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Reactive astrocytes undergo M1 microglia/macrohpages-induced necroptosis in spinal cord injury.

Overview of attention for article published in Molecular Neurodegeneration, January 2016
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Title
Reactive astrocytes undergo M1 microglia/macrohpages-induced necroptosis in spinal cord injury.
Published in
Molecular Neurodegeneration, January 2016
DOI 10.1186/s13024-016-0081-8
Pubmed ID
Authors

Fan, Hong, Zhang, Kun, Shan, Lequn, Kuang, Fang, Chen, Kun, Zhu, Keqing, Ma, Heng, Ju, Gong, Wang, Ya-Zhou

Abstract

A unique feature of the pathological change after spinal cord injury (SCI) is the progressive enlargement of lesion area, which usually results in cavity formation and is accompanied by reactive astrogliosis and chronic inflammation. Reactive astrocytes line the spinal cavity, walling off the lesion core from the normal spinal tissue, and are thought to play multiple important roles in SCI. The contribution of cell death, particularly the apoptosis of neurons and oligodendrocytes during the process of cavitation has been extensively studied. However, how reactive astrocytes are eliminated following SCI remains largely unclear. By immunohistochemistry, in vivo propidium iodide (PI)-labeling and electron microscopic examination, here we reported that in mice, reactive astrocytes died by receptor-interacting protein 3 and mixed lineage kinase domain-like protein (RIP3/MLKL) mediated necroptosis, rather than apoptosis or autophagy. Inhibiting receptor-interacting protein 1 (RIP1) or depleting RIP3 not only significantly attenuated astrocyte death but also rescued the neurotrophic function of astrocytes. The astrocytic expression of necroptotic markers followed the polarization of M1 microglia/macrophages after SCI. Depleting M1 microglia/macrophages or transplantation of M1 macrophages could significantly reduce or increase the necroptosis of astrocytes. Further, the inflammatory responsive genes Toll-like receptor 4 (TLR4) and myeloid differentiation primary response gene 88 (MyD88) are induced in necroptotic astrocytes. In vitro antagonizing MyD88 in astrocytes could significantly alleviate the M1 microglia/macrophages-induced cell death. Finally, our data showed that in human, necroptotic markers and TLR4/MyD88 were co-expressed in astrocytes of injured, but not normal spinal cord. Taken together, these results reveal that after SCI, reactive astrocytes undergo M1 microglia/macrophages-induced necroptosis, partially through TLR/MyD88 signaling, and suggest that inhibiting astrocytic necroptosis may be beneficial for preventing secondary SCI.

Twitter Demographics

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Mendeley readers

The data shown below were compiled from readership statistics for 74 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Spain 1 1%
Unknown 73 99%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 18 24%
Researcher 11 15%
Student > Master 10 14%
Student > Bachelor 8 11%
Professor > Associate Professor 5 7%
Other 15 20%
Unknown 7 9%
Readers by discipline Count As %
Neuroscience 17 23%
Agricultural and Biological Sciences 16 22%
Medicine and Dentistry 11 15%
Biochemistry, Genetics and Molecular Biology 8 11%
Immunology and Microbiology 5 7%
Other 5 7%
Unknown 12 16%

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 05 February 2016.
All research outputs
#5,327,361
of 7,103,144 outputs
Outputs from Molecular Neurodegeneration
#293
of 352 outputs
Outputs of similar age
#220,651
of 319,350 outputs
Outputs of similar age from Molecular Neurodegeneration
#20
of 21 outputs
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We're also able to compare this research output to 21 others from the same source and published within six weeks on either side of this one. This one is in the 1st percentile – i.e., 1% of its contemporaries scored the same or lower than it.