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. Author manuscript; available in PMC: 2020 Sep 1.
Published in final edited form as: Kidney Int. 2019 May 6;96(3):656–673. doi: 10.1016/j.kint.2019.03.023

Figure 8: Formoterol treatment induced the expression of mitochondrial proteins:

Figure 8:

(A) Markers of MB in mice kidney lysates were evaluated by western blotting using PGC-1α, OXPHOS (cocktail antibodies of mitochondrial ETC complex I to V) and GAPDH antibodies. (B–C) Densitometric analysis of immunoblots showed increased expression of PGC-1α (One-way ANOVA, *P≤0.05 NTS+vehicle vs. NTS+formoterol; ##P≤0.01 vehicle vs NTS+formoterol) and OXPHOS (mitochondrial complex I, III and V) proteins in NTS+formoterol treated mice (One-way ANOVA, **P≤0.01, ***P≤0.001 NTS+vehicle vs. NTS+formoterol; ##P≤0.01 vehicle vs NTS+formoterol). Data are presented in mean±SEM. (D) The qPCR analysis showed that formoterol treatment upregulated the expression of PGC-α, NDUFB8, ND6, COXIII and NRF1 genes that are involved in MB. Data are presented in mean±SEM. One-way ANOVA, **P≤0.05, **P≤0.01, ***P≤0.001 NTS+vehicle vs. NTS+formoterol; aaP≤0.01 control vs NTS+vehicle; #P≤0.05, ###P≤0.05 control vs NTS+formoterol. (E) mtDNA copy number analysis of kidney samples from NTS injured mice showed that mtDNA copy number significantly increased (~2fold) upon formoterol treatment. *P≤0.05 control vs NTS+formoterol.