DUSP22 Ameliorates Endothelial‐to‐Mesenchymal Transition in HUVECs through Smad2/3 and MAPK Signaling Pathways

Figures

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  Figure 1. DUSP22 expression level in TGF-β-induced EndMT. DUSP22 expression after TGF-β (10 ng/ml) induced HUVECs 48 h indicated (a) representative blots and (b) quantitative results of the phenotypic molecule of the EndMT, (c) RT-PCR analysis, and (d) the cell migration. ∗P < 0.01 vs. control.

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  Figure 2. DUSP22 downregulation in HUVECs aggravates EndMT. (a) sh-DUSP22 reduced expression of DUSP22 in HUVECs; (b) the cell activity after transfecting the sh-NC and sh-DUSP22; the (c) protein representative blots and (d) quantitative results and the (e) mRNA expression changes of the phenotypic molecule of EndMT after transfecting the sh-NC and sh-DUSP22; the (f) cell migration and (g) invasion changes after transfecting the sh-NC and sh-DUSP22. ∗P < 0.01 vs. sh-NC. #P < 0.01 vs. sh-NC+TGF-β.

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  Figure 3. DUSP22 overexpression in HUVECs ameliorates EndMT. (a) OEDUSP22 reduced expression of DUSP22 in HUVECs; (b) the cell activity after transfecting the OENC and OEDUSP22; the (c) protein representative blots and (d) quantitative results and the (e) mRNA expression changes of the phenotypic molecule of EndMT after transfecting the OENC and OEDUSP22; the (f) cell migration and (g) invasion changes after transfecting the OENC and OEDUSP22. ∗P < 0.01 vs. OENC. #P < 0.01 vs. OENC+TGF-β.

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  Figure 4. DUSP22 affects the smad2/3 signaling pathway. sh-DUSP22 activates the smad2/3 signaling pathway. The (a) protein representative blots and (b) quantitative results and the (c) mRNA expression changes of the downstream molecules of smad2/3 signaling pathway. ∗P < 0.01 vs. sh-NC. #P < 0.01 vs. sh-NC+TGF-β. OEDUSP22 inactivates the smad2/3 signaling pathway. The (d) protein representative blots and (e) quantitative results and the (f) mRNA expression changes of the downstream molecules of smad2/3 signaling pathway. ∗∗P < 0.01 vs. OENC. ##P < 0.01 vs. OENC+TGF-β. After adding with smad2/3 inhibitor ITD-1, the (g) mRNA expression changes and the (h) protein representative blots and (i) quantitative results of the phenotypic molecule of EndMT. 1P < 0.01 vs. sh-NC. 2P < 0.01 vs. sh-NC+TGF-β. 3P < 0.01 vs. sh-DUSP22. 4P < 0.01 vs. sh-DUSP22+TGF-β.

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  Figure 5. DUSP22 impacts the MAPK signaling pathway. sh-DUSP22 activates the MAPK signaling pathway. The (a) protein representative blots and (b) quantitative results of the p-JNK/JNK and p-ERK/ERK. ∗P < 0.01 vs. sh-NC. #P < 0.01 vs. sh-NC+TGF-β. OEDUSP22 inactivates the MAPK signaling pathway. The (c) protein representative blots and (d) quantitative results of the p-JNK/JNK and p-ERK/ERK. ∗∗P < 0.01 vs. OENC. ##P < 0.01 vs. OENC+TGF-β. After adding with JNK inhibitor SP600125, the (e) mRNA expression changes and the (f) protein representative blots and (g) quantitative results of the phenotypic molecule of EndMT. After adding with ERK inhibitor ravoxertinib, the (h) mRNA expression changes and the (i) protein representative blots and (j) quantitative results of the phenotypic molecule of EndMT. 1P < 0.01 vs. sh-NC. 2P < 0.01 vs. sh-NC+TGF-β. 3P < 0.01 vs. sh-DUSP22. 4P < 0.01 vs. sh-DUSP22+TGF-β.

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  Figure 6. The signaling pathways of DUSP22 in EndMT. During TGF-β-induced EndMT, the expression of DUSP22 is downregulated. This decrease in DUSP22 expression level aggravated EndMT, while the overexpression of DUSP22 ameliorated EndMT in HUVECs. DUPS22 affects EndMT through smad2/3 and MAPK signaling pathways.