The complement C3‐C3aR pathway mediates microglia–astrocyte interaction following status epilepticus
Gliosis is a histopathological characteristic of epilepsy that comprises activated microglia and astrocytes. It is unclear whether or how crosstalk occurs between microglia and astrocytes in the evolution of epilepsy. Here, we report in a mouse model of status epilepticus, induced by intracerebroven...
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| Published in | Glia Vol. 69; no. 5; pp. 1155 - 1169 |
|---|---|
| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Hoboken, USA
John Wiley & Sons, Inc
01.05.2021
Wiley Subscription Services, Inc |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0894-1491 1098-1136 1098-1136 |
| DOI | 10.1002/glia.23955 |
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| Abstract | Gliosis is a histopathological characteristic of epilepsy that comprises activated microglia and astrocytes. It is unclear whether or how crosstalk occurs between microglia and astrocytes in the evolution of epilepsy. Here, we report in a mouse model of status epilepticus, induced by intracerebroventricular injection of kainic acid (KA), sequential activation of microglia and astrocytes and their close spatial interaction in the hippocampal CA3 region. Microglial ablation reduced astrocyte activation and their upregulation of complement C3. When compared to wild‐type mice, both C3−/− and C3aR−/− mice had significantly less microglia–astrocyte interaction in response to KA‐induced status epilepticus. Additionally, KA‐injected C3−/− mice had significantly less histochemical evidence of neurodegeneration. The results suggest that the C3‐C3aR pathway contributes to KA‐induced neurodegeneration by mediating microglia–astrocyte communication. The C3‐C3aR pathway may prove to be a potential therapeutic target for epilepsy treatment.
Main Points
Microglia are required for astrocytes activation in experimental status epilepticus.
C3 from astrocytes activates microglia via C3a receptors.
Microglia–astrocyte interaction promotes gliosis and neuronal injury after seizures. |
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| AbstractList | Gliosis is a histopathological characteristic of epilepsy that comprises activated microglia and astrocytes. It is unclear whether or how crosstalk occurs between microglia and astrocytes in the evolution of epilepsy. Here, we report in a mouse model of status epilepticus, induced by intracerebroventricular injection of kainic acid (KA), sequential activation of microglia and astrocytes and their close spatial interaction in the hippocampal CA3 region. Microglial ablation reduced astrocyte activation and their upregulation of complement C3. When compared to wild‐type mice, both C3−/− and C3aR−/− mice had significantly less microglia–astrocyte interaction in response to KA‐induced status epilepticus. Additionally, KA‐injected C3−/− mice had significantly less histochemical evidence of neurodegeneration. The results suggest that the C3‐C3aR pathway contributes to KA‐induced neurodegeneration by mediating microglia–astrocyte communication. The C3‐C3aR pathway may prove to be a potential therapeutic target for epilepsy treatment. Gliosis is a histopathologic characteristic of epilepsy that comprises activated microglia and astrocytes. It is unclear whether or how crosstalk occurs between microglia and astrocytes in the evolution of epilepsy. Here, we report in a mouse model of status epilepticus, induced by intracerebroventricular injection of kainic acid (KA), sequential activation of microglia and astrocytes and their close spatial interaction in the hippocampal CA3 region. Microglial ablation reduced astrocyte activation and their upregulation of complement C3. When compared to wild-type mice, both C3−/− and C3aR−/− mice had significantly less microglia-astrocyte interaction in response to KA-induced status epilepticus. Additionally, KA-injected C3−/− mice had significantly less histochemical evidence of neurodegeneration. The results suggest that the C3-C3aR pathway contributes to KA-induced neurodegeneration by mediating microglia-astrocyte communication. The C3-C3aR pathway may prove to be a potential therapeutic target for epilepsy treatment. Gliosis is a histopathological characteristic of epilepsy that comprises activated microglia and astrocytes. It is unclear whether or how crosstalk occurs between microglia and astrocytes in the evolution of epilepsy. Here, we report in a mouse model of status epilepticus, induced by intracerebroventricular injection of kainic acid (KA), sequential activation of microglia and astrocytes and their close spatial interaction in the hippocampal CA3 region. Microglial ablation reduced astrocyte activation and their upregulation of complement C3. When compared to wild-type mice, both C3-/- and C3aR-/- mice had significantly less microglia-astrocyte interaction in response to KA-induced status epilepticus. Additionally, KA-injected C3-/- mice had significantly less histochemical evidence of neurodegeneration. The results suggest that the C3-C3aR pathway contributes to KA-induced neurodegeneration by mediating microglia-astrocyte communication. The C3-C3aR pathway may prove to be a potential therapeutic target for epilepsy treatment.Gliosis is a histopathological characteristic of epilepsy that comprises activated microglia and astrocytes. It is unclear whether or how crosstalk occurs between microglia and astrocytes in the evolution of epilepsy. Here, we report in a mouse model of status epilepticus, induced by intracerebroventricular injection of kainic acid (KA), sequential activation of microglia and astrocytes and their close spatial interaction in the hippocampal CA3 region. Microglial ablation reduced astrocyte activation and their upregulation of complement C3. When compared to wild-type mice, both C3-/- and C3aR-/- mice had significantly less microglia-astrocyte interaction in response to KA-induced status epilepticus. Additionally, KA-injected C3-/- mice had significantly less histochemical evidence of neurodegeneration. The results suggest that the C3-C3aR pathway contributes to KA-induced neurodegeneration by mediating microglia-astrocyte communication. The C3-C3aR pathway may prove to be a potential therapeutic target for epilepsy treatment. Gliosis is a histopathological characteristic of epilepsy that comprises activated microglia and astrocytes. It is unclear whether or how crosstalk occurs between microglia and astrocytes in the evolution of epilepsy. Here, we report in a mouse model of status epilepticus, induced by intracerebroventricular injection of kainic acid (KA), sequential activation of microglia and astrocytes and their close spatial interaction in the hippocampal CA3 region. Microglial ablation reduced astrocyte activation and their upregulation of complement C3. When compared to wild‐type mice, both C3 −/− and C3aR −/− mice had significantly less microglia–astrocyte interaction in response to KA‐induced status epilepticus. Additionally, KA‐injected C3 −/− mice had significantly less histochemical evidence of neurodegeneration. The results suggest that the C3‐C3aR pathway contributes to KA‐induced neurodegeneration by mediating microglia–astrocyte communication. The C3‐C3aR pathway may prove to be a potential therapeutic target for epilepsy treatment. Gliosis is a histopathological characteristic of epilepsy that comprises activated microglia and astrocytes. It is unclear whether or how crosstalk occurs between microglia and astrocytes in the evolution of epilepsy. Here, we report in a mouse model of status epilepticus, induced by intracerebroventricular injection of kainic acid (KA), sequential activation of microglia and astrocytes and their close spatial interaction in the hippocampal CA3 region. Microglial ablation reduced astrocyte activation and their upregulation of complement C3. When compared to wild‐type mice, both C3−/− and C3aR−/− mice had significantly less microglia–astrocyte interaction in response to KA‐induced status epilepticus. Additionally, KA‐injected C3−/− mice had significantly less histochemical evidence of neurodegeneration. The results suggest that the C3‐C3aR pathway contributes to KA‐induced neurodegeneration by mediating microglia–astrocyte communication. The C3‐C3aR pathway may prove to be a potential therapeutic target for epilepsy treatment. Main Points Microglia are required for astrocytes activation in experimental status epilepticus. C3 from astrocytes activates microglia via C3a receptors. Microglia–astrocyte interaction promotes gliosis and neuronal injury after seizures. Gliosis is a histopathological characteristic of epilepsy that comprises activated microglia and astrocytes. It is unclear whether or how crosstalk occurs between microglia and astrocytes in the evolution of epilepsy. Here, we report in a mouse model of status epilepticus, induced by intracerebroventricular injection of kainic acid (KA), sequential activation of microglia and astrocytes and their close spatial interaction in the hippocampal CA3 region. Microglial ablation reduced astrocyte activation and their upregulation of complement C3. When compared to wild-type mice, both C3 and C3aR mice had significantly less microglia-astrocyte interaction in response to KA-induced status epilepticus. Additionally, KA-injected C3 mice had significantly less histochemical evidence of neurodegeneration. The results suggest that the C3-C3aR pathway contributes to KA-induced neurodegeneration by mediating microglia-astrocyte communication. The C3-C3aR pathway may prove to be a potential therapeutic target for epilepsy treatment. |
| Author | Ying, Yanlu Dheer, Aastha Wu, Long‐Jun Zheng, Jiaying Wu, Qian Bosco, Dale B. Lennon, Vanda A. Wei, Yujia Chen, Tingjun Xie, Manling |
| AuthorAffiliation | 4 Department of Neuroscience, Mayo Clinic, Jacksonville, FL, 32224, USA 1 Department of Neurology, Mayo Clinic, Rochester, MN, 55905, USA 2 Department of Neurosurgery, Xinqiao Hospital, Army Military Medical University, Chongqing, 400037, China 3 Department of Immunology, Mayo Clinic, Rochester, MN, 55905, USA |
| AuthorAffiliation_xml | – name: 2 Department of Neurosurgery, Xinqiao Hospital, Army Military Medical University, Chongqing, 400037, China – name: 3 Department of Immunology, Mayo Clinic, Rochester, MN, 55905, USA – name: 4 Department of Neuroscience, Mayo Clinic, Jacksonville, FL, 32224, USA – name: 1 Department of Neurology, Mayo Clinic, Rochester, MN, 55905, USA |
| Author_xml | – sequence: 1 givenname: Yujia surname: Wei fullname: Wei, Yujia organization: Xinqiao Hospital, Army Military Medical University – sequence: 2 givenname: Tingjun surname: Chen fullname: Chen, Tingjun organization: Mayo Clinic – sequence: 3 givenname: Dale B. surname: Bosco fullname: Bosco, Dale B. organization: Mayo Clinic – sequence: 4 givenname: Manling surname: Xie fullname: Xie, Manling organization: Mayo Clinic – sequence: 5 givenname: Jiaying surname: Zheng fullname: Zheng, Jiaying organization: Mayo Clinic – sequence: 6 givenname: Aastha surname: Dheer fullname: Dheer, Aastha organization: Mayo Clinic – sequence: 7 givenname: Yanlu surname: Ying fullname: Ying, Yanlu organization: Mayo Clinic – sequence: 8 givenname: Qian surname: Wu fullname: Wu, Qian organization: Mayo Clinic – sequence: 9 givenname: Vanda A. surname: Lennon fullname: Lennon, Vanda A. organization: Mayo Clinic – sequence: 10 givenname: Long‐Jun orcidid: 0000-0001-8019-3380 surname: Wu fullname: Wu, Long‐Jun email: wu.longjun@mayo.edu organization: Mayo Clinic |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/33314324$$D View this record in MEDLINE/PubMed |
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| Snippet | Gliosis is a histopathological characteristic of epilepsy that comprises activated microglia and astrocytes. It is unclear whether or how crosstalk occurs... Gliosis is a histopathologic characteristic of epilepsy that comprises activated microglia and astrocytes. It is unclear whether or how crosstalk occurs... |
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| SubjectTerms | Ablation Animals Astrocytes C3a receptor Complement activation complement C3 Complement C3 - genetics Complement component C3 Complement component C3a Complement receptors Crosstalk Epilepsy Gliosis Hippocampus Kainic acid Kainic Acid - toxicity Mice Microglia Neurodegeneration seizures Status Epilepticus - chemically induced Therapeutic targets |
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| Title | The complement C3‐C3aR pathway mediates microglia–astrocyte interaction following status epilepticus |
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