Corrigendum to “Cobalt induces neurodegenerative damages through Pin1 inactivation in mice and human neuroglioma cells” [J Hazard Mater 419 (2021) 126378]

Abstract

The authors regret that the Fig. 5C/H and Fig. 6 was incorrect as the two identical blots of GAPDH were inadvertently used during the assembly of the final figures. The corrected Fig. 5 and Fig. 6 were re-assembled using the original data. The error does not change either the results or the conclusions of the data. The authors regret the error.

1. Download: Download high-res image (921KB)
2. Download: Download full-size image

Fig. 5. Neurodegenerative effects of cobalt in 2- and 12-month-old mice. (A) After exposure, Co²⁺ content increased in the blood, cortex, hippocampus of 12-month-old mice (n = 5). (B) Protein levels of Pin1 in the hippocampus and cortex were significantly downregulated by cobalt regardless of age. (C) The upregulation of Tau, T231 P-Tau protein levels as well as cis-/trans- P-Tau ratio by cobalt marks the involvement of Pin1 in the process. (D) Quantification of (C). (E) The upregulation of APP, Aβ_1–42 and GSK3β marks the neurodegeneration caused by cobalt. (F) quantification of (E). (G) Neuronal apoptosis detected by TUNEL assay in both the hippocampus and cortex of 12-month-old mice. Scale bars of the upper panels indicate 100 µm, while in the zoom-in images, the scale bars indicate 50 µm. (H) Cobalt caused upregulations of apoptosis relative protein Caspase-9 in both the hippocampus and cortex from 2- and 12-month-old mice. (I) Results of histopathological examination in both the hippocampal and cortex of 12-month-old mice (n = 3) are shown. Left panel: HE staining with pyknosis of neuron indicated as red arrow, while red nerve cell labelled as yellow arrow. Middle panel: Bielschowsky’s silver staining with fiber tangles and age spots marked with black arrow. Right panel: Nissl staining with Nissl’s body noticed with black arrow. Scale bar indicates 500 µm. (J–N) Morris water-maze test showed learning and recognition deficiencies were caused by cobalt exposure (n = 5). In training trials (J), the representative tracks for each group were shown. In 2-month-old mice, all exposure group presented significant differences in all days. In 12-month-old mice, escape latencies in 8 and 16 mg/kg groups are significantly longer than the control group of the same day, as well as day 2 and day 4 of 4 mg/kg groups (P < 0.05). Space prob trials results including representative tracks (K), number of virtual platform crossings (L), swimming speed (M, cm/s) and time spent (N) in the effective region (seconds) of the mice are presented. All data are shown as mean ± SD. * for P < 0.05, ** P < 0.01 and *** P < 0.001 compared with the control in respective age group; # for P < 0.05, ## P < 0.01 and ### P < 0.001 compared with relative 2-month-old mice.

1. Download: Download high-res image (201KB)
2. Download: Download full-size image

Fig. 6. Examinations of Pin1 protein level and function in human blood samples from hip joint replacement. Human sample data were divided into low Co (low cobalt) and high Co (high cobalt) groups according to the median plasma cobalt level (0.669 µg/l). Blood cell Pin1 and trans P-Tau protein levels were significantly decreased in the high cobalt group. * for P < 0.05 compared with the control.