair after sciatic nerve injury. This study was divided into two parts. The first part established the sciatic nerve injury model. In the second part, NLRP3 intervention was given on the basis of the sciatic nerve injury model. The results showed that The model of sciatic nerve injury in mice was established successfully. The sciatic nerve function of the MSU group and the MCC950 group recovered better than the control group, and the recovery of the MCC950 group was the best. It is concluded that moderate inhibition of nlrp3-mediated inflammatory response is helpful for peripheral nerve repair after injury.

Keywords

Nlrp3, Peripheral Nerve Injury, IL-1β

References

  1. Romero-Ortega, M., et al., Chronic and low charge injection wireless intraneural stimulation in vivo. Conf Proc IEEE Eng Med Biol Soc, 2015. 2015: p. 1013-6.
  2. Chavan, S.S., V.A. Pavlov, and K.J. Tracey, Mechanisms and Therapeutic Relevance of Neuro-immune Communication. Immunity, 2017. 46(6): p. 927-942.
  3. Yi, L., et al., Differential gene expression profile of CD4+/CD8+ T cells in patients with hepatitis C virus and/or human immunodeficiency virus infection. Hong Kong Med J, 2015. 21 Suppl 7: p. S11-3.
  4. Zambetti, L.P., et al., The rhapsody of NLRPs: master players of inflammation...and a lot more. Immunol Res, 2012. 53(1-3): p. 78-90.
  5. Xu, L., et al., MiR-34c Ameliorates Neuropathic Pain by Targeting NLRP3 in a Mouse Model of Chronic Constriction Injury. Neuroscience, 2019. 399: p. 125-134.
  6. Lamkanfi, M. and V.M. Dixit, Mechanisms and Functions of Inflammasomes. cell 2014. 157(Elsevier Inc. ): p. 1013.
  7. Lawrence, C.B., S.M. Allan, and N.J. Rothwell, Interleukin-1beta and the interleukin-1 receptor antagonist act in the striatum to modify excitotoxic brain damage in the rat. Eur J Neurosci, 1998. 10(3): p. 1188-95.
  8. Brough, D., P.J. Tyrrell, and S.M. Allan, Regulation of interleukin-1 in acute brain injury. Trends Pharmacol Sci, 2011. 32(10): p. 617-22.
  9. Houtman, J., et al., Beclin1-driven autophagy modulates the inflammatory response of microglia via NLRP3. EMBO J, 2019.
  10. Jia, M., et al., Activation of NLRP3 inflammasome in peripheral nerve contributes to paclitaxel-induced neuropathic pain. Mol Pain, 2017. 13: p. 1744806917719804.
  11. Mehto, S., et al., The Crohn's Disease Risk Factor IRGM Limits NLRP3 Inflammasome Activation by Impeding Its Assembly and by Mediating Its Selective Autophagy. Mol Cell, 2018.
  12. Xu, C., et al., Targeting of NLRP3 inflammasome with gene editing for the amelioration of inflammatory diseases. Nat Commun, 2018. 9(1): p. 4092.
  13. Suetomi, T., et al., Inflammation and NLRP3 Inflammasome Activation Initiated in Response to Pressure Overload by Ca(2+)/Calmodulin-Dependent Protein Kinase II delta Signaling in Cardiomyocytes Are Essential for Adverse Cardiac Remodeling. Circulation, 2018. 138(22): p. 2530-2544.
  14. Martini, R. and H. Willison, Neuroinflammation in the peripheral nerve: Cause, modulator, or bystander in peripheral neuropathies? Glia, 2016. 64(4): p. 475-86.
  15. Low, P.A., et al., Peripheral nerve microenvironment: collection of endoneurially enriched fluid. Exp Neurol, 1982. 77(1): p. 208-14.
  16. Zochodne, D.W., The microenvironment of injured and regenerating peripheral nerves. Muscle Nerve Suppl, 2000. 9: p. S33-8.
  17. Carroll, S.L.F., Paul W, Expression of JE monocyte chemoattr Source J Neuropathol Exp Neurol SO 1998 Oct 57 10 915 30[PMIDT9786242]. Journal of Neuropathology and Experimental Neurology, 1998. 57: p. 915-930.
  18. Hara H, F.R., Gagliardini V, Ayata C, Fink K, Huang Z, Shimizu-Sasamata M, Yuan J, Moskowitz MA, Inhibition of interleukin 1beta converting enzyme family proteases reduces ischemic and excitotoxic neuronal damage. National Academy of Sciences, 1997. 94(5): p. 2007-12.
  19. Gui, W.S., et al., Interleukin-1beta overproduction is a common cause for neuropathic pain, memory deficit, and depression following peripheral nerve injury in rodents. Mol Pain, 2016. 12.
  20. Nadeau, S., et al., Functional recovery after peripheral nerve injury is dependent on the pro-inflammatory cytokines IL-1beta and TNF: implications for neuropathic pain. J Neurosci, 2011. 31(35): p. 12533-42.
  21. Routtenberg, B.a.A., GAP 43 an intrinsic determinant of neuronal development and plasticity. Trends Neurosci, 1997. 20(2): p. 84-91.
  22. Meiri, K.F., K.H. Pfenninger, and M.B. Willard, Growth-associated protein, GAP-43, a polypeptide that is induced when neurons extend axons, is a component of growth cones and corresponds to pp46, a major polypeptide of a subcellular fraction enriched in growth cones. Proc Natl Acad Sci U S A, 1986. 83(10): p. 3537-41.

Cite this Article:

International Journal of Sciences is Open Access Journal.
This article is licensed under a Creative Commons Attribution 4.0 International (CC BY 4.0) License.
Author(s) retain the copyrights of this article, though, publication rights are with Alkhaer Publications.

Search Articles

Issue June 2024

Volume 13, June 2024


Table of Contents



World-wide Delivery is FREE

Share this Issue with Friends:


Submit your Paper