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Differential expression of genes in the CNS. (A) Autologous transplants. Graphs show expression levels of <t>CASP3,</t> IFN‐ß, IFN‐γ and VCAM after cell and gene therapies in the CNS of RR‐EAE mice at the peak of the second relapse (45 dpi) (n = 5 animals per experimental group). (B) Allogeneic transplants. Graphs show expression levels of SEMA3F, IFN‐ß and IFNAR2 after cell and gene therapies in the CNS of CP‐EAE mice in the chronic period (35 dpi) (n = 6 animals per experimental group). Mann–Whitney test; *P < 0.05 versus saline; #P < 0.05 cell therapy versus gene therapy.
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Differential expression of genes in the CNS. (A) Autologous transplants. Graphs show expression levels of <t>CASP3,</t> IFN‐ß, IFN‐γ and VCAM after cell and gene therapies in the CNS of RR‐EAE mice at the peak of the second relapse (45 dpi) (n = 5 animals per experimental group). (B) Allogeneic transplants. Graphs show expression levels of SEMA3F, IFN‐ß and IFNAR2 after cell and gene therapies in the CNS of CP‐EAE mice in the chronic period (35 dpi) (n = 6 animals per experimental group). Mann–Whitney test; *P < 0.05 versus saline; #P < 0.05 cell therapy versus gene therapy.
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Differential expression of genes in the CNS. (A) Autologous transplants. Graphs show expression levels of <t>CASP3,</t> IFN‐ß, IFN‐γ and VCAM after cell and gene therapies in the CNS of RR‐EAE mice at the peak of the second relapse (45 dpi) (n = 5 animals per experimental group). (B) Allogeneic transplants. Graphs show expression levels of SEMA3F, IFN‐ß and IFNAR2 after cell and gene therapies in the CNS of CP‐EAE mice in the chronic period (35 dpi) (n = 6 animals per experimental group). Mann–Whitney test; *P < 0.05 versus saline; #P < 0.05 cell therapy versus gene therapy.
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Differential expression of genes in the CNS. (A) Autologous transplants. Graphs show expression levels of <t>CASP3,</t> IFN‐ß, IFN‐γ and VCAM after cell and gene therapies in the CNS of RR‐EAE mice at the peak of the second relapse (45 dpi) (n = 5 animals per experimental group). (B) Allogeneic transplants. Graphs show expression levels of SEMA3F, IFN‐ß and IFNAR2 after cell and gene therapies in the CNS of CP‐EAE mice in the chronic period (35 dpi) (n = 6 animals per experimental group). Mann–Whitney test; *P < 0.05 versus saline; #P < 0.05 cell therapy versus gene therapy.
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Differential expression of genes in the CNS. (A) Autologous transplants. Graphs show expression levels of <t>CASP3,</t> IFN‐ß, IFN‐γ and VCAM after cell and gene therapies in the CNS of RR‐EAE mice at the peak of the second relapse (45 dpi) (n = 5 animals per experimental group). (B) Allogeneic transplants. Graphs show expression levels of SEMA3F, IFN‐ß and IFNAR2 after cell and gene therapies in the CNS of CP‐EAE mice in the chronic period (35 dpi) (n = 6 animals per experimental group). Mann–Whitney test; *P < 0.05 versus saline; #P < 0.05 cell therapy versus gene therapy.
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Differential expression of genes in the CNS. (A) Autologous transplants. Graphs show expression levels of <t>CASP3,</t> IFN‐ß, IFN‐γ and VCAM after cell and gene therapies in the CNS of RR‐EAE mice at the peak of the second relapse (45 dpi) (n = 5 animals per experimental group). (B) Allogeneic transplants. Graphs show expression levels of SEMA3F, IFN‐ß and IFNAR2 after cell and gene therapies in the CNS of CP‐EAE mice in the chronic period (35 dpi) (n = 6 animals per experimental group). Mann–Whitney test; *P < 0.05 versus saline; #P < 0.05 cell therapy versus gene therapy.
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Differential expression of genes in the CNS. (A) Autologous transplants. Graphs show expression levels of <t>CASP3,</t> IFN‐ß, IFN‐γ and VCAM after cell and gene therapies in the CNS of RR‐EAE mice at the peak of the second relapse (45 dpi) (n = 5 animals per experimental group). (B) Allogeneic transplants. Graphs show expression levels of SEMA3F, IFN‐ß and IFNAR2 after cell and gene therapies in the CNS of CP‐EAE mice in the chronic period (35 dpi) (n = 6 animals per experimental group). Mann–Whitney test; *P < 0.05 versus saline; #P < 0.05 cell therapy versus gene therapy.
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Differential expression of genes in the CNS. (A) Autologous transplants. Graphs show expression levels of CASP3, IFN‐ß, IFN‐γ and VCAM after cell and gene therapies in the CNS of RR‐EAE mice at the peak of the second relapse (45 dpi) (n = 5 animals per experimental group). (B) Allogeneic transplants. Graphs show expression levels of SEMA3F, IFN‐ß and IFNAR2 after cell and gene therapies in the CNS of CP‐EAE mice in the chronic period (35 dpi) (n = 6 animals per experimental group). Mann–Whitney test; *P < 0.05 versus saline; #P < 0.05 cell therapy versus gene therapy.

Journal: British Journal of Pharmacology

Article Title: Gene therapy with mesenchymal stem cells expressing IFN‐ß ameliorates neuroinflammation in experimental models of multiple sclerosis

doi: 10.1111/bph.13674

Figure Lengend Snippet: Differential expression of genes in the CNS. (A) Autologous transplants. Graphs show expression levels of CASP3, IFN‐ß, IFN‐γ and VCAM after cell and gene therapies in the CNS of RR‐EAE mice at the peak of the second relapse (45 dpi) (n = 5 animals per experimental group). (B) Allogeneic transplants. Graphs show expression levels of SEMA3F, IFN‐ß and IFNAR2 after cell and gene therapies in the CNS of CP‐EAE mice in the chronic period (35 dpi) (n = 6 animals per experimental group). Mann–Whitney test; *P < 0.05 versus saline; #P < 0.05 cell therapy versus gene therapy.

Article Snippet: The genes tested were SEMA3F (ref: Mm00441325_m1) and VCAM1 (ref: Mm01320970_m1) (both involved in cellular migration capacity); CD74 (ref: Mm00658576_m1), IL‐17 (ref: Mm00439618_m1) and SPP1 (ref: Mm00436767_m1) (all involved in inflammatory response); IFN‐β (ref: Mm00439552_s1), IFNAR2 (ref: Mm00494916_m1), IFN‐γ (ref: Mm01168134_m1), FoxP3 (ref: Mm00475162_m1) and IL‐4 (ref: Mm00445259_m1) (all with immunomodulatory activity); and PDGFA (ref: Mm01205760_m1), CSPG4 (ref: Mm00507257_m1), OLIG2 (ref: Mm01210556_m1) and CASP3 (ref: Mm01195085_m1) (all involved in neuronal damage and regeneration). β‐actin (Act B) (ref: Mm00607939_s1) was used as a reference gene.

Techniques: Quantitative Proteomics, Expressing, MANN-WHITNEY, Saline

Journal: British Journal of Pharmacology

Article Title: Gene therapy with mesenchymal stem cells expressing IFN‐ß ameliorates neuroinflammation in experimental models of multiple sclerosis

doi: 10.1111/bph.13674

Figure Lengend Snippet:

Article Snippet: The genes tested were SEMA3F (ref: Mm00441325_m1) and VCAM1 (ref: Mm01320970_m1) (both involved in cellular migration capacity); CD74 (ref: Mm00658576_m1), IL‐17 (ref: Mm00439618_m1) and SPP1 (ref: Mm00436767_m1) (all involved in inflammatory response); IFN‐β (ref: Mm00439552_s1), IFNAR2 (ref: Mm00494916_m1), IFN‐γ (ref: Mm01168134_m1), FoxP3 (ref: Mm00475162_m1) and IL‐4 (ref: Mm00445259_m1) (all with immunomodulatory activity); and PDGFA (ref: Mm01205760_m1), CSPG4 (ref: Mm00507257_m1), OLIG2 (ref: Mm01210556_m1) and CASP3 (ref: Mm01195085_m1) (all involved in neuronal damage and regeneration). β‐actin (Act B) (ref: Mm00607939_s1) was used as a reference gene.

Techniques: