miR-382 Contributes to Renal Tubulointerstitial Fibrosis by Downregulating HSPD1

Figure 8

Overexpression of HSPD1 restored renal antioxidant capacity and attenuated TGF-β1-induced loss of cell polarity in vitro. HK2 cells were not transfected or were transfected with Myc-DDK-tagged plasmid (pHSPD1) or an empty vector. Cells without plasmid transfection were transfected with LNA-anti-miR382/anti-scramble oligos. (a) Effects of anti-382 treatment or HSPD1 overexpression on ROS levels in HK2 cells under TGF-β1 exposure. Fluorescence intensity was measured at an excitation wavelength of 485 nm and an emission wavelength of 535 nm. (b) Relative mRNA level of E-cadherin. (c, d) Relative protein abundance of E-cadherin and HSPD1, examined by Western blot analysis. (e) ELISA assay of 3-NT (Abcam) with the cell homogenate. (f) ELISA assay of Trx (BioVendor R&D) with the cell homogenate. 3-NT indicates 3-nitrotyrosine; Trx indicates thioredoxin. , ^# compared with the control group; ^▲, ^Δ compared with the TGF-β1 group ().

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