Decreased expression of the voltage-dependent anion channel in differentiated PC-12 and SH-SY5Y cells following low-level Pb exposure

Toxicological Sciences

Volumn 113, Issue 1, 2009, Pages 169-176

  Prins, John M ^a   Park, Sunyoung ^a   Lurie, Diana I ^a,b  

^a UNIVERSITY OF MONTANA   (United States)

^b UNIVERSITY OF MONTANA   (United States)

Author keywords

Energy depression; Lead; PC 12 cells; SH SY5Y cells; Voltage dependent anion channel

Indexed keywords

ADENOSINE TRIPHOSPHATE; LEAD; VOLTAGE DEPENDENT ANION CHANNEL; VOLTAGE DEPENDENT ANION CHANNEL 1; VOLTAGE DEPENDENT ANION CHANNEL 2; VOLTAGE DEPENDENT ANION CHANNEL 3;

ANIMAL CELL; ARTICLE; CONTROLLED STUDY; DOWN REGULATION; ENERGY METABOLISM; GENE EXPRESSION; GENETIC TRANSCRIPTION; HUMAN; HUMAN CELL; HYPOXIA; NERVE CELL DIFFERENTIATION; NEUROBLASTOMA CELL; NONHUMAN; NUCLEOTIDE SEQUENCE; PHEOCHROMOCYTOMA CELL; PROTEIN EXPRESSION; REVERSE TRANSCRIPTION POLYMERASE CHAIN REACTION;

ADENOSINE TRIPHOSPHATE; ANIMALS; BLOTTING, WESTERN; CELL DIFFERENTIATION; CELL HYPOXIA; CELL LINE, TUMOR; DOSE-RESPONSE RELATIONSHIP, DRUG; DOWN-REGULATION; HUMANS; NEURONS; ORGANOMETALLIC COMPOUNDS; RATS; REVERSE TRANSCRIPTASE POLYMERASE CHAIN REACTION; RNA, MESSENGER; TIME FACTORS; TRANSCRIPTION, GENETIC; VOLTAGE-DEPENDENT ANION CHANNEL 1; VOLTAGE-DEPENDENT ANION CHANNELS;

MUS;

EID: 75249104229     PISSN: 10966080     EISSN: 10960929     Source Type: Journal    
DOI: 10.1093/toxsci/kfp249     Document Type: Article

References (37)

1. Abu-Hamad, S., Sivan, S., and Shoshan-Barmatz, V. (2006). The expression level of the voltage-dependent anion channel controls life and death of the cell. Proc. Natl. Acad. Sci. U.S.A. 103, 5787-5792.
2. Atkins, D.S., Basha, M.R., and Zawia, N.H. (2003). Intracellular signaling pathways involved in mediating the effects of lead on the transcription factor Sp1. Int. J. Dev. Neurosci. 21, 235-244.
3. Baines, C.P., Kaiser, R.A., Sheiko, T., Craigen, W.J., and Molkentin, J.D. (2007). Voltage-dependent anion channels are dispensable for mitochondrial-dependent cell death. Nat. Cell Biol. 9, 550-555.
4. Basha, M.R., Wei, W., Brydie, M., Razmiafshari, M., and Zawia, N.H. (2003). Lead-induced developmental perturbations in hippocampal Sp1 DNA-binding are prevented by zinc supplementation: in vivo evidence for Pb and Zn competition. Int. J. Dev. Neurosci. 21, 1-12.
5. Blachly-Dyson, E., and Forte, M. (2001). VDAC channels. IUBMB Life 52, 113-118.
6. Braun, J.M., Kahn, R.S., Froehlich, T., Auinger, P., and Lanphear, B.P. (2006). Exposures to environmental toxicants and attention deficit hyperactivity disorder in U.S. children. Environ. Health Perspect. 114, 1904-1909.
7. Cordova, F.M., Rodrigues, A.L., Giacomelli, M.B., Oliveira, C.S., Posser, T., Dunkley, P.R., and Leal, R.B. (2004). Lead stimulates ERK1/2 and p38MAPK phosphorylation in the hippocampus of immature rats. Brain Res. 998, 65-72.
8. Crumpton, T., Atkins, D.S., Zawia, N.H., and Barone, S., Jr. (2001). Lead exposure in pheochromocytoma (PC12) cells alters neural differentiation and Sp1 DNA-binding. Neurotoxicology 22, 49-62.
9. Fox, D.A., Kala, S.V., Hamilton, W.R., Johnson, J.E., and O'Callaghan, J.P. (2008). Low-level human equivalent gestational lead exposure produces supernormal scotopic electroretinograms, increased retinal neurogenesis, and decreased retinal dopamine utilization in rats. Environ. Health Perspect. 116, 618-625.
10. Garza, A., Vega, R., and Soto, E. (2006). Cellular mechanisms of lead neurotoxicity. Med. Sci. Monit. 12, RA57-RA-65.
11. Greene, L.A., and Tischler, A.S. (1976). Establishment of a noradrenergic clonal line of rat adrenal pheochromocytoma cells which respond to nerve growth factor. Proc. Natl. Acad. Sci. U.S.A. 73, 2424-2428.
12. Hanas, J.S., Rodgers, J.S., Bantle, J.A., and Cheng, Y.G. (1999). Lead inhibition of DNA-binding mechanism of Cys(2)His(2) zinc finger proteins. Mol. Pharmacol. 56, 982-988.
13. Jones, L.G., Prins, J., Park, S., Walton, J.P., Luebke, A.E., and Lurie, D.I. (2008). Lead exposure during development results in increased neurofilament phosphorylation, neuritic beading, and temporal processing deficits within the murine auditory brainstem. J. Comp. Neurol. 506, 1003-1017.
14. Kann, O., and Kovacs, R. (2007). Mitochondria and neuronal activity. Am. J. Physiol. Cell Physiol. 292, C641-C657.
15. Leal, R.B., Cordova, F.M., Herd, L., Bobrovskaya, L., and Dunkley, P.R. (2002). Lead-stimulated p38MAPK-dependent Hsp27 phosphorylation. Toxicol. Appl. Pharmacol. 178, 44-51.
16. Levy, M., Faas, G.C., Saggau, P., Craigen, W.J., and Sweatt, J.D. (2003). Mitochondrial regulation of synaptic plasticity in the hippocampus. J. Biol. Chem. 278, 17727-17734.
17. Lidsky, T.I., and Schneider, J.S. (2003). Lead neurotoxicity in children: basic mechanisms and clinical correlates. Brain 126, 5-19.
18. Livak, K.J., and Schmittgen, T.D. (2001). Analysis of relative gene expression data using real time quantitative PCR and the 2(-Delta Delta C(T)) method. Methods 25, 402-408.
19. Oertel, D. (1999). The role of timing in the brain stem auditory nuclei of vertebrates. Annu. Rev. Physiol. 61, 497-519.
20. Rafalowska, U., Struzynska, L., Dabrowska-Bouta, B., and Lenkiewicz, A. (1996). Is lead toxicosis a reflection of altered energy metabolism in brain synaptosomes? Acta Neurobiol. Exp. (Wars) 56, 611-617.
21. Robson, J.A., and Sidell, N. (1985). Ultrastructural features of a human neuroblastoma cell line treated with retinoic acid. Neuroscience 14, 1149-1162.
22. Rowland, K.C., Irby, N.K., and Spirou, G.A. (2000). Specialized synapse-associated structures within the calyx of Held. J. Neurosci. 20, 9135-9144.
23. Sampson, M.J., Decker, W.K., Beaudet, A.L., Ruitenbeek, W., Armstrong, D., Hicks, M.J., and Craigen, W.J. (2001). Immotile sperm and infertility in mice lacking mitochondrial voltage-dependent anion channel type 3. J. Biol. Chem. 276, 39206-39212.
24. Sampson, M.J., Lovell, R.S., and Craigen, W.J. (1997). The murine voltage-dependent anion channel gene family. Conserved structure and function. J. Biol. Chem. 272, 18966-18973.
25. Seppet, E., Gruno, M., Peetsalu, A., Gizatullina, Z., Nguyen, H.P., Vielhaber, S., Wussling, M.H.P., Trumbekaite, S., Arandarcikaite, O., Jerzembeck, D., et al. (2009). Mitochondria and energetic depression in cell pathophysiology. Int. J. Mol. Sci. 10, 2252-2303.
26. Shoshan-Barmatz, V., and Gincel, D. (2003). The voltage-dependent anion channel: characterization, modulation, and role in mitochondrial function in cell life and death. Cell Biochem. Biophys. 39, 279-292.
27. Shoshan-Barmatz, V., and Israelson, A. (2005). The voltage-dependent anion channel in endoplasmic/sarcoplasmic reticulum: characterization, modulation and possible function. J. Membr. Biol. 204, 57-66.
28. Shoshan-Barmatz, V., Israelson, A., Brdiczka, D., and Sheu, S.S. (2006). The voltage-dependent anion channel (VDAC): function in intracellular signalling, cell life and cell death. Curr. Pharm. Des. 12, 2249-2270.
29. Sterling, G.H., O'Neill, K.J., McCafferty, M.R., and O'Neill, J.J. (1982). Effect of chronic lead ingestion by rats on glucose metabolism and acetylcholine synthesis in cerebral cortex slices. J. Neurochem. 39, 592-596.
30. Vignali, G., Niclas, J., Sprocati, M.T., Vale, R.D., Sirtori, C., and Navone, F. (1996). Differential expression of ubiquitous and neuronal kinesin heavy chains during differentiation of human neuroblastoma and PC12 cells. Eur. J. Neurosci. 8, 536-544.
31. von Gersdorff, H., and Borst, J.G. (2002). Short-term plasticity at the calyx of held. Nat. Rev. Neurosci. 3, 53-64.
32. Weeber, E.J., Levy, M., Sampson, M.J., Anflous, K., Armstrong, D.L., Brown, S.E., Sweatt, J.D., and Craigen, W.J. (2002). The role of mitochondrial porins and the permeability transition pore in learning and synaptic plasticity. J. Biol. Chem. 277, 18891-18897.
33. Wilson, M.A., Johnston, M.V., Goldstein, G.W., and Blue, M.E. (2000). Neonatal lead exposure impairs development of rodent barrel field cortex. Proc. Natl. Acad. Sci. U.S.A. 97, 5540-5545.
34. Wu, S., Sampson, M.J., Decker, W.K., and Craigen, W.J. (1999). Each mammalian mitochondrial outer membrane porin protein is dispensable: effects on cellular respiration. Biochim. Biophys. Acta 1452, 68-78.
35. Zawia, N.H. (2003). Transcriptional involvement in neurotoxicity. Toxicol. Appl. Pharmacol. 190, 177-188.
36. Zawia, N.H., Sharan, R., Brydie, M., Oyama, T., and Crumpton, T. (1998). Sp1 as a target site for metal-induced perturbations of transcriptional regulation of developmental brain gene expression. Brain Res. Dev. Brain Res. 107, 291-298.
37. Zhao, Q., Slavkovich, V., and Zheng, W. (1998). Lead exposure promotes translocation of protein kinase C activities in rat choroid plexus in vitro, but not in vivo. Toxicol. Appl. Pharmacol. 149, 99-106.