Fig. 8: VEGFA-mediated promotion of smad7 expression mainly occurs through Dll4/Notch4 signaling. | Cell Death & Disease

Fig. 8: VEGFA-mediated promotion of smad7 expression mainly occurs through Dll4/Notch4 signaling.

From: Vascular endothelial growth factor 165 inhibits pro-fibrotic differentiation of stromal cells via the DLL4/Notch4/smad7 pathway

Fig. 8

a, b The mRNA and protein levels of Notch1 and Notch4 in human endometrial stromal cells were decreased significantly at 24 h after transfection with siNotch1 or siNotch4, respectively. N = 3, *P < 0.05. Unpaired t-test. c–f Endometrial stromal cells stimulated with 10 ng/mL TGFβ1 for 48 h were transfected with siNotch1 and siNotch4 for 24 h and/or cocultured with 10 ng/mL VEGF165 for another 12 or 24 h. The mRNA and protein levels of Notch1, Notch4, smad7, α-SMA, and collagen 1 were examined. N = 3, *P < 0.05. Two-way ANOVA and SNK-q. T: TGFβ1, VEGF: VEGF165. g A model illustrating the role of VEGF165 in inhibiting endometrial fibrosis via DLL4/Notch4/Smad7 signaling. VEGF165 expression is decreased in the endometrium in Asherman’s syndrome, especially in stromal cells, which results in endometrial fibrosis, manifested as increased collagen 1 and α-SMA expression and hydroxyproline levels. Exogenous VEGF165 can reverse stromal cell differentiation into myofibroblasts and endometrial fibrosis by binding to VEGFR2 to induce DLL4/Notch4/Smad7 signaling

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