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hiPSC–NSC–Exos enhance neurological deficits and alleviate brain edema after ICH via activation of the PI3K-AKT signaling pathway. (A) Scatter plot of differentially expressed genes in the affected hemisphere after ICH ( n = 3). (B) Gene Ontology (GO) analysis of differentially expressed genes. (C) Kyoto Encyclopedia of Genes and Genomic (KEGG) pathway enrichment analysis of the top 10 differentially expressed genes, with a focus on the PI3K-AKT signaling pathway. (D–F) Representative western blotting and quantitative analysis of p-PI3K, PI3K, p-AKT, and AKT expression levels ( n = 6). (G–I) Neurobehavioral function tests (rotarod test, corner turn test, and mNSS) were conducted on days 1 and 3 after ICH ( n = 6). The longer fall latency in rotarod tests and the fewer ipsilateral turnings in the corner turn test indicated better neurological function. (J) Quantification of water content in the ipsilateral hemisphere, contralateral hemisphere, and cerebellum ( n = 6). Data are presented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, vs. PBS group; # P < 0.05, ## P < 0.01, ### P < 0.001, vs. hiPSC-NSC-Exo group (Student’s t -test [E, F] or repeated-measures two-way analysis of variance followed by least significant difference post hoc tests [G–J]). All statistical values are presented in . AKT: Protein kinase B; DMSO: dimethyl sulfoxide; Exo: exosomes; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; hiPSC: human induced pluripotent stem cell; ICH: intracerebral hemorrhage; LY294002: a PI3K/AKT inhibitor; MCP-1: monocyte chemoattractant protein-1; mNSS: modified Neurological Severity Score; NSC: neural stem cell; p-AKT: phosphorylated protein kinase B; p-PI3K: phosphorylated phosphoinositide 3-kinase; PI3K: phosphoinositide 3-kinase; PBS: phosphate-buffered saline.
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hiPSC–NSC–Exos enhance neurological deficits and alleviate brain edema after ICH via activation of the PI3K-AKT signaling pathway. (A) Scatter plot of differentially expressed genes in the affected hemisphere after ICH ( n = 3). (B) Gene Ontology (GO) analysis of differentially expressed genes. (C) Kyoto Encyclopedia of Genes and Genomic (KEGG) pathway enrichment analysis of the top 10 differentially expressed genes, with a focus on the PI3K-AKT signaling pathway. (D–F) Representative western blotting and quantitative analysis of p-PI3K, PI3K, p-AKT, and AKT expression levels ( n = 6). (G–I) Neurobehavioral function tests (rotarod test, corner turn test, and mNSS) were conducted on days 1 and 3 after ICH ( n = 6). The longer fall latency in rotarod tests and the fewer ipsilateral turnings in the corner turn test indicated better neurological function. (J) Quantification of water content in the ipsilateral hemisphere, contralateral hemisphere, and cerebellum ( n = 6). Data are presented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, vs. PBS group; # P < 0.05, ## P < 0.01, ### P < 0.001, vs. hiPSC-NSC-Exo group (Student’s t -test [E, F] or repeated-measures two-way analysis of variance followed by least significant difference post hoc tests [G–J]). All statistical values are presented in . AKT: Protein kinase B; DMSO: dimethyl sulfoxide; Exo: exosomes; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; hiPSC: human induced pluripotent stem cell; ICH: intracerebral hemorrhage; LY294002: a PI3K/AKT inhibitor; MCP-1: monocyte chemoattractant protein-1; mNSS: modified Neurological Severity Score; NSC: neural stem cell; p-AKT: <t>phosphorylated</t> protein kinase B; p-PI3K: phosphorylated phosphoinositide 3-kinase; PI3K: phosphoinositide 3-kinase; PBS: phosphate-buffered saline.
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hiPSC–NSC–Exos enhance neurological deficits and alleviate brain edema after ICH via activation of the PI3K-AKT signaling pathway. (A) Scatter plot of differentially expressed genes in the affected hemisphere after ICH ( n = 3). (B) Gene Ontology (GO) analysis of differentially expressed genes. (C) Kyoto Encyclopedia of Genes and Genomic (KEGG) pathway enrichment analysis of the top 10 differentially expressed genes, with a focus on the PI3K-AKT signaling pathway. (D–F) Representative western blotting and quantitative analysis of p-PI3K, PI3K, p-AKT, and AKT expression levels ( n = 6). (G–I) Neurobehavioral function tests (rotarod test, corner turn test, and mNSS) were conducted on days 1 and 3 after ICH ( n = 6). The longer fall latency in rotarod tests and the fewer ipsilateral turnings in the corner turn test indicated better neurological function. (J) Quantification of water content in the ipsilateral hemisphere, contralateral hemisphere, and cerebellum ( n = 6). Data are presented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, vs. PBS group; # P < 0.05, ## P < 0.01, ### P < 0.001, vs. hiPSC-NSC-Exo group (Student’s t -test [E, F] or repeated-measures two-way analysis of variance followed by least significant difference post hoc tests [G–J]). All statistical values are presented in . AKT: Protein kinase B; DMSO: dimethyl sulfoxide; Exo: exosomes; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; hiPSC: human induced pluripotent stem cell; ICH: intracerebral hemorrhage; LY294002: a PI3K/AKT inhibitor; MCP-1: monocyte chemoattractant protein-1; mNSS: modified Neurological Severity Score; NSC: neural stem cell; p-AKT: <t>phosphorylated</t> protein kinase B; p-PI3K: phosphorylated phosphoinositide 3-kinase; PI3K: phosphoinositide 3-kinase; PBS: phosphate-buffered saline.
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Image Search Results


hiPSC–NSC–Exos enhance neurological deficits and alleviate brain edema after ICH via activation of the PI3K-AKT signaling pathway. (A) Scatter plot of differentially expressed genes in the affected hemisphere after ICH ( n = 3). (B) Gene Ontology (GO) analysis of differentially expressed genes. (C) Kyoto Encyclopedia of Genes and Genomic (KEGG) pathway enrichment analysis of the top 10 differentially expressed genes, with a focus on the PI3K-AKT signaling pathway. (D–F) Representative western blotting and quantitative analysis of p-PI3K, PI3K, p-AKT, and AKT expression levels ( n = 6). (G–I) Neurobehavioral function tests (rotarod test, corner turn test, and mNSS) were conducted on days 1 and 3 after ICH ( n = 6). The longer fall latency in rotarod tests and the fewer ipsilateral turnings in the corner turn test indicated better neurological function. (J) Quantification of water content in the ipsilateral hemisphere, contralateral hemisphere, and cerebellum ( n = 6). Data are presented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, vs. PBS group; # P < 0.05, ## P < 0.01, ### P < 0.001, vs. hiPSC-NSC-Exo group (Student’s t -test [E, F] or repeated-measures two-way analysis of variance followed by least significant difference post hoc tests [G–J]). All statistical values are presented in . AKT: Protein kinase B; DMSO: dimethyl sulfoxide; Exo: exosomes; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; hiPSC: human induced pluripotent stem cell; ICH: intracerebral hemorrhage; LY294002: a PI3K/AKT inhibitor; MCP-1: monocyte chemoattractant protein-1; mNSS: modified Neurological Severity Score; NSC: neural stem cell; p-AKT: phosphorylated protein kinase B; p-PI3K: phosphorylated phosphoinositide 3-kinase; PI3K: phosphoinositide 3-kinase; PBS: phosphate-buffered saline.

Journal: Neural Regeneration Research

Article Title: Human-induced pluripotent stem cell–derived neural stem cell exosomes improve blood–brain barrier function after intracerebral hemorrhage by activating astrocytes via PI3K/AKT/MCP-1 axis

doi: 10.4103/NRR.NRR-D-23-01889

Figure Lengend Snippet: hiPSC–NSC–Exos enhance neurological deficits and alleviate brain edema after ICH via activation of the PI3K-AKT signaling pathway. (A) Scatter plot of differentially expressed genes in the affected hemisphere after ICH ( n = 3). (B) Gene Ontology (GO) analysis of differentially expressed genes. (C) Kyoto Encyclopedia of Genes and Genomic (KEGG) pathway enrichment analysis of the top 10 differentially expressed genes, with a focus on the PI3K-AKT signaling pathway. (D–F) Representative western blotting and quantitative analysis of p-PI3K, PI3K, p-AKT, and AKT expression levels ( n = 6). (G–I) Neurobehavioral function tests (rotarod test, corner turn test, and mNSS) were conducted on days 1 and 3 after ICH ( n = 6). The longer fall latency in rotarod tests and the fewer ipsilateral turnings in the corner turn test indicated better neurological function. (J) Quantification of water content in the ipsilateral hemisphere, contralateral hemisphere, and cerebellum ( n = 6). Data are presented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, vs. PBS group; # P < 0.05, ## P < 0.01, ### P < 0.001, vs. hiPSC-NSC-Exo group (Student’s t -test [E, F] or repeated-measures two-way analysis of variance followed by least significant difference post hoc tests [G–J]). All statistical values are presented in . AKT: Protein kinase B; DMSO: dimethyl sulfoxide; Exo: exosomes; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; hiPSC: human induced pluripotent stem cell; ICH: intracerebral hemorrhage; LY294002: a PI3K/AKT inhibitor; MCP-1: monocyte chemoattractant protein-1; mNSS: modified Neurological Severity Score; NSC: neural stem cell; p-AKT: phosphorylated protein kinase B; p-PI3K: phosphorylated phosphoinositide 3-kinase; PI3K: phosphoinositide 3-kinase; PBS: phosphate-buffered saline.

Article Snippet: The membranes were incubated overnight at 4°C with primary antibodies against ZO-1 (rabbit, 1:300, Cell Signaling Technology, Cat# 13663, RRID: AB_2798287), claudin-5 (mouse, 1:1000, Thermo Fisher Scientific, Cat# 35-2500, RRID: AB_2533200), phosphorylated phosphoinositide 3-kinase (p-PI3K, rabbit, 1:1000, Cell Signaling Technology, Cat# 4228S, RRID: AB_659940), phosphoinositide 3-kinase (PI3K, rabbit, 1:1000, Cell Signaling Technology, Cat# 4255, RRID: AB_659888), phosphorylated protein kinase B (p-AKT, rabbit,1:1000, Cell Signaling Technology Cat# 4060S, RRID: AB_2315049), protein kinase B (AKT; rabbit, 1:1000, Cell Signaling Technology, Cat# 9272S, RRID: AB_329827), CD9 (rabbit, 1:1000, Cell Signaling Technology, Cat# 13403, RRID: AB_2732848), CD63 (rabbit, 1:1000, Abcam, Cat# ab134045, RRID: AB_2800495), Alix (mouse, 1:1000, Cell Signaling Technology, Cat# 2171, RRID: AB_2299455), and glyceraldehyde-3-phosphate dehydrogenase (GAPDH, rabbit, 1:3000, Cell Signaling Technology, Cat# 2118, RRID: AB_561053).

Techniques: Activation Assay, Western Blot, Expressing, Modification, Saline

hiPSC–NSC–Exos improve blood–brain barrier function after intracerebral hemorrhage by activating astrocytes via the PI3K/AKT/MCP-1 axis. (A) Hemin/exosome + LY294002/DMSO treatment of astrocytes. (B–D) Representative western blot image and quantitative analysis of p-PI3K, PI3K, p-AKT, and AKT expression levels ( n = 6). (E) MCP-1 content in the medium ( n = 3). (F) LY294002 and C1142 treatment of the hemin-treated BBB model. (G) MCP-1 content in the medium of the BBB model ( n = 6). (H, I) EB leakage and TEER in the BBB model under different conditions ( n = 6). Data are presented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, vs . astrocyte group; # P < 0.05, ## P < 0.01, ### P < 0.001, vs . astrocyte + hemin group; && P < 0.01, &&& P < 0.001, vs . astrocyte + hemin + Exo group. All statistical values are presented in . AKT: Protein kinase B; BBB: blood–brain barrier; C1142: a MCP-1 neutralizing agent; DMSO: dimethyl sulfoxide; Exo: exosomes; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; hiPSC: human induced pluripotent stem cell; LY294002: a PI3K/AKT inhibitor; MCP-1: monocyte chemoattractant protein-1; NSC: neural stem cell; p-AKT: phosphorylated protein kinase B; p-PI3K: phosphorylated phosphoinositide 3-kinase; PI3K: phosphoinositide 3-kinase.

Journal: Neural Regeneration Research

Article Title: Human-induced pluripotent stem cell–derived neural stem cell exosomes improve blood–brain barrier function after intracerebral hemorrhage by activating astrocytes via PI3K/AKT/MCP-1 axis

doi: 10.4103/NRR.NRR-D-23-01889

Figure Lengend Snippet: hiPSC–NSC–Exos improve blood–brain barrier function after intracerebral hemorrhage by activating astrocytes via the PI3K/AKT/MCP-1 axis. (A) Hemin/exosome + LY294002/DMSO treatment of astrocytes. (B–D) Representative western blot image and quantitative analysis of p-PI3K, PI3K, p-AKT, and AKT expression levels ( n = 6). (E) MCP-1 content in the medium ( n = 3). (F) LY294002 and C1142 treatment of the hemin-treated BBB model. (G) MCP-1 content in the medium of the BBB model ( n = 6). (H, I) EB leakage and TEER in the BBB model under different conditions ( n = 6). Data are presented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, vs . astrocyte group; # P < 0.05, ## P < 0.01, ### P < 0.001, vs . astrocyte + hemin group; && P < 0.01, &&& P < 0.001, vs . astrocyte + hemin + Exo group. All statistical values are presented in . AKT: Protein kinase B; BBB: blood–brain barrier; C1142: a MCP-1 neutralizing agent; DMSO: dimethyl sulfoxide; Exo: exosomes; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; hiPSC: human induced pluripotent stem cell; LY294002: a PI3K/AKT inhibitor; MCP-1: monocyte chemoattractant protein-1; NSC: neural stem cell; p-AKT: phosphorylated protein kinase B; p-PI3K: phosphorylated phosphoinositide 3-kinase; PI3K: phosphoinositide 3-kinase.

Article Snippet: The membranes were incubated overnight at 4°C with primary antibodies against ZO-1 (rabbit, 1:300, Cell Signaling Technology, Cat# 13663, RRID: AB_2798287), claudin-5 (mouse, 1:1000, Thermo Fisher Scientific, Cat# 35-2500, RRID: AB_2533200), phosphorylated phosphoinositide 3-kinase (p-PI3K, rabbit, 1:1000, Cell Signaling Technology, Cat# 4228S, RRID: AB_659940), phosphoinositide 3-kinase (PI3K, rabbit, 1:1000, Cell Signaling Technology, Cat# 4255, RRID: AB_659888), phosphorylated protein kinase B (p-AKT, rabbit,1:1000, Cell Signaling Technology Cat# 4060S, RRID: AB_2315049), protein kinase B (AKT; rabbit, 1:1000, Cell Signaling Technology, Cat# 9272S, RRID: AB_329827), CD9 (rabbit, 1:1000, Cell Signaling Technology, Cat# 13403, RRID: AB_2732848), CD63 (rabbit, 1:1000, Abcam, Cat# ab134045, RRID: AB_2800495), Alix (mouse, 1:1000, Cell Signaling Technology, Cat# 2171, RRID: AB_2299455), and glyceraldehyde-3-phosphate dehydrogenase (GAPDH, rabbit, 1:3000, Cell Signaling Technology, Cat# 2118, RRID: AB_561053).

Techniques: Western Blot, Expressing

hiPSC–NSC–Exos enhance neurological deficits and alleviate brain edema after ICH via activation of the PI3K-AKT signaling pathway. (A) Scatter plot of differentially expressed genes in the affected hemisphere after ICH ( n = 3). (B) Gene Ontology (GO) analysis of differentially expressed genes. (C) Kyoto Encyclopedia of Genes and Genomic (KEGG) pathway enrichment analysis of the top 10 differentially expressed genes, with a focus on the PI3K-AKT signaling pathway. (D–F) Representative western blotting and quantitative analysis of p-PI3K, PI3K, p-AKT, and AKT expression levels ( n = 6). (G–I) Neurobehavioral function tests (rotarod test, corner turn test, and mNSS) were conducted on days 1 and 3 after ICH ( n = 6). The longer fall latency in rotarod tests and the fewer ipsilateral turnings in the corner turn test indicated better neurological function. (J) Quantification of water content in the ipsilateral hemisphere, contralateral hemisphere, and cerebellum ( n = 6). Data are presented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, vs. PBS group; # P < 0.05, ## P < 0.01, ### P < 0.001, vs. hiPSC-NSC-Exo group (Student’s t -test [E, F] or repeated-measures two-way analysis of variance followed by least significant difference post hoc tests [G–J]). All statistical values are presented in . AKT: Protein kinase B; DMSO: dimethyl sulfoxide; Exo: exosomes; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; hiPSC: human induced pluripotent stem cell; ICH: intracerebral hemorrhage; LY294002: a PI3K/AKT inhibitor; MCP-1: monocyte chemoattractant protein-1; mNSS: modified Neurological Severity Score; NSC: neural stem cell; p-AKT: phosphorylated protein kinase B; p-PI3K: phosphorylated phosphoinositide 3-kinase; PI3K: phosphoinositide 3-kinase; PBS: phosphate-buffered saline.

Journal: Neural Regeneration Research

Article Title: Human-induced pluripotent stem cell–derived neural stem cell exosomes improve blood–brain barrier function after intracerebral hemorrhage by activating astrocytes via PI3K/AKT/MCP-1 axis

doi: 10.4103/NRR.NRR-D-23-01889

Figure Lengend Snippet: hiPSC–NSC–Exos enhance neurological deficits and alleviate brain edema after ICH via activation of the PI3K-AKT signaling pathway. (A) Scatter plot of differentially expressed genes in the affected hemisphere after ICH ( n = 3). (B) Gene Ontology (GO) analysis of differentially expressed genes. (C) Kyoto Encyclopedia of Genes and Genomic (KEGG) pathway enrichment analysis of the top 10 differentially expressed genes, with a focus on the PI3K-AKT signaling pathway. (D–F) Representative western blotting and quantitative analysis of p-PI3K, PI3K, p-AKT, and AKT expression levels ( n = 6). (G–I) Neurobehavioral function tests (rotarod test, corner turn test, and mNSS) were conducted on days 1 and 3 after ICH ( n = 6). The longer fall latency in rotarod tests and the fewer ipsilateral turnings in the corner turn test indicated better neurological function. (J) Quantification of water content in the ipsilateral hemisphere, contralateral hemisphere, and cerebellum ( n = 6). Data are presented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, vs. PBS group; # P < 0.05, ## P < 0.01, ### P < 0.001, vs. hiPSC-NSC-Exo group (Student’s t -test [E, F] or repeated-measures two-way analysis of variance followed by least significant difference post hoc tests [G–J]). All statistical values are presented in . AKT: Protein kinase B; DMSO: dimethyl sulfoxide; Exo: exosomes; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; hiPSC: human induced pluripotent stem cell; ICH: intracerebral hemorrhage; LY294002: a PI3K/AKT inhibitor; MCP-1: monocyte chemoattractant protein-1; mNSS: modified Neurological Severity Score; NSC: neural stem cell; p-AKT: phosphorylated protein kinase B; p-PI3K: phosphorylated phosphoinositide 3-kinase; PI3K: phosphoinositide 3-kinase; PBS: phosphate-buffered saline.

Article Snippet: The membranes were incubated overnight at 4°C with primary antibodies against ZO-1 (rabbit, 1:300, Cell Signaling Technology, Cat# 13663, RRID: AB_2798287), claudin-5 (mouse, 1:1000, Thermo Fisher Scientific, Cat# 35-2500, RRID: AB_2533200), phosphorylated phosphoinositide 3-kinase (p-PI3K, rabbit, 1:1000, Cell Signaling Technology, Cat# 4228S, RRID: AB_659940), phosphoinositide 3-kinase (PI3K, rabbit, 1:1000, Cell Signaling Technology, Cat# 4255, RRID: AB_659888), phosphorylated protein kinase B (p-AKT, rabbit,1:1000, Cell Signaling Technology Cat# 4060S, RRID: AB_2315049), protein kinase B (AKT; rabbit, 1:1000, Cell Signaling Technology, Cat# 9272S, RRID: AB_329827), CD9 (rabbit, 1:1000, Cell Signaling Technology, Cat# 13403, RRID: AB_2732848), CD63 (rabbit, 1:1000, Abcam, Cat# ab134045, RRID: AB_2800495), Alix (mouse, 1:1000, Cell Signaling Technology, Cat# 2171, RRID: AB_2299455), and glyceraldehyde-3-phosphate dehydrogenase (GAPDH, rabbit, 1:3000, Cell Signaling Technology, Cat# 2118, RRID: AB_561053).

Techniques: Activation Assay, Western Blot, Expressing, Modification, Saline

hiPSC–NSC–Exos improve blood–brain barrier function after intracerebral hemorrhage by activating astrocytes via the PI3K/AKT/MCP-1 axis. (A) Hemin/exosome + LY294002/DMSO treatment of astrocytes. (B–D) Representative western blot image and quantitative analysis of p-PI3K, PI3K, p-AKT, and AKT expression levels ( n = 6). (E) MCP-1 content in the medium ( n = 3). (F) LY294002 and C1142 treatment of the hemin-treated BBB model. (G) MCP-1 content in the medium of the BBB model ( n = 6). (H, I) EB leakage and TEER in the BBB model under different conditions ( n = 6). Data are presented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, vs . astrocyte group; # P < 0.05, ## P < 0.01, ### P < 0.001, vs . astrocyte + hemin group; && P < 0.01, &&& P < 0.001, vs . astrocyte + hemin + Exo group. All statistical values are presented in . AKT: Protein kinase B; BBB: blood–brain barrier; C1142: a MCP-1 neutralizing agent; DMSO: dimethyl sulfoxide; Exo: exosomes; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; hiPSC: human induced pluripotent stem cell; LY294002: a PI3K/AKT inhibitor; MCP-1: monocyte chemoattractant protein-1; NSC: neural stem cell; p-AKT: phosphorylated protein kinase B; p-PI3K: phosphorylated phosphoinositide 3-kinase; PI3K: phosphoinositide 3-kinase.

Journal: Neural Regeneration Research

Article Title: Human-induced pluripotent stem cell–derived neural stem cell exosomes improve blood–brain barrier function after intracerebral hemorrhage by activating astrocytes via PI3K/AKT/MCP-1 axis

doi: 10.4103/NRR.NRR-D-23-01889

Figure Lengend Snippet: hiPSC–NSC–Exos improve blood–brain barrier function after intracerebral hemorrhage by activating astrocytes via the PI3K/AKT/MCP-1 axis. (A) Hemin/exosome + LY294002/DMSO treatment of astrocytes. (B–D) Representative western blot image and quantitative analysis of p-PI3K, PI3K, p-AKT, and AKT expression levels ( n = 6). (E) MCP-1 content in the medium ( n = 3). (F) LY294002 and C1142 treatment of the hemin-treated BBB model. (G) MCP-1 content in the medium of the BBB model ( n = 6). (H, I) EB leakage and TEER in the BBB model under different conditions ( n = 6). Data are presented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, vs . astrocyte group; # P < 0.05, ## P < 0.01, ### P < 0.001, vs . astrocyte + hemin group; && P < 0.01, &&& P < 0.001, vs . astrocyte + hemin + Exo group. All statistical values are presented in . AKT: Protein kinase B; BBB: blood–brain barrier; C1142: a MCP-1 neutralizing agent; DMSO: dimethyl sulfoxide; Exo: exosomes; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; hiPSC: human induced pluripotent stem cell; LY294002: a PI3K/AKT inhibitor; MCP-1: monocyte chemoattractant protein-1; NSC: neural stem cell; p-AKT: phosphorylated protein kinase B; p-PI3K: phosphorylated phosphoinositide 3-kinase; PI3K: phosphoinositide 3-kinase.

Article Snippet: The membranes were incubated overnight at 4°C with primary antibodies against ZO-1 (rabbit, 1:300, Cell Signaling Technology, Cat# 13663, RRID: AB_2798287), claudin-5 (mouse, 1:1000, Thermo Fisher Scientific, Cat# 35-2500, RRID: AB_2533200), phosphorylated phosphoinositide 3-kinase (p-PI3K, rabbit, 1:1000, Cell Signaling Technology, Cat# 4228S, RRID: AB_659940), phosphoinositide 3-kinase (PI3K, rabbit, 1:1000, Cell Signaling Technology, Cat# 4255, RRID: AB_659888), phosphorylated protein kinase B (p-AKT, rabbit,1:1000, Cell Signaling Technology Cat# 4060S, RRID: AB_2315049), protein kinase B (AKT; rabbit, 1:1000, Cell Signaling Technology, Cat# 9272S, RRID: AB_329827), CD9 (rabbit, 1:1000, Cell Signaling Technology, Cat# 13403, RRID: AB_2732848), CD63 (rabbit, 1:1000, Abcam, Cat# ab134045, RRID: AB_2800495), Alix (mouse, 1:1000, Cell Signaling Technology, Cat# 2171, RRID: AB_2299455), and glyceraldehyde-3-phosphate dehydrogenase (GAPDH, rabbit, 1:3000, Cell Signaling Technology, Cat# 2118, RRID: AB_561053).

Techniques: Western Blot, Expressing