Fig 1: miR-218 affected renal cell viability and apoptosis by targeting DACH1. (a) CCK-8 assays were emplyed to determine the cells proliferation in different groups. (b) Cell apoptosis was evaluated by flow cytometry analysis in different groups. (c) Cell apoptosis was quantified. **p < 0.01. HG: high glucose; Con: control.
Fig 2: miR-218/DACH1 axis affected the EMT process. (a) Following treatment with miR-218 inhibitor/si-DACH1, the protein expression of EMT-related markers was determined by western blot. (b) Following treatment with miR-218 mimic/pcDNA3.1-DACH1, the protein expression of EMT-related markers was determined by western blot. Con: control; HG: high glucose; EMT: epithelial-mesenchymal transition.
Fig 3: DACH1 was a direct target of miR-218. (a) The website Targetscan was used to predict the binding sites between miR-218 and the 3'-UTR region of DACH1. (b) A luciferase reporter assay was used to determine the luciferase activities in different groups. (c) Expression of DACH1 in tissues was analyzed by bioinformatics tools in GSE30528 dataset. (d) Expression of DACH1 under HG conditions. QRT-PCR (e, f) and western blot (g, h) were adopted to detect the mRNA and protein levels of DACH1 in different groups in HEK-2 cells. **p < 0.01. NC: negative control; WT: wide type; MUT: mutant type; DKD: diabetic kidney disease; HG: high glucose; Con: control.
Fig 4: miR-218/DACH1 axis affected inflammatory response. MiR-218/DACH1 axis regulated the concentration of pro-inflammatory cytokines TNF-a (a) and IL-1ß (b) and anti-inflammatory cytokine IL-10 in HG-treated renal cells. The levels of inflammatory cytokines in different groups were measured by ELISA assay. **p < 0.01. HG: high glucose; Con: control.
Supplier Page from Thermo Fisher Scientific for DACH1 Antibody