Inhibition of TGFBIp expression by lithium: Implications for TGFBI-linked corneal dystrophy therapy

Investigative Ophthalmology and Visual Science

Volumn 52, Issue 6, 2011, Pages 3293-3300

  Choi, Seung Il ^a   Kim, Bong Yoon ^a   Dadakhujaev, Shorafidinkhuja ^a   Jester, James V ^b   Ryu, Hyunmi ^a   Kim, Tae Im ^a   Kim, Eung Kweon ^a,c  

^a Yonsei University College of Medicine   (South Korea)

^b UNIVERSITY OF CALIFORNIA   (United States)

^c Yonsei University   (South Korea)

Author keywords

[No Author keywords available]

Indexed keywords

BETA ACTIN; CELL ADHESION MOLECULE; GLYCOGEN SYNTHASE KINASE 3ALPHA; GLYCOGEN SYNTHASE KINASE 3BETA; LITHIUM CHLORIDE; MESSENGER RNA; MICROTUBULE ASSOCIATED PROTEIN; MICROTUBULE ASSOCIATED PROTEIN 3; POTASSIUM CHLORIDE; SMAD3 PROTEIN; TRANSFORMING GROWTH FACTOR BETA INDUCED GENE PROTEIN; UNCLASSIFIED DRUG; BETAIG H3 PROTEIN; BETAIG-H3 PROTEIN; GLYCOGEN SYNTHASE KINASE 3; GLYCOGEN SYNTHASE KINASE 3 ALPHA; GLYCOGEN SYNTHASE KINASE 3 BETA; SCLEROPROTEIN; SMAD3 PROTEIN, HUMAN; TRANSFORMING GROWTH FACTOR BETA;

ARTICLE; AUTOPHAGY; CELL VIABILITY; CONTROLLED STUDY; CORNEA DYSTROPHY; DOWN REGULATION; FIBROBLAST; HUMAN; HUMAN CELL; IMMUNOBLOTTING; IMMUNOPRECIPITATION; NUCLEOTIDE SEQUENCE; PRIORITY JOURNAL; PROTEIN EXPRESSION; REAL TIME POLYMERASE CHAIN REACTION; REVERSE TRANSCRIPTION POLYMERASE CHAIN REACTION; SIGNAL TRANSDUCTION; WESTERN BLOTTING; CELL CULTURE; CONGENITAL CORNEA DYSTROPHY; CORNEA; CYTOLOGY; DOSE RESPONSE; DRUG ANTAGONISM; DRUG EFFECT; GENE EXPRESSION REGULATION; GENETICS; METABOLISM; PATHOLOGY; PHOSPHORYLATION; TIME;

AUTOPHAGY; BLOTTING, WESTERN; CELLS, CULTURED; CORNEA; CORNEAL DYSTROPHIES, HEREDITARY; DOSE-RESPONSE RELATIONSHIP, DRUG; EXTRACELLULAR MATRIX PROTEINS; FIBROBLASTS; GENE EXPRESSION REGULATION; GLYCOGEN SYNTHASE KINASE 3; HUMANS; LITHIUM CHLORIDE; PHOSPHORYLATION; REVERSE TRANSCRIPTASE POLYMERASE CHAIN REACTION; RNA, MESSENGER; SMAD3 PROTEIN; TIME FACTORS; TRANSFORMING GROWTH FACTOR BETA;

EID: 79960972837     PISSN: 01460404     EISSN: 15525783     Source Type: Journal    
DOI: 10.1167/iovs.10-6405     Document Type: Article

References (52)

1. Skonier J, Neubauer M, Madisen L, Bennett K, Plowman GD, Purchio AF. cDNA cloning and sequence analysis of beta Ig-h3, a novel gene induced in a human adenocarcinoma cell line after treatment with transforming growth factor-beta. DNA Cell Biol. 1992;11:511-522.
2. Zhao Y, Shao G, Piao CQ, Berenguer J, Hei TK. Down-regulation of Betaig-h3 gene is involved in the tumorigenesis in human bronchial epithelial cells induced by heavy-ion radiation. Radiat Res. 2004;162:655-659.
3. Zhao YL, Piao CQ, Hei TK. Downregulation of Betaig-h3 gene is causally linked to tumorigenic phenotype in asbestos treated immortalized human bronchial epithelial cells. Oncogene. 2002;21: 7471-7477.
4. Zhang Y, Wen G, Shao G, et al. TGFBI deficiency predisposes mice to spontaneous tumor development. Cancer Res. 2009;69:37-44.
5. LeBaron RG, Bezverkov KI, Zimber MP, Pavelec R, Skonier J, Purchio AF. Beta IG-H3, a novel secretory protein inducible by transforming growth factor-beta, is present in normal skin and promotes the adhesion and spreading of dermal fibroblasts in vitro. J Invest Dermatol. 1995;104:844-849.
6. Billings PC, Herrick DJ, Kucich U, et al. Extracellular matrix and nuclear localization of beta ig-h3 in human bladder smooth muscle and fibroblast cells. J Cell Biochem. 2000;79:261-273.
7. Kim JE, Jeong HW, Nam JO, et al. Identification of motifs in the fasciclin domains of the transforming growth factor-beta-induced matrix protein betaig-h3 that interact with the alphavbeta5 integrin. J Biol Chem. 2002;277:46159-46165.
8. Klintworth GK. Advances in the molecular genetics of corneal dystrophies. Am J Ophthalmol. 1999;128:747-754.
9. Korvatska E, Henry H, Mashima Y, et al. Amyloid and non-amyloid forms of 5q31-linked corneal dystrophy resulting from keratoepithelin mutations at Arg-124 are associated with abnormal turnover of the protein. J Biol Chem. 2000;275:11465-11469.
10. Moon JW, Kim SW, Kim TI, Cristol SM, Chung ES, Kim EK. Homozygous granular corneal dystrophy type II (Avellino corneal dystrophy): natural history and progression after treatment. Cornea. 2007;26:1095-1100.
11. Woodgett JR. Judging a protein by more than its name: GSK-3. Sci STKE. 2001;2001:re12.
12. Cadigan KM, Nusse R. Wnt signaling: a common theme in animal development. Genes Dev. 1997;11:3286-3305.
13. Wodarz A, Nusse R. Mechanisms of Wnt signaling in development. Annu Rev Cell Dev Biol. 1998;14:59-88.
14. Frame S, Cohen P. GSK3 takes centre stage more than 20 years after its discovery. Biochem J. 2001;359:1-16.
15. Grimes CA, Jope RS. The multifaceted roles of glycogen synthase kinase 3beta in cellular signaling. Prog Neurobiol. 2001;65:391-426.
16. Hedgepeth CM, Conrad LJ, Zhang J, Huang HC, Lee VM, Klein PS. Activation of the Wnt signaling pathway: a molecular mechanism for lithium action. Dev Biol. 1997;185:82-91.
17. Phiel CJ, Klein PS. Molecular targets of lithium action. Annu Rev Pharmacol Toxicol. 2001;41:789-813.
18. Stambolic V, Ruel L, Woodgett JR. Lithium inhibits glycogen synthase kinase-3 activity and mimics wingless signalling in intact cells. Curr Biol. 1996;6:1664-1668.
19. Klein PS, Melton DA. A molecular mechanism for the effect of lithium on development. Proc Natl Acad Sci U S A. 1996;93:8455-8459.
20. Fukumoto T, Morinobu S, Okamoto Y, Kagaya A, Yamawaki S. Chronic lithium treatment increases the expression of brain-derived neurotrophic factor in the rat brain. Psychopharmacology (Berl). 2001;158:100-106.
21. Gould TD, Manji HK. The Wnt signaling pathway in bipolar disorder. Neuroscientist. 2002;8:497-511.
22. Doble BW, Woodgett JR. GSK-3: tricks of the trade for a multitasking kinase. J Cell Sci. 2003;116:1175-1186.
23. Chalecka-Franaszek E, Chuang DM. Lithium activates the serine/ threonine kinase Akt-1 and suppresses glutamate-induced inhibition of Akt-1 activity in neurons. Proc Natl Acad Sci U S A. 1999;96:8745-8750.
24. De Sarno P, Li X, Jope RS. Regulation of Akt and glycogen synthase kinase-3 beta phosphorylation by sodium valproate and lithium. Neuropharmacology. 2002;43:1158-1164.
25. Zhang F, Phiel CJ, Spece L, Gurvich N, Klein PS. Inhibitory phosphorylation of glycogen synthase kinase-3 (GSK-3) in response to lithium: evidence for autoregulation of GSK-3. J Biol Chem. 2003; 278:33067-33077.
26. Gould TD, Quiroz JA, Singh J, Zarate CA, Manji HK. Emerging experimental therapeutics for bipolar disorder: insights from the molecular and cellular actions of current mood stabilizers. Mol Psychiatry. 2004;9:734-755.
27. Jope RS. Anti-bipolar therapy: mechanism of action of lithium. Mol Psychiatry. 1999;4:117-128.
28. Kirshenboim N, Plotkin B, Shlomo SB, Kaidanovich-Beilin O, Eldar-Finkelman H. Lithium-mediated phosphorylation of glycogen synthase kinase-3beta involves PI3 kinase-dependent activation of protein kinase C-alpha. J Mol Neurosci. 2004;24:237-245.
29. Liang MH, Chuang DM. Regulation and function of glycogen synthase kinase-3 isoforms in neuronal survival. J Biol Chem. 2007; 282:3904-3917.
30. Liang MH, Chuang DM. Differential roles of glycogen synthase kinase-3 isoforms in the regulation of transcriptional activation. J Biol Chem. 2006;281:30479-30484.
31. Derynck R, Zhang YE. Smad-dependent and Smad-independent pathways in TGF-beta family signalling. Nature. 2003;425:577-584.
32. Shi Y, Massague J. Mechanisms of TGF-beta signaling from cell membrane to the nucleus. Cell. 2003;113:685-700.
33. Sanyal S, Kim SM, Ramaswami M. Retrograde regulation in the CNS; neuron-specific interpretations of TGF-beta signaling. Neuron. 2004;41:845-848.
34. Gomes FC, Sousa Vde O, Romao L. Emerging roles for TGF-beta1 in nervous system development. Int J Dev Neurosci. 2005;23:413-424.
35. Choi SI, Kim TI, Kim KS, et al. Decreased catalase expression and increased susceptibility to oxidative stress in primary cultured corneal fibroblasts from patients with granular corneal dystrophy type II. Am J Pathol. 2009;175:248-261.
36. Jester JV, Huang J, Fisher S, et al. Myofibroblast differentiation of normal human keratocytes and hTERT, extended-life human corneal fibroblasts. Invest Ophthalmol Vis Sci. 2003;44:1850-1858.
37. Guo X, Ramirez A, Waddell DS, Li Z, Liu X, Wang XF. Axin and GSK3-control Smad3 protein stability and modulate TGF-signaling. Genes Dev. 2008;22:106-120.
38. Sarkar S, Floto RA, Berger Z, et al. Lithium induces autophagy by inhibiting inositol monophosphatase. J Cell Biol. 2005;170:1101-1111.
39. Koike M, Shibata M, Waguri S, et al. Participation of autophagy in storage of lysosomes in neurons from mouse models of neuronal ceroid-lipofuscinoses (Batten disease). Am J Pathol. 2005;167: 1713-1728.
40. Klionsky DJ, Abeliovich H, Agostinis P, et al. Guidelines for the use and interpretation of assays for monitoring autophagy in higher eukaryotes. Autophagy. 2008;4:151-175.
41. Jope RS. Lithium and GSK-3: one inhibitor, two inhibitory actions, multiple outcomes. Trends Pharmacol Sci. 2003;24:441-443.
42. Ryves WJ, Harwood AJ. Lithium inhibits glycogen synthase kinase-3 by competition for magnesium. Biochem Biophys Res Commun. 2001;280:720-725.
43. Millet C, Yamashita M, Heller M, Yu LR, Veenstra TD, Zhang YE. A negative feedback control of transforming growth factor-beta signaling by glycogen synthase kinase 3-mediated Smad3 linker phosphorylation at Ser-204. J Biol Chem. 2009;284:19808-19816.
44. Sarkar S, Krishna G, Imarisio S, Saiki S, O'Kane CJ, Rubinsztein DC. A rational mechanism for combination treatment of Huntington's disease using lithium and rapamycin. Hum Mol Genet. 2008;17: 170-178.
45. Sarkar S, Rubinsztein DC. Inositol and IP3 levels regulate autophagy: biology and therapeutic speculations. Autophagy. 2006;2:132-134.
46. Lai JS, Zhao C, Warsh JJ, Li PP. Cytoprotection by lithium and valproate varies between cell types and cellular stresses. Eur J Pharmacol. 2006;539:18-26.
47. Bowerman B. Cell biology: oxidative stress and cancer: a betacatenin convergence. Science. 2005;308:1119-1120.
48. Maiese K, Chong ZZ. Insights into oxidative stress and potential novel therapeutic targets for Alzheimer disease. Restor Neurol Neurosci. 2004;22:87-104.
49. Schafer M, Goodenough S, Moosmann B, Behl C. Inhibition of glycogen synthase kinase 3 beta is involved in the resistance to oxidative stress in neuronal HT22 cells. Brain Res. 2004;1005:84-89.
50. King TD, Jope RS. Inhibition of glycogen synthase kinase-3 protects cells from intrinsic but not extrinsic oxidative stress. Neuroreport. 2005;16:597-601.
51. Chen RW, Chuang DM. Long term lithium treatment suppresses p53 and Bax expression but increases Bcl-2 expression: a prominent role in neuroprotection against excitotoxicity. J Biol Chem. 1999;274:6039-6042.
52. Rowe MK, Chuang DM. Lithium neuroprotection: molecular mechanisms and clinical implications. Expert Rev Mol Med. 2004;6:1-18.