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Fig. 1. Patients with chronic kidney disease (CKD) show an increased level of HK2, and CKD mice-derived mesenchymal stem/stromal cells (MSCs) show impaired mitochondrial functionality. (A) Serum samples from patients with CKD (n=30) and healthy controls (n=30) were subjected to enzyme-linked immunosorbent assay (ELISA) for HK2. (B) Methylglyoxal (MG) content in human serum samples from the same experimental groups (CKD patients vs. healthy control group). (C) Expression of HK1 and HK2 in mitochondrial fractions of MSCs derived from the CKD mouse model (CKD-mMSCs) and normal control mice (Nor-mMSCs), as detected by immunoblotting (n=5). Expression levels of HK1 and HK2 were normalized relative to levels of the mitochondrial marker VDAC1. (D) Normal-mMSCs and CKD-mMSCs were assayed using MitoSOX to assess mitochondrial oxidative stress. MitoSOX signals were quantified using flow cytometry (n=5). (E) Normal-mMSCs and CKD-mMSCs were assayed using TMRE to assess the mitochondrial membrane potential. TMRE signals were quantified using flow cytometry (n=5). Values represent the mean ± standard error of the mean (SEM). *p<0.05 or **p<0.01 vs. control.
Biomolecules & Therapeutics 2022;30:28~37 https://doi.org/10.4062/biomolther.2021.058
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