L‑carnitine attenuates TGF‑β1‑induced EMT in retinal pigment epithelial cells via a PPARγ‑dependent mechanism

Abstract

The epithelial‑mesenchymal transition (EMT) of retinal pigment epithelial (RPE) cells is an important underlying mechanism of proliferative vitreoretinopathy (PVR). We previously found that L‑carnitine (β‑hydroxy‑γ‑N-trimethylammonium‑butyrate, LC) was significantly lower during the transforming growth factor‑β1 (TGF‑β1)‑induced EMT process in ARPE‑19 cells. The present study assessed the role of LC in the EMT of RPE cells. The migration of RPE cells was detected using a Transwell migration assay. Then, EMT‑related biomarkers were measured via western blotting, immunofluorescence and reverse transcription‑quantitative PCR. It was observed that LC attenuated the TGF‑β1‑induced downregulation of the epithelial markers E‑Cadherin and zonula occludens‑1, as well as the expression of mesenchymal markers fibronectin and α‑smooth muscle actin. Meanwhile, LC blocked Erk1/2 and JNK pathways in the EMT of RPE cells. Moreover, treatment with a peroxisome proliferator‑activated receptor γ (PPARγ) inhibitor prevented the effect of LC on EMT. Taken together, these data suggested that LC attenuated EMT induced by TGF‑β1 via inhibition of the Erk1/2 and JNK pathways and upregulation of PPARγ expression.

Keywords: L‑carnitine; epithelial‑mesenchymal transition; proliferative vitreoretinopathy; retinal pigment epithelial cell.