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. 2023 Oct 14;26(11):108211. doi: 10.1016/j.isci.2023.108211

Figure 4.

Figure 4

Down-regulation of E-cadherin was induced by shedding of syndecan-1 (SDC-1) and activation of STAT3 signaling in hypoxia/reoxygenation (H/R) treated proximal tubular epithelial cells (PTECs)

(A) H/R resulted in the increased apoptosis in PTES, ∗p < 0.05.

(B) H/R could result in the phosphorylation of STAT3 and decreased expression of E-cadherin in the PTECs, ∗p < 0.05.

(C) GM6001 pretreatment could alleviate the apoptosis of PTES, ∗p < 0.05.

(D) Western blot analysis showed that the activation of STAT3 was suppressed. Decreased E-cadherin was alleviated after inhibition of the SDC-1 shedding by GM6001. ∗p < 0.05, ∗∗p < 0.01.

(E) Expression of E-cadherin was increased after S3I-201 (5μM) treatment under H/R condition. ∗p < 0.05 vs. DMSO+H/R group.

(F) AG490 (100μM) was also used to inhibit the activation of STAT3, which could restore the decreased expression of E-cadherin in the PTECs, ∗p < 0.05 vs. DMSO+H/R group, n = 3–4.