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. 2018 Aug 17;50(8):105. doi: 10.1038/s12276-018-0124-z

Fig. 5. CAMP-hMT1A increases mitochondrial function in neuronal cells without cytotoxicity.

Fig. 5

a Confocal microscopy images of CAMP-hMT1A in the mitochondria of SH-SY5Y neuronal cells (×400, scale bar = 10 μm). Cells were treated with 2 μM CAMP-hMT1A protein for 24 h, stained with MitoTracker (MitoT, red), and immunostained with 6xHis-tag antibody (green). b Western blot of tyrosine hydroxylase (TH) levels in CAMP-MT1A- or PBS-treated cells. β-Actin was detected as a loading control. c Time- and dose-dependent effects of CAMP-hMT1A on complex 1 of OXPHOS, NADH dehydrogenase activity. d Dose-dependent effects of CAMP-hMT1A on intracellular ATP content. e The oxygen consumption rate (OCR) of isolated mitochondria for state 2 (–ADP) and state 3 (+1.5 mM ADP) respiration were measured, with mitochondrial complex 1 inhibitors MPP+ (1 mM) and rotenone (1 μM) used as positive controls. The data are presented as the mean ± SEM, n = 3