Genetic influences on secondary degeneration and wound healing following spinal cord injury in various strains of mice

2002 ◽  
Vol 451 (3) ◽  
pp. 225-235 ◽  
Author(s):  
Denise Inman ◽  
Lloyd Guth ◽  
Oswald Steward
2017 ◽  
Vol 34 (6) ◽  
pp. 1149-1155 ◽  
Author(s):  
Jessica M. Marbourg ◽  
Anna Bratasz ◽  
Xiaokui Mo ◽  
Phillip G. Popovich

2003 ◽  
Vol 74 (2) ◽  
pp. 227-239 ◽  
Author(s):  
William D. Whetstone ◽  
Jung-Yu C. Hsu ◽  
Manuel Eisenberg ◽  
Zena Werb ◽  
Linda J. Noble-Haeusslein

2012 ◽  
Vol 29 (5) ◽  
pp. 957-970 ◽  
Author(s):  
Cameron Lutton ◽  
Yun Wai Young ◽  
Richard Williams ◽  
Adrian C.B. Meedeniya ◽  
Alan Mackay-Sim ◽  
...  

2021 ◽  
Author(s):  
Floriane Bretheau ◽  
Adrian Castellanos-Molina ◽  
Benoit Mailhot ◽  
Maxime Kusik ◽  
Dominic Belanger ◽  
...  

Abstract Spinal cord injury (SCI) triggers neuroinflammation, and subsequently secondary degeneration and oligodendrocyte (OL) death. We report that the alarmin interleukin (IL)-1α is released by damaged microglia after SCI. Intra-cisterna magna injection of IL-1α in mice rapidly induced neutrophil infiltration and OL death throughout the spinal cord, mimicking what is seen at sites of SCI. These effects were abolished by co-treatment with the IL-1R1 antagonist anakinra, as well as in IL-1R1-knockout mice which showed enhanced locomotor recovery after SCI. Conditional restoration of IL-1R1 expression in astrocytes or endothelial cells (ECs), but not in OLs or microglia, restored IL-1α-induced effects, while astrocyte- or EC-specific Il1r1 deletion reduced OL loss. Conditioned medium derived from IL-1α-stimulated astrocytes is toxic for OLs; further, IL-1α-stimulated astrocytes generate reactive oxygen species (ROS) and blocking ROS production in IL-1α-treated or SCI mice prevented OL loss. Thus, after SCI, microglia release IL-1α, which induces astrocyte- and EC-mediated OL degeneration.


2021 ◽  
Vol 1 (2) ◽  
Author(s):  
Andrea Paola Ibarra-García ◽  
Antonio Ibarra

Spinal cord injury (SCI) induces several destructive events that develop immediately after the primary insult. These phenomena increase tissue damage; that is why, numerous therapeutic approaches are studied in order to neutralize these destructive mechanisms. In line with this, several studies indicate that after injury, neural tissue could be protected by an adaptive immune response directed against self-antigens. Immunization with neural-derived peptides (INDP) reduces secondary degeneration of neurons after spinal cord insult and promotes a significant motor recovery. The combination of antioxidants or other immunomodulatory peptides after SCI can improve the protective effect induced by INDP. INDP in acute SCI is a promising strategy, so further studies should be addressed to be able to formulate the best strategy.


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