Dynamics of spinal microglia repopulation following an acute depletion View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2016-03-10

AUTHORS

Yao Yao, Stefania Echeverry, Xiang Qun Shi, Mu Yang, Qiu Zi Yang, Guan Yun Frances Wang, Julien Chambon, Yi Chen Wu, Kai Yuan Fu, Yves De Koninck, Ji Zhang

ABSTRACT

Our understanding on the function of microglia has been revolutionized in the recent 20 years. However, the process of maintaining microglia homeostasis has not been fully understood. In this study, we dissected the features of spinal microglia repopulation following an acute partial depletion. By injecting intrathecally Mac-1-saporin, a microglia selective immunotoxin, we ablated 50% microglia in the spinal cord of naive mice. Spinal microglia repopulated rapidly and local homeostasis was re-established within 14 days post-depletion. Mac-1-saporin treatment resulted in microglia cell proliferation and circulating monocyte infiltration. The latter is indeed part of an acute, transient inflammatory reaction that follows cell depletion, and was characterized by an increase in the expression of inflammatory molecules and by the breakdown of the blood spinal cord barrier. During this period, microglia formed cell clusters and exhibited a M1-like phenotype. MCP-1/CCR2 signaling was essential in promoting this depletion associated spinal inflammatory reaction. Interestingly, ruling out MCP-1-mediated secondary inflammation, including blocking recruitment of monocyte-derived microglia, did not affect depletion-triggered microglia repopulation. Our results also demonstrated that newly generated microglia kept their responsiveness to peripheral nerve injury and their contribution to injury-associated neuropathic pain was not significantly altered. More... »

PAGES

22839

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/srep22839

DOI

http://dx.doi.org/10.1038/srep22839

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1039982357

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/26961247


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