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TGM2 specific inhibitor significantly attenuates colitis and angiogenesis in DSS colitis model. (A) Body lost of <t>GK921</t> treatment group and solvent treatment group after DSS colitis model establishment (n = 9 in Con group, n = 7 in DSS-DMSO, n = 8 in DSS-GK921 treatment group). (B) Representative colonic images of GK921 treatment group and solvent treatment group after DSS colitis model establishment. (C) Appearance of colon length of GK921 treatment group and solvent treatment group after DSS establishment (n = 9 in Con group, n = 7 in DSS-DMSO, n = 8 in DSS-GK921 treatment group). (D, E) DAI and CDMI score of GK921 treatment group and solvent treatment group after DSS colitis model establishment (n = 9 in Con group, n = 7 in DSS-DMSO, n = 8 in DSS-GK921 treatment group). (F, H) Representative HE staining and TGM2, CD31 immunohistochemical images of GK921 treatment group and solvent treatment group after DSS colitis model establishment show decreased MVD in DSS mice after GK921 treatment. (G) WB result display that GK921 treatment significantly reduce the phosphorylation of VEGFR2 at Tyr1059 and Tyr1214 after DSS treatment. (I) GK921 treatment exhibit decrease in the number of CD31 (green), TGM2 (red), Ki-67 (cyan) positive proliferative vascular endothelial cells comparing to controls. (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001). (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
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TGM2 specific inhibitor significantly attenuates colitis and angiogenesis in DSS colitis model. (A) Body lost of <t>GK921</t> treatment group and solvent treatment group after DSS colitis model establishment (n = 9 in Con group, n = 7 in DSS-DMSO, n = 8 in DSS-GK921 treatment group). (B) Representative colonic images of GK921 treatment group and solvent treatment group after DSS colitis model establishment. (C) Appearance of colon length of GK921 treatment group and solvent treatment group after DSS establishment (n = 9 in Con group, n = 7 in DSS-DMSO, n = 8 in DSS-GK921 treatment group). (D, E) DAI and CDMI score of GK921 treatment group and solvent treatment group after DSS colitis model establishment (n = 9 in Con group, n = 7 in DSS-DMSO, n = 8 in DSS-GK921 treatment group). (F, H) Representative HE staining and TGM2, CD31 immunohistochemical images of GK921 treatment group and solvent treatment group after DSS colitis model establishment show decreased MVD in DSS mice after GK921 treatment. (G) WB result display that GK921 treatment significantly reduce the phosphorylation of VEGFR2 at Tyr1059 and Tyr1214 after DSS treatment. (I) GK921 treatment exhibit decrease in the number of CD31 (green), TGM2 (red), Ki-67 (cyan) positive proliferative vascular endothelial cells comparing to controls. (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001). (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
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TGM2 specific inhibitor significantly attenuates colitis and angiogenesis in DSS colitis model. (A) Body lost of <t>GK921</t> treatment group and solvent treatment group after DSS colitis model establishment (n = 9 in Con group, n = 7 in DSS-DMSO, n = 8 in DSS-GK921 treatment group). (B) Representative colonic images of GK921 treatment group and solvent treatment group after DSS colitis model establishment. (C) Appearance of colon length of GK921 treatment group and solvent treatment group after DSS establishment (n = 9 in Con group, n = 7 in DSS-DMSO, n = 8 in DSS-GK921 treatment group). (D, E) DAI and CDMI score of GK921 treatment group and solvent treatment group after DSS colitis model establishment (n = 9 in Con group, n = 7 in DSS-DMSO, n = 8 in DSS-GK921 treatment group). (F, H) Representative HE staining and TGM2, CD31 immunohistochemical images of GK921 treatment group and solvent treatment group after DSS colitis model establishment show decreased MVD in DSS mice after GK921 treatment. (G) WB result display that GK921 treatment significantly reduce the phosphorylation of VEGFR2 at Tyr1059 and Tyr1214 after DSS treatment. (I) GK921 treatment exhibit decrease in the number of CD31 (green), TGM2 (red), Ki-67 (cyan) positive proliferative vascular endothelial cells comparing to controls. (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001). (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
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TGM2 specific inhibitor significantly attenuates colitis and angiogenesis in DSS colitis model. (A) Body lost of <t>GK921</t> treatment group and solvent treatment group after DSS colitis model establishment (n = 9 in Con group, n = 7 in DSS-DMSO, n = 8 in DSS-GK921 treatment group). (B) Representative colonic images of GK921 treatment group and solvent treatment group after DSS colitis model establishment. (C) Appearance of colon length of GK921 treatment group and solvent treatment group after DSS establishment (n = 9 in Con group, n = 7 in DSS-DMSO, n = 8 in DSS-GK921 treatment group). (D, E) DAI and CDMI score of GK921 treatment group and solvent treatment group after DSS colitis model establishment (n = 9 in Con group, n = 7 in DSS-DMSO, n = 8 in DSS-GK921 treatment group). (F, H) Representative HE staining and TGM2, CD31 immunohistochemical images of GK921 treatment group and solvent treatment group after DSS colitis model establishment show decreased MVD in DSS mice after GK921 treatment. (G) WB result display that GK921 treatment significantly reduce the phosphorylation of VEGFR2 at Tyr1059 and Tyr1214 after DSS treatment. (I) GK921 treatment exhibit decrease in the number of CD31 (green), TGM2 (red), Ki-67 (cyan) positive proliferative vascular endothelial cells comparing to controls. (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001). (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
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TGM2 specific inhibitor significantly attenuates colitis and angiogenesis in DSS colitis model. (A) Body lost of <t>GK921</t> treatment group and solvent treatment group after DSS colitis model establishment (n = 9 in Con group, n = 7 in DSS-DMSO, n = 8 in DSS-GK921 treatment group). (B) Representative colonic images of GK921 treatment group and solvent treatment group after DSS colitis model establishment. (C) Appearance of colon length of GK921 treatment group and solvent treatment group after DSS establishment (n = 9 in Con group, n = 7 in DSS-DMSO, n = 8 in DSS-GK921 treatment group). (D, E) DAI and CDMI score of GK921 treatment group and solvent treatment group after DSS colitis model establishment (n = 9 in Con group, n = 7 in DSS-DMSO, n = 8 in DSS-GK921 treatment group). (F, H) Representative HE staining and TGM2, CD31 immunohistochemical images of GK921 treatment group and solvent treatment group after DSS colitis model establishment show decreased MVD in DSS mice after GK921 treatment. (G) WB result display that GK921 treatment significantly reduce the phosphorylation of VEGFR2 at Tyr1059 and Tyr1214 after DSS treatment. (I) GK921 treatment exhibit decrease in the number of CD31 (green), TGM2 (red), Ki-67 (cyan) positive proliferative vascular endothelial cells comparing to controls. (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001). (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
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TGM2 specific inhibitor significantly attenuates colitis and angiogenesis in DSS colitis model. (A) Body lost of <t>GK921</t> treatment group and solvent treatment group after DSS colitis model establishment (n = 9 in Con group, n = 7 in DSS-DMSO, n = 8 in DSS-GK921 treatment group). (B) Representative colonic images of GK921 treatment group and solvent treatment group after DSS colitis model establishment. (C) Appearance of colon length of GK921 treatment group and solvent treatment group after DSS establishment (n = 9 in Con group, n = 7 in DSS-DMSO, n = 8 in DSS-GK921 treatment group). (D, E) DAI and CDMI score of GK921 treatment group and solvent treatment group after DSS colitis model establishment (n = 9 in Con group, n = 7 in DSS-DMSO, n = 8 in DSS-GK921 treatment group). (F, H) Representative HE staining and TGM2, CD31 immunohistochemical images of GK921 treatment group and solvent treatment group after DSS colitis model establishment show decreased MVD in DSS mice after GK921 treatment. (G) WB result display that GK921 treatment significantly reduce the phosphorylation of VEGFR2 at Tyr1059 and Tyr1214 after DSS treatment. (I) GK921 treatment exhibit decrease in the number of CD31 (green), TGM2 (red), Ki-67 (cyan) positive proliferative vascular endothelial cells comparing to controls. (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001). (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
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TGM2 specific inhibitor significantly attenuates colitis and angiogenesis in DSS colitis model. (A) Body lost of <t>GK921</t> treatment group and solvent treatment group after DSS colitis model establishment (n = 9 in Con group, n = 7 in DSS-DMSO, n = 8 in DSS-GK921 treatment group). (B) Representative colonic images of GK921 treatment group and solvent treatment group after DSS colitis model establishment. (C) Appearance of colon length of GK921 treatment group and solvent treatment group after DSS establishment (n = 9 in Con group, n = 7 in DSS-DMSO, n = 8 in DSS-GK921 treatment group). (D, E) DAI and CDMI score of GK921 treatment group and solvent treatment group after DSS colitis model establishment (n = 9 in Con group, n = 7 in DSS-DMSO, n = 8 in DSS-GK921 treatment group). (F, H) Representative HE staining and TGM2, CD31 immunohistochemical images of GK921 treatment group and solvent treatment group after DSS colitis model establishment show decreased MVD in DSS mice after GK921 treatment. (G) WB result display that GK921 treatment significantly reduce the phosphorylation of VEGFR2 at Tyr1059 and Tyr1214 after DSS treatment. (I) GK921 treatment exhibit decrease in the number of CD31 (green), TGM2 (red), Ki-67 (cyan) positive proliferative vascular endothelial cells comparing to controls. (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001). (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
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TGM2 specific inhibitor significantly attenuates colitis and angiogenesis in DSS colitis model. (A) Body lost of GK921 treatment group and solvent treatment group after DSS colitis model establishment (n = 9 in Con group, n = 7 in DSS-DMSO, n = 8 in DSS-GK921 treatment group). (B) Representative colonic images of GK921 treatment group and solvent treatment group after DSS colitis model establishment. (C) Appearance of colon length of GK921 treatment group and solvent treatment group after DSS establishment (n = 9 in Con group, n = 7 in DSS-DMSO, n = 8 in DSS-GK921 treatment group). (D, E) DAI and CDMI score of GK921 treatment group and solvent treatment group after DSS colitis model establishment (n = 9 in Con group, n = 7 in DSS-DMSO, n = 8 in DSS-GK921 treatment group). (F, H) Representative HE staining and TGM2, CD31 immunohistochemical images of GK921 treatment group and solvent treatment group after DSS colitis model establishment show decreased MVD in DSS mice after GK921 treatment. (G) WB result display that GK921 treatment significantly reduce the phosphorylation of VEGFR2 at Tyr1059 and Tyr1214 after DSS treatment. (I) GK921 treatment exhibit decrease in the number of CD31 (green), TGM2 (red), Ki-67 (cyan) positive proliferative vascular endothelial cells comparing to controls. (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001). (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Journal: Journal of Advanced Research

Article Title: Transglutaminase 2 modulates inflammatory angiogenesis via vascular endothelial growth factor receptor 2 pathway in inflammatory bowel disease

doi: 10.1016/j.jare.2025.07.002

Figure Lengend Snippet: TGM2 specific inhibitor significantly attenuates colitis and angiogenesis in DSS colitis model. (A) Body lost of GK921 treatment group and solvent treatment group after DSS colitis model establishment (n = 9 in Con group, n = 7 in DSS-DMSO, n = 8 in DSS-GK921 treatment group). (B) Representative colonic images of GK921 treatment group and solvent treatment group after DSS colitis model establishment. (C) Appearance of colon length of GK921 treatment group and solvent treatment group after DSS establishment (n = 9 in Con group, n = 7 in DSS-DMSO, n = 8 in DSS-GK921 treatment group). (D, E) DAI and CDMI score of GK921 treatment group and solvent treatment group after DSS colitis model establishment (n = 9 in Con group, n = 7 in DSS-DMSO, n = 8 in DSS-GK921 treatment group). (F, H) Representative HE staining and TGM2, CD31 immunohistochemical images of GK921 treatment group and solvent treatment group after DSS colitis model establishment show decreased MVD in DSS mice after GK921 treatment. (G) WB result display that GK921 treatment significantly reduce the phosphorylation of VEGFR2 at Tyr1059 and Tyr1214 after DSS treatment. (I) GK921 treatment exhibit decrease in the number of CD31 (green), TGM2 (red), Ki-67 (cyan) positive proliferative vascular endothelial cells comparing to controls. (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001). (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Article Snippet: For the GK921 inhibitor experiment, mice received daily intraperitoneal injections of GK921 (10 mg/kg, MedChemExpress, USA).

Techniques: Solvent, Staining, Immunohistochemical staining, Phospho-proteomics