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. 2018 May 11;42(2):946–956. doi: 10.3892/ijmm.2018.3670

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Copyright: © Liu et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Protective effect of HO-1 overexpression on BMSC survival. BMSCs indirectly cultured with AKI- KHS were used to simulate implanted BMSCs trapped in the AKI in vivo. (A) Cell cycle profiles. (B) Quantitative analysis of the cell cycle profile. The cell cycle of BMSCs induced by AKI-KHS arrested at the G0/G1 phase. However, the expression of HO-1 decreased the proportion of BMSCs at the G0/G1 phase. (C) Immunohistochemical staining of PCNA in BMSCs (×200 magnification). Brown nuclei indicated PCNA⁺ cells. (D) Quantitative analysis of the PCNA expression. The proportion of the PCNA⁺ cells in the HO-1-BMSCs/AKI-KHS group was increased significantly compared with the BMSCs/AKI-KHS group. Results are presented as the mean ± standard deviation (n=6). ^aP<0.05 vs. control group; ^bP<0.05 vs. BMSCs/AKI-KHS group. HO-1, heme oxygenase-1; BMSC, bone marrow-derived mesenchymal stem cell; AKI, acute kidney injury; KHS, kidney homogenate supernatant; PCNA, proliferating cell nuclear antigen; blank, blank group (BMSCs with medium); con, control group (BMSCs with normal KHS); eGFP, enhanced green fluorescent protein.