ArticleCell death & disease2018
Induced neural stem cell-derived astrocytes modulate complement activation and mediate neuroprotection following closed head injury.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.
- A Systematic Review of Closed Head Injury Models of Mild Traumatic Brain Injury in Mice and Rats.Journal of neurotrauma · 2019Pooled it
- Targeted complement inhibition ameliorates the pathological and cognitive outcomes in repetitive mild closed head injury.Signal transduction and targeted therapy · 2025Article
- Nanozymes in neuropathic pain: strategies bridging oxidative stress, mitochondrial repair, and neuroimmune modulation for targeted therapy.Journal of neuroinflammation · 2025Review
- Long non-coding RNA Malat1 modulates CXCR4 expression to regulate the interaction between induced neural stem cells and microglia following closed head injury.Stem cell research & therapy · 2025Article
- Astrocytes originated from neural stem cells drive the regenerative remodeling of pathologic CSPGs in spinal cord injury.Stem cell reports · 2024Article
- Long non-coding RNANeural regeneration research · 2024Article
- Induced neural stem cell grafts exert neuroprotection through an interaction between Crry and Akt in a mouse model of closed head injury.Stem cell research & therapy · 2021Article
- Endothelial progenitor cell transplantation alleviated ischemic brain injury via inhibiting C3/C3aR pathway in mice.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2020Article
- Xeno- and transgene-free reprogramming of mesenchymal stem cells toward the cells expressing neural markers using exosome treatments.PloS one · 2020Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The complement system is a crucial component of immunity, and its activation has critical roles in neuroinflammatory response and cellular damage following closed head injury (CHI). We previously demonstrated that systemically injected induced neural stem cells (iNSCs) could modulate complement activation to ameliorate neuronal apoptosis in mouse CHI models. However, it remains unknown whether iNSC derivatives can regulate complement activation. In the present study, after CHI mouse serum treatment, we found dramatic decreases in the cellular viabilities of differentiated iNSCs. Interestingly, following CHI mouse serum treatment, the death of astrocytes derived from iNSCs which were pre-treated with CHI mouse serum was significantly decreased. Meanwhile, the deposition of C3 (C3d) and C5b-9 in these astrocytes was substantially reduced. Remarkably, we detected increased expression of complement receptor type 1-related protein y (Crry) in these astrocytes. Moreover, these astrocytes could reduce the numbers of apoptotic neurons via Crry expression post-CHI mouse serum treatment. Additionally, intracerebral-transplanted iNSCs, pre-treated with CHI mouse serum, significantly increased the levels of Crry expression in astrocytes to reduce the accumulation of C3d and C9 and the death of neurons in the brains of CHI mice. In summary, iNSCs receiving CHI mouse serum pre-treatment could enhance the expression of Crry in iNSC-derived astrocytes to modulate complement activation and mediate neuroprotection following CHI.
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