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Fig. 2 | Cell Communication and Signaling

Fig. 2

From: Epithelial and interstitial Notch1 activity contributes to the myofibroblastic phenotype and fibrosis

Fig. 2

Notch1 signalling is activated in TECs after AA injury. a RTCA assay indicating the survival index of NRK-52E cells treated with AA with or without DAPT. b Upregulated Ki67 expression, determined by immunofluorescence staining, was inhibited by DAPT treatment. Bar = 20 μm. c The ratio of Ki67-positive cells in total cells according to the results of immunofluorescence staining. d qRT-PCR showed that increased mRNA expression levels of Col1α1, Col3α1 and α-SMA, and decreased mRNA levels of E-cadherin and BMP-7 in AA-treated NRK-52E cells were inhibited by DAPT treatment. e Elevated expression levels of α-SMA and collagen III in AA-treated NRK-52E cells were inhibited by DAPT treatment. Bar = 20 μm. f Increased expression levels of α-SMA, vimentin and collagen I, and decreased expression of E-cadherin in AA-treated NRK-52E cells were inhibited by DAPT treatment. g Increased mRNA expression levels of Notch1, Jagged1 and Numb in AA-treated NRK-52E cells were inhibited by DAPT treatment. h Elevated expression levels of Notch1, NICD and Jagged1 in AA-treated NRK-52E cells were inhibited by DAPT treatment. Bar = 20 μm. i Enhanced expression levels of Notch1, Jagged1 and NICD in AA-treated NRK-52E cells were inhibited by DAPT treatment. All data are presented as means ± SDs. AA, 10 ng/ml; DAPT (HD), high-dose (10 μmol/L); DAPT (LD), low-dose (1 μmol/L). *P < 0.05, **P < 0.01 versus the control; #P < 0.01, #P < 0.05 versus the AA-treated group

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