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PPAR Research
Volume 2014, Article ID 349525, 11 pages
http://dx.doi.org/10.1155/2014/349525
Research Article

Effect of Chronic Valproic Acid Treatment on Hepatic Gene Expression Profile in Wfs1 Knockout Mouse

1Institute of Biomedicine and Translational Medicine, Department of Physiology, University of Tartu, 19 Ravila Street, 50411 Tartu, Estonia
2Centre of Excellence for Translational Medicine, 19 Ravila Street, 50411 Tartu, Estonia
3SGDP, Institute of Psychiatry at the Maudsley, King’s College London, De Crespigny Park, London SE5 8AF, UK
4Institute of Biomedicine and Translational Medicine, Department of Biochemistry, University of Tartu, 19 Ravila Street, 50411 Tartu, Estonia

Received 21 December 2013; Revised 17 February 2014; Accepted 17 February 2014; Published 1 April 2014

Academic Editor: Constantinos Giaginis

Copyright © 2014 Marite Punapart et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Linked References

  1. R. S. Jope and G. V. W. Johnson, “The glamour and gloom of glycogen synthase kinase-3,” Trends in Biochemical Sciences, vol. 29, no. 2, pp. 95–102, 2004. View at Publisher · View at Google Scholar · View at Scopus
  2. S. Chateauvieux, F. Morceau, M. Dicato, and M. Diederich, “Molecular and therapeutic potential and toxicity of valproic acid,” Journal of Biomedicine and Biotechnology, vol. 2010, Article ID 479364, 18 pages, 2010. View at Publisher · View at Google Scholar · View at Scopus
  3. A. Verrotti, C. D'Egidio, A. Mohn, G. Coppola, and F. Chiarelli, “Weight gain following treatment with valproic acid: pathogenetic mechanisms and clinical implications,” Obesity Reviews, vol. 12, no. 501, pp. e32–e43, 2011. View at Publisher · View at Google Scholar · View at Scopus
  4. H. H. Chang, C. H. Chou, P. S. Chen et al., “High prevalence of metabolic disturbances in patients with bipolar disorder in Taiwan,” Journal of Affective Disorders, vol. 117, no. 1-2, pp. 124–129, 2009. View at Publisher · View at Google Scholar · View at Scopus
  5. T. Kato, “Molecular neurobiology of bipolar disorder: a disease of “mood-stabilizing neurons”?” Trends in Neurosciences, vol. 31, no. 10, pp. 495–503, 2008. View at Publisher · View at Google Scholar · View at Scopus
  6. C. Kakiuchi, M. Ishiwata, T. Umekage et al., “Association of the XBP1-116C/G polymorphism with schizophrenia in the Japanese population,” Psychiatry and Clinical Neurosciences, vol. 58, no. 4, pp. 438–440, 2004. View at Publisher · View at Google Scholar · View at Scopus
  7. C. Kakiuchi, K. Iwamoto, M. Ishiwata et al., “Impaired feedback regulation of XBP1 as a genetic risk factor for bipolar disorder,” Nature Genetics, vol. 35, no. 2, pp. 171–175, 2003. View at Publisher · View at Google Scholar · View at Scopus
  8. J. So, J. J. Warsh, and P. P. Li, “Impaired endoplasmic reticulum stress response in B-lymphoblasts from patients with bipolar-I disorder,” Biological Psychiatry, vol. 62, no. 2, pp. 141–147, 2007. View at Publisher · View at Google Scholar · View at Scopus
  9. C. Kakiuchi, M. Ishiwata, A. Hayashi, and T. Kato, “XBP1 induces WFS1 through an endoplasmic reticulum stress response element-like motif in SH-SY5Y cells,” Journal of Neurochemistry, vol. 97, no. 2, pp. 545–555, 2006. View at Publisher · View at Google Scholar · View at Scopus
  10. D.-M. Chuang, “The antiapoptotic actions of mood stabilizers: molecular mechanisms and therapeutic potentials,” Annals of the New York Academy of Sciences, vol. 1053, pp. 195–204, 2005. View at Publisher · View at Google Scholar · View at Scopus
  11. C. Kakiuchi, S. Ishigaki, C. M. Oslowski, S. G. Fonseca, T. Kato, and F. Urano, “Valproate, a mood stabilizer, induces WFS1 expression and modulates its interaction with ER stress protein GRP94,” PLoS ONE, vol. 4, no. 1, Article ID e4134, 2009. View at Publisher · View at Google Scholar · View at Scopus
  12. C. D. Bown, J.-F. Wang, and L. T. Young, “Increased expression of endoplasmic reticulum stress proteins following chronic valproate treatment of rat C6 glioma cells,” Neuropharmacology, vol. 39, no. 11, pp. 2162–2169, 2000. View at Publisher · View at Google Scholar · View at Scopus
  13. L. Shao, X. Sun, L. Xu, L. T. Young, and J.-F. Wang, “Mood stabilizing drug lithium increases expression of endoplasmic reticulum stress proteins in primary cultured rat cerebral cortical cells,” Life Sciences, vol. 78, no. 12, pp. 1317–1323, 2006. View at Publisher · View at Google Scholar · View at Scopus
  14. B. Chen, J. F. Wang, and L. T. Young, “Chronic valproate treatment increases expression of endoplasmic reticulum stress proteins in the rat cerebral cortex and hippocampus,” Biological Psychiatry, vol. 48, no. 7, pp. 658–664, 2000. View at Publisher · View at Google Scholar · View at Scopus
  15. T. Yamada, H. Ishihara, A. Tamura et al., “WFS1-deficiency increases endoplasmic reticulum stress, impairs cell cycle progression and triggers the apoptotic pathway specifically in pancreatic β-cells,” Human Molecular Genetics, vol. 15, no. 10, pp. 1600–1609, 2006. View at Publisher · View at Google Scholar · View at Scopus
  16. K. Ueda, J. Kawano, K. Takeda et al., “Endoplasmic reticulum stress induces Wfs1 gene expression in pancreatic β-cells via transcriptional activation,” European Journal of Endocrinology, vol. 153, no. 1, pp. 167–176, 2005. View at Publisher · View at Google Scholar · View at Scopus
  17. S. G. Fonseca, M. Fukuma, K. L. Lipson et al., “WFS1 is a novel component of the unfolded protein response and maintains homeostasis of the endoplasmic reticulum in pacreatic β-cells,” The Journal of Biological Chemistry, vol. 280, no. 47, pp. 39609–39615, 2005. View at Publisher · View at Google Scholar · View at Scopus
  18. T. M. Strom, K. Hörtnagel, S. Hofmann et al., “Diabetes insipidus, diabetes mellitus, optic atrophy and deafness (DIDMOAD) caused by mutations in a novel gene (Wolframin) coding for a predicted transmembrane protein,” Human Molecular Genetics, vol. 7, no. 13, pp. 2021–2028, 1998. View at Publisher · View at Google Scholar · View at Scopus
  19. H. Inoue, Y. Tanizawa, J. Wasson et al., “A gene encoding a transmembrane protein is mutated in patients with diabetes mellitus and optic atrophy (Wolfram syndrome),” Nature Genetics, vol. 20, no. 2, pp. 143–148, 1998. View at Publisher · View at Google Scholar · View at Scopus
  20. R. G. Swift, D. O. Perkins, C. L. Chase, D. B. Sadler, and M. Swift, “Psychiatric disorders in 36 families with Wolfram syndrome,” The American Journal of Psychiatry, vol. 148, no. 6, pp. 775–779, 1991. View at Google Scholar · View at Scopus
  21. M. Swift and R. G. Swift, “Psychiatric disorders and mutations at the Wolfram syndrome locus,” Biological Psychiatry, vol. 47, no. 9, pp. 787–793, 2000. View at Publisher · View at Google Scholar · View at Scopus
  22. T. D. Als, H. A. Dahl, T. J. Flint et al., “Possible evidence for a common risk locus for bipolar affective disorder and schizophrenia on chromosome 4p16 in patients from the Faroe Islands,” Molecular Psychiatry, vol. 9, no. 1, pp. 93–98, 2004. View at Publisher · View at Google Scholar · View at Scopus
  23. R. Cheng, S. H. Juo, J. E. Loth et al., “Genome-wide linkage scan in a large bipolar disorder sample from the National Institute of Mental Health genetics initiative suggests putative loci for bipolar disorder, psychosis, suicide, and panic disorder,” Molecular Psychiatry, vol. 11, no. 3, pp. 252–260, 2006. View at Publisher · View at Google Scholar · View at Scopus
  24. H. Ewald, B. Degn, O. Mors, and T. A. Kruse, “Support for the possible locus on chromosome 4p16 for bipolar affective disorder,” Molecular Psychiatry, vol. 3, no. 5, pp. 442–448, 1998. View at Google Scholar · View at Scopus
  25. H. Ewald, T. Flint, T. A. Kruse, and O. Mors, “A genome-wide scan shows significant linkage between bipolar disorder and chromosome 12q24.3 and suggestive linkage to chromosomes 1p22-21, 4p16, 6q14-22, 10q26 and 16p13.3,” Molecular Psychiatry, vol. 7, no. 7, pp. 734–744, 2002. View at Publisher · View at Google Scholar · View at Scopus
  26. S. D. Detera-Wadleigh, C.-Y. Liu, M. Maheshwari et al., “Sequence variation in DOCK9 and heterogeneity in bipolar disorder,” Psychiatric Genetics, vol. 17, no. 5, pp. 274–286, 2007. View at Publisher · View at Google Scholar · View at Scopus
  27. T. Ohtsuki, H. Ishiguro, T. Yoshikawa, and T. Arinami, “WFS1 gene mutation search in depressive patients: detection of five missense polymorphisms but no association with depression or bipolar affective disorder,” Journal of Affective Disorders, vol. 58, no. 1, pp. 11–17, 2000. View at Publisher · View at Google Scholar · View at Scopus
  28. L. Martorell, M. Gómez Zaera, J. Valero et al., “The WFS1 (Wolfram syndrome 1) is not a major susceptibility gene for the development of psychiatric disorders,” Psychiatric Genetics, vol. 13, no. 1, pp. 29–32, 2003. View at Publisher · View at Google Scholar · View at Scopus
  29. R. Torres, E. Leroy, X. Hu et al., “Mutation screening of the Wolfram syndrome gene in psychiatric patients,” Molecular Psychiatry, vol. 6, no. 1, pp. 39–43, 2001. View at Publisher · View at Google Scholar · View at Scopus
  30. J. Crawford, M. A. Zielinski, L. J. Fisher, G. R. Sutherland, and R. D. Goldney, “Is there a relationship between Wolfram syndrome carrier status and suicide?” American Journal of Medical Genetics—Neuropsychiatric Genetics, vol. 114, no. 3, pp. 343–346, 2002. View at Publisher · View at Google Scholar · View at Scopus
  31. K. L. Evans, D. Lawson, T. Meitinger, D. H. Blackwood, and D. J. Porteous, “Mutational analysis of the Wolfram syndrome gene in two families with chromosome 4p-linked bipolar affective disorder,” American Journal of Medical Genetics, vol. 96, no. 2, pp. 158–160, 2000. View at Google Scholar
  32. T. Kato, K. Iwamoto, S. Washizuka et al., “No association of mutations and mRNA expression of WFS1/wolframin with bipolar disorder in humans,” Neuroscience Letters, vol. 338, no. 1, pp. 21–24, 2003. View at Publisher · View at Google Scholar · View at Scopus
  33. F. Seifuddin, M. Pirooznia, J. T. Judy et al., “Systematic review of genome-wide gene expression studies of bipolar disorder,” BMC Psychiatry, vol. 13, article 213, 2013. View at Publisher · View at Google Scholar
  34. T. Kato, M. Ishiwata, K. Yamada et al., “Behavioral and gene expression analyses of Wfs1 knockout mice as a possible animal model of mood disorder,” Neuroscience Research, vol. 61, no. 2, pp. 143–158, 2008. View at Publisher · View at Google Scholar · View at Scopus
  35. S. Kõks, U. Soomets, J. L. Paya-Cano et al., “Wfs1 gene deletion causes growth retardation in mice and interferes with the growth hormone pathway,” Physiological Genomics, vol. 37, no. 3, pp. 249–259, 2009. View at Publisher · View at Google Scholar · View at Scopus
  36. A. Terasmaa, U. Soomets, J. Oflijan et al., “Wfs1 mutation makes mice sensitive to insulin-like effect of acute valproic acid and resistant to streptozocin,” Journal of Physiology and Biochemistry, vol. 67, no. 3, pp. 381–390, 2011. View at Publisher · View at Google Scholar · View at Scopus
  37. M. de Falco, L. Manente, A. Lucariello et al., “Localization and distribution of Wolframin in human tissues,” Frontiers in Bioscience, vol. 4, pp. 1986–1998, 2012. View at Google Scholar
  38. R. Edgar, M. Domrachev, and A. E. Lash, “Gene Expression Omnibus: NCBI gene expression and hybridization array data repository,” Nucleic Acids Research, vol. 30, no. 1, pp. 207–210, 2002. View at Google Scholar · View at Scopus
  39. K. J. Livak and T. D. Schmittgen, “Analysis of relative gene expression data using real-time quantitative PCR and the 2-CT method,” Methods, vol. 25, no. 4, pp. 402–408, 2001. View at Publisher · View at Google Scholar · View at Scopus
  40. M.-H. Lee, M. Kim, B.-H. Lee et al., “Subchronic effects of valproic acid on gene expression profiles for lipid metabolism in mouse liver,” Toxicology and Applied Pharmacology, vol. 226, no. 3, pp. 271–284, 2008. View at Publisher · View at Google Scholar · View at Scopus
  41. M.-H. Lee, I. Hong, M. Kim et al., “Gene expression profiles of murine fatty liver induced by the administration of valproic acid,” Toxicology and Applied Pharmacology, vol. 220, no. 1, pp. 45–59, 2007. View at Publisher · View at Google Scholar · View at Scopus
  42. J. Yan, H. Wang, Y. Liu, and C. Shao, “Analysis of gene regulatory networks in the mammalian circadian rhythm,” PLoS Computational Biology, vol. 4, no. 10, Article ID e1000193, 2008. View at Publisher · View at Google Scholar · View at Scopus
  43. M. Göttlicher, S. Heck, and P. Herrlich, “Transcriptional cross-talk, the second mode of steroid hormone receptor action,” Journal of Molecular Medicine, vol. 76, no. 7, pp. 480–489, 1998. View at Publisher · View at Google Scholar · View at Scopus
  44. A. Lampen, S. Siehler, U. Ellerbeck, M. Göttlicher, and H. Nau, “New molecular bioassays for the estimation of the teratogenic potency of valproic acid derivatives in vitro: activation of the peroxisomal proliferator-activated receptor (PPARδ),” Toxicology and Applied Pharmacology, vol. 160, no. 3, pp. 238–249, 1999. View at Publisher · View at Google Scholar · View at Scopus
  45. E. Szalowska, B. van der Burg, H. Y. Man, P. J. Hendriksen, and A. A. Peijnenburg, “Model steatogenic compounds (amiodarone, valproic Acid, and tetracycline) alter lipid metabolism by different mechanisms in mouse liver slices,” PLoS ONE, vol. 9, no. 1, Article ID e86795, 2014. View at Publisher · View at Google Scholar
  46. N. di-Po, N. S. Tan, L. Michalik, W. Wahli, and B. Desvergne, “Antiapoptotic role of PPARβ in keratinocytes via transcriptional control of the Akt1 signaling pathway,” Molecular Cell, vol. 10, no. 4, pp. 721–733, 2002. View at Publisher · View at Google Scholar · View at Scopus
  47. P. A. Grimaldi, “Regulatory role of peroxisome proliferator-activated receptor delta (PPARδ) in muscle metabolism. A new target for metabolic syndrome treatment?” Biochimie, vol. 87, no. 1, pp. 5–8, 2005. View at Publisher · View at Google Scholar · View at Scopus
  48. S. Takahashi, T. Tanaka, and J. Sakai, “New therapeutic target for metabolic syndrome: PPARδ,” Endocrine Journal, vol. 54, no. 3, pp. 347–357, 2007. View at Publisher · View at Google Scholar · View at Scopus
  49. M. Adiels, S.-O. Olofsson, M.-R. Taskinen, and J. Borén, “Overproduction of very low-density lipoproteins is the hallmark of the dyslipidemia in the metabolic syndrome,” Arteriosclerosis, Thrombosis, and Vascular Biology, vol. 28, no. 7, pp. 1225–1236, 2008. View at Publisher · View at Google Scholar · View at Scopus
  50. P. Balakumar, M. Rose, S. S. Ganti, P. Krishan, and M. Singh, “PPAR dual agonists: are they opening Pandora's Box?” Pharmacological Research, vol. 56, no. 2, pp. 91–98, 2007. View at Publisher · View at Google Scholar · View at Scopus
  51. J. Lee and W. Y. Chung, “The role played by the peroxisome proliferator-activated receptor-β/δ (PPARβ/δ) activator, GW501516, in control of fatty acid metabolism: a new potential therapeutic target for treating metabolic syndrome,” Endocrinology, vol. 152, no. 5, pp. 1742–1744, 2011. View at Publisher · View at Google Scholar · View at Scopus
  52. S. Liu, J. D. Brown, K. J. Stanya et al., “A diurnal serum lipid integrates hepatic lipogenesis and peripheral fatty acid use,” Nature, vol. 502, no. 7472, pp. 550–554, 2013. View at Publisher · View at Google Scholar
  53. C. H. Lee, P. Olson, A. Hevener et al., “PPARδ regulates glucose metabolism and insulin sensitivity,” Proceedings of the National Academy of Sciences of the United States of America, vol. 103, no. 9, pp. 3444–3449, 2006. View at Publisher · View at Google Scholar
  54. P. P. Zandi, P. L. Belmonte, V. L. Willour et al., “Association study of Wnt signaling pathway genes in bipolar disorder,” Archives of General Psychiatry, vol. 65, no. 7, pp. 785–793, 2008. View at Publisher · View at Google Scholar
  55. G. D. Barish, V. A. Narkar, and R. M. Evans, “PPARδ: a dagger in the heart of the metabolic syndrome,” The Journal of Clinical Investigation, vol. 116, no. 3, pp. 590–597, 2006. View at Publisher · View at Google Scholar · View at Scopus
  56. E. Barroso, R. Rodríguez-Calvo, L. Serrano-Marco et al., “The PPARβ/δ activator GW501516 prevents the down-regulation of AMPK caused by a high-fat diet in liver and amplifies the PGC-1α-lipin 1-PPARα pathway leading to increased fatty acid oxidation,” Endocrinology, vol. 152, no. 5, pp. 1848–1859, 2011. View at Publisher · View at Google Scholar · View at Scopus