ILEI is an important intermediate participating in the formation of TGF-β1-induced renal tubular EMT.

Renal interstitial fibrosis is the most common process by which chronic kidney diseases progress to end-stage renal failure. Epithelial-to-mesenchymal transitions (EMTs) play a crucial role in the progression of renal interstitial fibrosis. A newly identified cytokine, interleukin-like EMT inducer (ILEI), has been linked to EMT in some diseases. However, the effects of ILEI on renal tubular EMT have not yet been well established. Here, we characterize the expression of ILEI in tubular EMT and describe the role and mechanism of ILEI in transforming growth factor beta 1 (TGF-β1)-induced renal tubular EMT. The results indicate that ILEI is involved in renal tubular EMT induced by TGF-β1, as overexpression of ILEI not only induces EMT of HK-2 cells independently but also profoundly enhances EMT in response to TGF-β1. Supporting this finding, ILEI small interfering RNA was found to block the EMT of HK-2 cells induced by TGF-β1. This work additionally suggests ILEI mediates TGF-β1-dependent EMT via the extracellular regulated protein kinases (ERKs) and protein kinase B (Akt) signalling pathways. In conclusion, ILEI appears to play a crucial role in mediating TGF-β1-induced EMT through the Akt and ERK pathways, which may provide a therapeutic target for the treatment of fibrotic kidney diseases. SIGNIFICANCE OF THE STUDY:There is no study reporting the effect of ILEI in renal EMTs. In this research, we examined the role and mechanism of ILEI in EMT using tubular epithelial cell; we found that ILEI participated in renal tubular EMT, and overexpression of ILEI can not only induce EMT of HK-2 cells independently but also enhance EMT in response to TGF-β1. Meanwhile, we found ILEI small interfering RNA blocked the EMT induced by TGF-β1, and ILEI participates in the EMT caused by TGF-β1 via ERK and Akt signalling pathways. We hoped to provide new ideas in further study on the prevention and treatment of fibrotic kidney diseases.

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