Blood–brain barrier disruption and neuroinflammation in the hippocampus of a cardiac arrest porcine model: Single-cell RNA sequencing analysis

Global brain ischemia and neurological deficit are consequences of cardiac arrest that lead to high mortality. Despite advancements in resuscitation science, our limited understanding of the cellular and molecular mechanisms underlying post-cardiac arrest brain injury have hindered the development o...

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Main Authors: Tangxing Jiang, Yaning Li, Hehui Liu, Yijun Sun, Huidan Zhang, Qirui Zhang, Shuyao Tang, Xu Niu, Han Du, Yinxia Yu, Hongwei Yue, Yunyun Guo, Yuguo Chen, Feng Xu
Format: Article
Language:English
Published: Wolters Kluwer Medknow Publications 2026-02-01
Series:Neural Regeneration Research
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Online Access:https://journals.lww.com/10.4103/NRR.NRR-D-24-01269
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author Tangxing Jiang
Yaning Li
Hehui Liu
Yijun Sun
Huidan Zhang
Qirui Zhang
Shuyao Tang
Xu Niu
Han Du
Yinxia Yu
Hongwei Yue
Yunyun Guo
Yuguo Chen
Feng Xu
author_facet Tangxing Jiang
Yaning Li
Hehui Liu
Yijun Sun
Huidan Zhang
Qirui Zhang
Shuyao Tang
Xu Niu
Han Du
Yinxia Yu
Hongwei Yue
Yunyun Guo
Yuguo Chen
Feng Xu
author_sort Tangxing Jiang
collection DOAJ
description Global brain ischemia and neurological deficit are consequences of cardiac arrest that lead to high mortality. Despite advancements in resuscitation science, our limited understanding of the cellular and molecular mechanisms underlying post-cardiac arrest brain injury have hindered the development of effective neuroprotective strategies. Previous studies primarily focused on neuronal death, potentially overlooking the contributions of non-neuronal cells and intercellular communication to the pathophysiology of cardiac arrest-induced brain injury. To address these gaps, we hypothesized that single-cell transcriptomic analysis could uncover previously unidentified cellular subpopulations, altered cell communication networks, and novel molecular mechanisms involved in post–cardiac arrest brain injury. In this study, we performed a single-cell transcriptomic analysis of the hippocampus from pigs with ventricular fibrillation-induced cardiac arrest at 6 and 24 hours following the return of spontaneous circulation, and from sham control pigs. Sequencing results revealed changes in the proportions of different cell types, suggesting post-arrest disruption in the blood–brain barrier and infiltration of neutrophils. These results were validated through western blotting, quantitative reverse transcription-polymerase chain reaction, and immunofluorescence staining. We also identified and validated a unique subcluster of activated microglia with high expression of S100A8, which increased over time following cardiac arrest. This subcluster simultaneously exhibited significant M1/M2 polarization and expressed key functional genes related to chemokines and interleukins. Additionally, we revealed the post-cardiac arrest dysfunction of oligodendrocytes and the differentiation of oligodendrocyte precursor cells into oligodendrocytes. Cell communication analysis identified enhanced post–cardiac arrest communication between neutrophils and microglia that was mediated by neutrophil-derived resistin, driving pro-inflammatory microglial polarization. Our findings provide a comprehensive single-cell map of the post-cardiac arrest hippocampus, offering potential novel targets for neuroprotection and repair following cardiac arrest.
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spelling doaj-art-c8492a723c2c49cb8f9d36c6901102cd2025-08-20T02:02:01ZengWolters Kluwer Medknow PublicationsNeural Regeneration Research1673-53741876-79582026-02-0121274275510.4103/NRR.NRR-D-24-01269Blood–brain barrier disruption and neuroinflammation in the hippocampus of a cardiac arrest porcine model: Single-cell RNA sequencing analysisTangxing JiangYaning LiHehui LiuYijun SunHuidan ZhangQirui ZhangShuyao TangXu NiuHan DuYinxia YuHongwei YueYunyun GuoYuguo ChenFeng XuGlobal brain ischemia and neurological deficit are consequences of cardiac arrest that lead to high mortality. Despite advancements in resuscitation science, our limited understanding of the cellular and molecular mechanisms underlying post-cardiac arrest brain injury have hindered the development of effective neuroprotective strategies. Previous studies primarily focused on neuronal death, potentially overlooking the contributions of non-neuronal cells and intercellular communication to the pathophysiology of cardiac arrest-induced brain injury. To address these gaps, we hypothesized that single-cell transcriptomic analysis could uncover previously unidentified cellular subpopulations, altered cell communication networks, and novel molecular mechanisms involved in post–cardiac arrest brain injury. In this study, we performed a single-cell transcriptomic analysis of the hippocampus from pigs with ventricular fibrillation-induced cardiac arrest at 6 and 24 hours following the return of spontaneous circulation, and from sham control pigs. Sequencing results revealed changes in the proportions of different cell types, suggesting post-arrest disruption in the blood–brain barrier and infiltration of neutrophils. These results were validated through western blotting, quantitative reverse transcription-polymerase chain reaction, and immunofluorescence staining. We also identified and validated a unique subcluster of activated microglia with high expression of S100A8, which increased over time following cardiac arrest. This subcluster simultaneously exhibited significant M1/M2 polarization and expressed key functional genes related to chemokines and interleukins. Additionally, we revealed the post-cardiac arrest dysfunction of oligodendrocytes and the differentiation of oligodendrocyte precursor cells into oligodendrocytes. Cell communication analysis identified enhanced post–cardiac arrest communication between neutrophils and microglia that was mediated by neutrophil-derived resistin, driving pro-inflammatory microglial polarization. Our findings provide a comprehensive single-cell map of the post-cardiac arrest hippocampus, offering potential novel targets for neuroprotection and repair following cardiac arrest.https://journals.lww.com/10.4103/NRR.NRR-D-24-01269blood–brain barrier disruptioncardiac arresthippocampusmicroglianeuroinflammationneuroprotectionneutrophiloligodendrocyte dysfunctions100a8single-cell rna sequencing
spellingShingle Tangxing Jiang
Yaning Li
Hehui Liu
Yijun Sun
Huidan Zhang
Qirui Zhang
Shuyao Tang
Xu Niu
Han Du
Yinxia Yu
Hongwei Yue
Yunyun Guo
Yuguo Chen
Feng Xu
Blood–brain barrier disruption and neuroinflammation in the hippocampus of a cardiac arrest porcine model: Single-cell RNA sequencing analysis
Neural Regeneration Research
blood–brain barrier disruption
cardiac arrest
hippocampus
microglia
neuroinflammation
neuroprotection
neutrophil
oligodendrocyte dysfunction
s100a8
single-cell rna sequencing
title Blood–brain barrier disruption and neuroinflammation in the hippocampus of a cardiac arrest porcine model: Single-cell RNA sequencing analysis
title_full Blood–brain barrier disruption and neuroinflammation in the hippocampus of a cardiac arrest porcine model: Single-cell RNA sequencing analysis
title_fullStr Blood–brain barrier disruption and neuroinflammation in the hippocampus of a cardiac arrest porcine model: Single-cell RNA sequencing analysis
title_full_unstemmed Blood–brain barrier disruption and neuroinflammation in the hippocampus of a cardiac arrest porcine model: Single-cell RNA sequencing analysis
title_short Blood–brain barrier disruption and neuroinflammation in the hippocampus of a cardiac arrest porcine model: Single-cell RNA sequencing analysis
title_sort blood brain barrier disruption and neuroinflammation in the hippocampus of a cardiac arrest porcine model single cell rna sequencing analysis
topic blood–brain barrier disruption
cardiac arrest
hippocampus
microglia
neuroinflammation
neuroprotection
neutrophil
oligodendrocyte dysfunction
s100a8
single-cell rna sequencing
url https://journals.lww.com/10.4103/NRR.NRR-D-24-01269
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