Upregulation of AQP4 Improves Blood–Brain Barrier Integrity and Perihematomal Edema Following Intracerebral Hemorrhage
Abstract In intracerebral hemorrhage (ICH), delayed secondary neural damages largely occur from perihematomal edema (PHE) resulting from the disruption of the blood–brain barrier (BBB). PHE is often considered the principal cause of morbidity and mortality in patients with ICH. Nevertheless, the mai...
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| Autor*in: |
Jeon, Hanwool [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2021 |
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| Schlagwörter: |
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| Anmerkung: |
© The American Society for Experimental NeuroTherapeutics, Inc. 2021 |
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| Übergeordnetes Werk: |
Enthalten in: NeuroRX - Springer-Verlag, 2006, 18(2021), 4 vom: 20. Sept., Seite 2692-2706 |
|---|---|
| Übergeordnetes Werk: |
volume:18 ; year:2021 ; number:4 ; day:20 ; month:09 ; pages:2692-2706 |
| Links: |
|---|
| DOI / URN: |
10.1007/s13311-021-01126-2 |
|---|
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SPR046114769 |
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| 520 | |a Abstract In intracerebral hemorrhage (ICH), delayed secondary neural damages largely occur from perihematomal edema (PHE) resulting from the disruption of the blood–brain barrier (BBB). PHE is often considered the principal cause of morbidity and mortality in patients with ICH. Nevertheless, the main cellular mechanism as well as the specific BBB component involved in the formation of PHE after ICH remains elusive. Herein, we evaluated the role of AQP4, a water channel expressed on the astrocytes of the BBB, in the formation of PHE in ICH. The static and dynamic functions of the BBB were evaluated by analyzing the microstructure and leakage assay. Protein changes in the PHE lesion were analyzed and the control mechanism of AQP4 expression by reactive oxygen species was also investigated. Delayed PHE formation due to BBB disruption after ICH was confirmed by the decreased coverage of multiple BBB components and increased dynamic leakages. Microstructure assay showed that among the BBB components, AQP4 showed a markedly decreased expression in the PHE lesions. The decrease in AQP4 was due to microenvironmental ROS derived from the hemorrhage and was restored by treatment with ROS scavenger. AQP4-deficient mice had significantly larger PHE lesions and unfavorable survival outcomes compared with wild-type mice. Our data identify AQP4 as a specific BBB-modulating target for alleviating PHE in ICH. Further comprehensive studies are needed to form the preclinical basis for the use of AQP4 enhancers as BBB modulators for preventing delayed cerebral edema after ICH. | ||
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10.1007/s13311-021-01126-2 doi (DE-627)SPR046114769 (SPR)s13311-021-01126-2-e DE-627 ger DE-627 rakwb eng Jeon, Hanwool verfasserin aut Upregulation of AQP4 Improves Blood–Brain Barrier Integrity and Perihematomal Edema Following Intracerebral Hemorrhage 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The American Society for Experimental NeuroTherapeutics, Inc. 2021 Abstract In intracerebral hemorrhage (ICH), delayed secondary neural damages largely occur from perihematomal edema (PHE) resulting from the disruption of the blood–brain barrier (BBB). PHE is often considered the principal cause of morbidity and mortality in patients with ICH. Nevertheless, the main cellular mechanism as well as the specific BBB component involved in the formation of PHE after ICH remains elusive. Herein, we evaluated the role of AQP4, a water channel expressed on the astrocytes of the BBB, in the formation of PHE in ICH. The static and dynamic functions of the BBB were evaluated by analyzing the microstructure and leakage assay. Protein changes in the PHE lesion were analyzed and the control mechanism of AQP4 expression by reactive oxygen species was also investigated. Delayed PHE formation due to BBB disruption after ICH was confirmed by the decreased coverage of multiple BBB components and increased dynamic leakages. Microstructure assay showed that among the BBB components, AQP4 showed a markedly decreased expression in the PHE lesions. The decrease in AQP4 was due to microenvironmental ROS derived from the hemorrhage and was restored by treatment with ROS scavenger. AQP4-deficient mice had significantly larger PHE lesions and unfavorable survival outcomes compared with wild-type mice. Our data identify AQP4 as a specific BBB-modulating target for alleviating PHE in ICH. Further comprehensive studies are needed to form the preclinical basis for the use of AQP4 enhancers as BBB modulators for preventing delayed cerebral edema after ICH. Perihematomal edema (dpeaa)DE-He213 Vasogenic edema (dpeaa)DE-He213 Intracerebral hemorrhage (dpeaa)DE-He213 Vascular biology (dpeaa)DE-He213 Kim, Moinay aut Park, Wonhyoung aut Lim, Joon Seo aut Lee, Eunyeup aut Cha, Hyeuk aut Ahn, Jae Sung aut Kim, Jeong Hoon aut Hong, Seok Ho aut Park, Ji Eun aut Lee, Eun-Jae aut Woo, Chul-Woong aut Lee, Seungjoo (orcid)0000-0003-0641-3917 aut Enthalten in NeuroRX Springer-Verlag, 2006 18(2021), 4 vom: 20. Sept., Seite 2692-2706 (DE-627)SPR031264964 nnns volume:18 year:2021 number:4 day:20 month:09 pages:2692-2706 https://dx.doi.org/10.1007/s13311-021-01126-2 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER AR 18 2021 4 20 09 2692-2706 |
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10.1007/s13311-021-01126-2 doi (DE-627)SPR046114769 (SPR)s13311-021-01126-2-e DE-627 ger DE-627 rakwb eng Jeon, Hanwool verfasserin aut Upregulation of AQP4 Improves Blood–Brain Barrier Integrity and Perihematomal Edema Following Intracerebral Hemorrhage 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The American Society for Experimental NeuroTherapeutics, Inc. 2021 Abstract In intracerebral hemorrhage (ICH), delayed secondary neural damages largely occur from perihematomal edema (PHE) resulting from the disruption of the blood–brain barrier (BBB). PHE is often considered the principal cause of morbidity and mortality in patients with ICH. Nevertheless, the main cellular mechanism as well as the specific BBB component involved in the formation of PHE after ICH remains elusive. Herein, we evaluated the role of AQP4, a water channel expressed on the astrocytes of the BBB, in the formation of PHE in ICH. The static and dynamic functions of the BBB were evaluated by analyzing the microstructure and leakage assay. Protein changes in the PHE lesion were analyzed and the control mechanism of AQP4 expression by reactive oxygen species was also investigated. Delayed PHE formation due to BBB disruption after ICH was confirmed by the decreased coverage of multiple BBB components and increased dynamic leakages. Microstructure assay showed that among the BBB components, AQP4 showed a markedly decreased expression in the PHE lesions. The decrease in AQP4 was due to microenvironmental ROS derived from the hemorrhage and was restored by treatment with ROS scavenger. AQP4-deficient mice had significantly larger PHE lesions and unfavorable survival outcomes compared with wild-type mice. Our data identify AQP4 as a specific BBB-modulating target for alleviating PHE in ICH. Further comprehensive studies are needed to form the preclinical basis for the use of AQP4 enhancers as BBB modulators for preventing delayed cerebral edema after ICH. Perihematomal edema (dpeaa)DE-He213 Vasogenic edema (dpeaa)DE-He213 Intracerebral hemorrhage (dpeaa)DE-He213 Vascular biology (dpeaa)DE-He213 Kim, Moinay aut Park, Wonhyoung aut Lim, Joon Seo aut Lee, Eunyeup aut Cha, Hyeuk aut Ahn, Jae Sung aut Kim, Jeong Hoon aut Hong, Seok Ho aut Park, Ji Eun aut Lee, Eun-Jae aut Woo, Chul-Woong aut Lee, Seungjoo (orcid)0000-0003-0641-3917 aut Enthalten in NeuroRX Springer-Verlag, 2006 18(2021), 4 vom: 20. Sept., Seite 2692-2706 (DE-627)SPR031264964 nnns volume:18 year:2021 number:4 day:20 month:09 pages:2692-2706 https://dx.doi.org/10.1007/s13311-021-01126-2 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER AR 18 2021 4 20 09 2692-2706 |
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10.1007/s13311-021-01126-2 doi (DE-627)SPR046114769 (SPR)s13311-021-01126-2-e DE-627 ger DE-627 rakwb eng Jeon, Hanwool verfasserin aut Upregulation of AQP4 Improves Blood–Brain Barrier Integrity and Perihematomal Edema Following Intracerebral Hemorrhage 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The American Society for Experimental NeuroTherapeutics, Inc. 2021 Abstract In intracerebral hemorrhage (ICH), delayed secondary neural damages largely occur from perihematomal edema (PHE) resulting from the disruption of the blood–brain barrier (BBB). PHE is often considered the principal cause of morbidity and mortality in patients with ICH. Nevertheless, the main cellular mechanism as well as the specific BBB component involved in the formation of PHE after ICH remains elusive. Herein, we evaluated the role of AQP4, a water channel expressed on the astrocytes of the BBB, in the formation of PHE in ICH. The static and dynamic functions of the BBB were evaluated by analyzing the microstructure and leakage assay. Protein changes in the PHE lesion were analyzed and the control mechanism of AQP4 expression by reactive oxygen species was also investigated. Delayed PHE formation due to BBB disruption after ICH was confirmed by the decreased coverage of multiple BBB components and increased dynamic leakages. Microstructure assay showed that among the BBB components, AQP4 showed a markedly decreased expression in the PHE lesions. The decrease in AQP4 was due to microenvironmental ROS derived from the hemorrhage and was restored by treatment with ROS scavenger. AQP4-deficient mice had significantly larger PHE lesions and unfavorable survival outcomes compared with wild-type mice. Our data identify AQP4 as a specific BBB-modulating target for alleviating PHE in ICH. Further comprehensive studies are needed to form the preclinical basis for the use of AQP4 enhancers as BBB modulators for preventing delayed cerebral edema after ICH. Perihematomal edema (dpeaa)DE-He213 Vasogenic edema (dpeaa)DE-He213 Intracerebral hemorrhage (dpeaa)DE-He213 Vascular biology (dpeaa)DE-He213 Kim, Moinay aut Park, Wonhyoung aut Lim, Joon Seo aut Lee, Eunyeup aut Cha, Hyeuk aut Ahn, Jae Sung aut Kim, Jeong Hoon aut Hong, Seok Ho aut Park, Ji Eun aut Lee, Eun-Jae aut Woo, Chul-Woong aut Lee, Seungjoo (orcid)0000-0003-0641-3917 aut Enthalten in NeuroRX Springer-Verlag, 2006 18(2021), 4 vom: 20. Sept., Seite 2692-2706 (DE-627)SPR031264964 nnns volume:18 year:2021 number:4 day:20 month:09 pages:2692-2706 https://dx.doi.org/10.1007/s13311-021-01126-2 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER AR 18 2021 4 20 09 2692-2706 |
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10.1007/s13311-021-01126-2 doi (DE-627)SPR046114769 (SPR)s13311-021-01126-2-e DE-627 ger DE-627 rakwb eng Jeon, Hanwool verfasserin aut Upregulation of AQP4 Improves Blood–Brain Barrier Integrity and Perihematomal Edema Following Intracerebral Hemorrhage 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The American Society for Experimental NeuroTherapeutics, Inc. 2021 Abstract In intracerebral hemorrhage (ICH), delayed secondary neural damages largely occur from perihematomal edema (PHE) resulting from the disruption of the blood–brain barrier (BBB). PHE is often considered the principal cause of morbidity and mortality in patients with ICH. Nevertheless, the main cellular mechanism as well as the specific BBB component involved in the formation of PHE after ICH remains elusive. Herein, we evaluated the role of AQP4, a water channel expressed on the astrocytes of the BBB, in the formation of PHE in ICH. The static and dynamic functions of the BBB were evaluated by analyzing the microstructure and leakage assay. Protein changes in the PHE lesion were analyzed and the control mechanism of AQP4 expression by reactive oxygen species was also investigated. Delayed PHE formation due to BBB disruption after ICH was confirmed by the decreased coverage of multiple BBB components and increased dynamic leakages. Microstructure assay showed that among the BBB components, AQP4 showed a markedly decreased expression in the PHE lesions. The decrease in AQP4 was due to microenvironmental ROS derived from the hemorrhage and was restored by treatment with ROS scavenger. AQP4-deficient mice had significantly larger PHE lesions and unfavorable survival outcomes compared with wild-type mice. Our data identify AQP4 as a specific BBB-modulating target for alleviating PHE in ICH. Further comprehensive studies are needed to form the preclinical basis for the use of AQP4 enhancers as BBB modulators for preventing delayed cerebral edema after ICH. Perihematomal edema (dpeaa)DE-He213 Vasogenic edema (dpeaa)DE-He213 Intracerebral hemorrhage (dpeaa)DE-He213 Vascular biology (dpeaa)DE-He213 Kim, Moinay aut Park, Wonhyoung aut Lim, Joon Seo aut Lee, Eunyeup aut Cha, Hyeuk aut Ahn, Jae Sung aut Kim, Jeong Hoon aut Hong, Seok Ho aut Park, Ji Eun aut Lee, Eun-Jae aut Woo, Chul-Woong aut Lee, Seungjoo (orcid)0000-0003-0641-3917 aut Enthalten in NeuroRX Springer-Verlag, 2006 18(2021), 4 vom: 20. Sept., Seite 2692-2706 (DE-627)SPR031264964 nnns volume:18 year:2021 number:4 day:20 month:09 pages:2692-2706 https://dx.doi.org/10.1007/s13311-021-01126-2 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER AR 18 2021 4 20 09 2692-2706 |
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10.1007/s13311-021-01126-2 doi (DE-627)SPR046114769 (SPR)s13311-021-01126-2-e DE-627 ger DE-627 rakwb eng Jeon, Hanwool verfasserin aut Upregulation of AQP4 Improves Blood–Brain Barrier Integrity and Perihematomal Edema Following Intracerebral Hemorrhage 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The American Society for Experimental NeuroTherapeutics, Inc. 2021 Abstract In intracerebral hemorrhage (ICH), delayed secondary neural damages largely occur from perihematomal edema (PHE) resulting from the disruption of the blood–brain barrier (BBB). PHE is often considered the principal cause of morbidity and mortality in patients with ICH. Nevertheless, the main cellular mechanism as well as the specific BBB component involved in the formation of PHE after ICH remains elusive. Herein, we evaluated the role of AQP4, a water channel expressed on the astrocytes of the BBB, in the formation of PHE in ICH. The static and dynamic functions of the BBB were evaluated by analyzing the microstructure and leakage assay. Protein changes in the PHE lesion were analyzed and the control mechanism of AQP4 expression by reactive oxygen species was also investigated. Delayed PHE formation due to BBB disruption after ICH was confirmed by the decreased coverage of multiple BBB components and increased dynamic leakages. Microstructure assay showed that among the BBB components, AQP4 showed a markedly decreased expression in the PHE lesions. The decrease in AQP4 was due to microenvironmental ROS derived from the hemorrhage and was restored by treatment with ROS scavenger. AQP4-deficient mice had significantly larger PHE lesions and unfavorable survival outcomes compared with wild-type mice. Our data identify AQP4 as a specific BBB-modulating target for alleviating PHE in ICH. Further comprehensive studies are needed to form the preclinical basis for the use of AQP4 enhancers as BBB modulators for preventing delayed cerebral edema after ICH. Perihematomal edema (dpeaa)DE-He213 Vasogenic edema (dpeaa)DE-He213 Intracerebral hemorrhage (dpeaa)DE-He213 Vascular biology (dpeaa)DE-He213 Kim, Moinay aut Park, Wonhyoung aut Lim, Joon Seo aut Lee, Eunyeup aut Cha, Hyeuk aut Ahn, Jae Sung aut Kim, Jeong Hoon aut Hong, Seok Ho aut Park, Ji Eun aut Lee, Eun-Jae aut Woo, Chul-Woong aut Lee, Seungjoo (orcid)0000-0003-0641-3917 aut Enthalten in NeuroRX Springer-Verlag, 2006 18(2021), 4 vom: 20. Sept., Seite 2692-2706 (DE-627)SPR031264964 nnns volume:18 year:2021 number:4 day:20 month:09 pages:2692-2706 https://dx.doi.org/10.1007/s13311-021-01126-2 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER AR 18 2021 4 20 09 2692-2706 |
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Enthalten in NeuroRX 18(2021), 4 vom: 20. Sept., Seite 2692-2706 volume:18 year:2021 number:4 day:20 month:09 pages:2692-2706 |
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Jeon, Hanwool misc Perihematomal edema misc Vasogenic edema misc Intracerebral hemorrhage misc Vascular biology Upregulation of AQP4 Improves Blood–Brain Barrier Integrity and Perihematomal Edema Following Intracerebral Hemorrhage |
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Upregulation of AQP4 Improves Blood–Brain Barrier Integrity and Perihematomal Edema Following Intracerebral Hemorrhage Perihematomal edema (dpeaa)DE-He213 Vasogenic edema (dpeaa)DE-He213 Intracerebral hemorrhage (dpeaa)DE-He213 Vascular biology (dpeaa)DE-He213 |
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Jeon, Hanwool Kim, Moinay Park, Wonhyoung Lim, Joon Seo Lee, Eunyeup Cha, Hyeuk Ahn, Jae Sung Kim, Jeong Hoon Hong, Seok Ho Park, Ji Eun Lee, Eun-Jae Woo, Chul-Woong Lee, Seungjoo |
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upregulation of aqp4 improves blood–brain barrier integrity and perihematomal edema following intracerebral hemorrhage |
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Upregulation of AQP4 Improves Blood–Brain Barrier Integrity and Perihematomal Edema Following Intracerebral Hemorrhage |
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Abstract In intracerebral hemorrhage (ICH), delayed secondary neural damages largely occur from perihematomal edema (PHE) resulting from the disruption of the blood–brain barrier (BBB). PHE is often considered the principal cause of morbidity and mortality in patients with ICH. Nevertheless, the main cellular mechanism as well as the specific BBB component involved in the formation of PHE after ICH remains elusive. Herein, we evaluated the role of AQP4, a water channel expressed on the astrocytes of the BBB, in the formation of PHE in ICH. The static and dynamic functions of the BBB were evaluated by analyzing the microstructure and leakage assay. Protein changes in the PHE lesion were analyzed and the control mechanism of AQP4 expression by reactive oxygen species was also investigated. Delayed PHE formation due to BBB disruption after ICH was confirmed by the decreased coverage of multiple BBB components and increased dynamic leakages. Microstructure assay showed that among the BBB components, AQP4 showed a markedly decreased expression in the PHE lesions. The decrease in AQP4 was due to microenvironmental ROS derived from the hemorrhage and was restored by treatment with ROS scavenger. AQP4-deficient mice had significantly larger PHE lesions and unfavorable survival outcomes compared with wild-type mice. Our data identify AQP4 as a specific BBB-modulating target for alleviating PHE in ICH. Further comprehensive studies are needed to form the preclinical basis for the use of AQP4 enhancers as BBB modulators for preventing delayed cerebral edema after ICH. © The American Society for Experimental NeuroTherapeutics, Inc. 2021 |
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Abstract In intracerebral hemorrhage (ICH), delayed secondary neural damages largely occur from perihematomal edema (PHE) resulting from the disruption of the blood–brain barrier (BBB). PHE is often considered the principal cause of morbidity and mortality in patients with ICH. Nevertheless, the main cellular mechanism as well as the specific BBB component involved in the formation of PHE after ICH remains elusive. Herein, we evaluated the role of AQP4, a water channel expressed on the astrocytes of the BBB, in the formation of PHE in ICH. The static and dynamic functions of the BBB were evaluated by analyzing the microstructure and leakage assay. Protein changes in the PHE lesion were analyzed and the control mechanism of AQP4 expression by reactive oxygen species was also investigated. Delayed PHE formation due to BBB disruption after ICH was confirmed by the decreased coverage of multiple BBB components and increased dynamic leakages. Microstructure assay showed that among the BBB components, AQP4 showed a markedly decreased expression in the PHE lesions. The decrease in AQP4 was due to microenvironmental ROS derived from the hemorrhage and was restored by treatment with ROS scavenger. AQP4-deficient mice had significantly larger PHE lesions and unfavorable survival outcomes compared with wild-type mice. Our data identify AQP4 as a specific BBB-modulating target for alleviating PHE in ICH. Further comprehensive studies are needed to form the preclinical basis for the use of AQP4 enhancers as BBB modulators for preventing delayed cerebral edema after ICH. © The American Society for Experimental NeuroTherapeutics, Inc. 2021 |
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Abstract In intracerebral hemorrhage (ICH), delayed secondary neural damages largely occur from perihematomal edema (PHE) resulting from the disruption of the blood–brain barrier (BBB). PHE is often considered the principal cause of morbidity and mortality in patients with ICH. Nevertheless, the main cellular mechanism as well as the specific BBB component involved in the formation of PHE after ICH remains elusive. Herein, we evaluated the role of AQP4, a water channel expressed on the astrocytes of the BBB, in the formation of PHE in ICH. The static and dynamic functions of the BBB were evaluated by analyzing the microstructure and leakage assay. Protein changes in the PHE lesion were analyzed and the control mechanism of AQP4 expression by reactive oxygen species was also investigated. Delayed PHE formation due to BBB disruption after ICH was confirmed by the decreased coverage of multiple BBB components and increased dynamic leakages. Microstructure assay showed that among the BBB components, AQP4 showed a markedly decreased expression in the PHE lesions. The decrease in AQP4 was due to microenvironmental ROS derived from the hemorrhage and was restored by treatment with ROS scavenger. AQP4-deficient mice had significantly larger PHE lesions and unfavorable survival outcomes compared with wild-type mice. Our data identify AQP4 as a specific BBB-modulating target for alleviating PHE in ICH. Further comprehensive studies are needed to form the preclinical basis for the use of AQP4 enhancers as BBB modulators for preventing delayed cerebral edema after ICH. © The American Society for Experimental NeuroTherapeutics, Inc. 2021 |
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Upregulation of AQP4 Improves Blood–Brain Barrier Integrity and Perihematomal Edema Following Intracerebral Hemorrhage |
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Kim, Moinay Park, Wonhyoung Lim, Joon Seo Lee, Eunyeup Cha, Hyeuk Ahn, Jae Sung Kim, Jeong Hoon Hong, Seok Ho Park, Ji Eun Lee, Eun-Jae Woo, Chul-Woong Lee, Seungjoo |
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