Cadmium induces alterations in the human spinal cord morphogenesis |
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Authors: | Erica Sarchielli Stefania Pacini Gabriele Morucci Tiziana Punzi Mirca Marini Gabriella B Vannelli Massimo Gulisano |
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Institution: | (1) Department of Anatomy, Histology and Forensic Medicine, University of Firenze, Viale Morgagni 85, 50134 Florence, Italy; |
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Abstract: | The effects of cadmium on the central nervous system are still relatively poorly understood and its role in neurodegenerative
diseases has been debated. In our research, cultured explants from 25 human foetal spinal cords (10–11 weeks gestational age)
were incubated with 10 and 100 μM cadmium chloride (CdCl2) for 24 h. After treatment, an immunohistochemical study for Sglial fibrillary acidic protein (GFAP) and choline acetyltransferase
(ChAT)], a Western blot analysis (for GFAP, β-Tubulin III, nerve growth factor receptor, Caspase 8 and poly (ADP-ribose) polymerase),
and a terminal deoxynucleotidyl transferase biotin-dUTP nick end labelling (TUNEL) assay (for detection of apoptotic bodies)
were performed. The treatment with CdCl2 induced a significant and dose-dependent change in the ratio motor neurons/glial cells in the ventral horns of human foetal
spinal cord. The decrease of the choline acetyltransferase-positive cells (motor neurons) and the reduction of β Tubulin III
indicate that CdCl2 specifically affects motor neurons of the ventral horns. While the number of motor neurons decreased for the activation of
apoptotic pathways (as shown by the increased expression of Caspase 8, nerve growth factor receptor, and poly (ADP-ribose)
polymerase), glial cells, both in the subependymal zone and in the gray matter of the ventral horns, increased (as shown by
the increase of GFAP expression). These results provide the evidence that during human spinal cord development, CdCl2 may affect the fate of neural and glial cells thus, being potentially involved in the etiopathogenesis of neurodegenerative
diseases. |
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