Suberoylanilide hydroxamic acid: A potential epigenetic therapeutic agent for lung fibrosis?

European Respiratory Journal

Volumn 34, Issue 1, 2009, Pages 145-155

  Wang, Z ^a   Chen, C ^a   Finger, S N ^a   Do Kwajah MM, S ^a   Jung, M ^c   Schwarz, H ^a   Swanson, N ^d   Lareu, R R ^a,d   Raghunath, M ^a,b  

^a NATIONAL UNIVERSITY OF SINGAPORE   (Singapore)

^b NATIONAL UNIVERSITY OF SINGAPORE   (Singapore)

^c UNIVERSITY OF FREIBURG   (Germany)

^d UNIVERSITY OF WESTERN AUSTRALIA   (Australia)

Author keywords

Antifibrotic; Collagen; Fibroblast; Histone deacetylase inhibitor; Pulmonary fibrosis; Suberoylanilide hydroxamic acid

Indexed keywords

ALPHA SMOOTH MUSCLE ACTIN; ALPHA TUBULIN; COLLAGEN; CYTOKINE; HISTONE; INTERSTITIAL COLLAGENASE; TISSUE INHIBITOR OF METALLOPROTEINASE 1; TRANSFORMING GROWTH FACTOR BETA1; VORINOSTAT;

ACETYLATION; ADULT; ANTIINFLAMMATORY ACTIVITY; APOPTOSIS; ARTICLE; CELL PROLIFERATION; CELL SUBPOPULATION; CELL TRANSDIFFERENTIATION; CONCENTRATION RESPONSE; CONTROLLED STUDY; CYTOKINE RELEASE; DRUG EFFECT; DRUG INHIBITION; ENZYME ACTIVITY; ENZYME SYNTHESIS; FETUS; HUMAN; HUMAN CELL; IN VITRO STUDY; LUNG FIBROBLAST; LUNG FIBROSIS; LYMPHOCYTE; MYOFIBROBLAST; PERIPHERAL BLOOD MONONUCLEAR CELL; PRIORITY JOURNAL; PROTEIN AGGREGATION; PROTEIN DETERMINATION; PROTEIN EXPRESSION;

ACTINS; ANTI-INFLAMMATORY AGENTS; CELL LINE; CELL PROLIFERATION; COLLAGEN; EPIGENESIS, GENETIC; FIBROBLASTS; FIBROSIS; HUMANS; HYDROXAMIC ACIDS; IMMUNOHISTOCHEMISTRY; LUNG; MATRIX METALLOPROTEINASE 1; MUSCLE, SMOOTH; TISSUE INHIBITOR OF METALLOPROTEINASE-1;

EID: 69249114634     PISSN: 09031936     EISSN: 13993003     Source Type: Journal    
DOI: 10.1183/09031936.00084808     Document Type: Article

References (30)

1. American Thoracic Society/European Respiratory Society International Multidisciplinary Consensus Classification of the Idiopathic Interstitial Pneumonia. Am J Respir Crit Care Med 2002; 165: 277-304.
2. Scotton CJ, Chambers RC. Molecular targets in pulmonary fibrosis: the myofibroblast in focus. Chest 2007; 132: 1311-1321.
3. Gauldie J. Pro: Inflammatory mechanisms are a minor component of the pathogenesis of idiopathic pulmonary fibrosis. Am J Respir Crit Care Med 2002; 165: 1205-1206.
4. Strieter RM. Con: Inflammatory mechanisms are not a minor component of the pathogenesis of idiopathic pulmonary fibrosis. Am J Respir Crit Care Med 2002; 165: 1206-1207.
5. Maher TM, Wells AU, Laurent GJ. Idiopathic pulmonary fibrosis: multiple causes and multiple mechanisms? Eur Respir J 2007; 30: 835-839.
6. Bhatt N, Baran CP, Allen J, et al. Promising pharmacologic innovations in treating pulmonary fibrosis. Curr Opin Pharmacol 2006; 6: 284-292.
7. Bolden JE, Peart MJ, Johnstone RW. Anticancer activities of histone deacetylase inhibitors. Nat Rev Drug Discov 2006; 5: 769-784.
8. Rishikof DC, Ricupero DA, Liu H, et al. Phenylbutyrate decreases type I collagen production in human lung fibroblasts. J Cell Biochem 2004; 91: 740-748.
9. Niki T, Rombouts K, De Bleser P, et al. A histone deacetylase inhibitor, trichostatin A, suppresses myofibroblastic differentiation of rat hepatic stellate cells in primary culture. Hematology 1999; 29: 858-867.
10. Rombouts K, Niki T, Greenwel P, et al. Trichostatin A, a histone deacetylase inhibitor, suppresses collagen synthesis and prevents TGF-β(1)-induced fibrogenesis in skin fibroblasts. Exp Cell Res 2002; 278: 184-197.
11. Huber LC, Distler JH, Moritz F, et al. Trichostatin A prevents the accumulation of extracellular matrix in a mouse model of bleomycin-induced skin fibrosis. Arthritis Rheum 2007; 56: 2755-2764.
12. Marks PA, Breslow R. Dimethyl sulfoxide to vorinostat: development of this histone deacetylase inhibitor as an anticancer drug. Nat Biotechnol 2007; 25: 84-90.
13. Stowell JC, Huot RI, Van Voast L. The synthesis of N-hydroxy-N′ phenyloctanediamide and its inhibitory effect on proliferation of AXC rat prostate cancer cells. J Med Chem 1995; 38: 1411-1413.
14. Lareu RR, Subramhanya KH, Peng Y, et al. Collagen matrix deposition is dramatically enhanced in vitro when crowded with charged macromolecules: the biological relevance of the excluded volume effect. FEBS Lett 2007; 581: 2709-2714.
15. Gribbin J, Hubbard RB, Le Jeune I, et al. Incidence and mortality of idiopathic pulmonary fibrosis and sarcoidosis in the UK. Thorax 2006; 61: 980-985.
16. Young DA, Billingham O, Sampieri CL, et al. Differential effects of histone deacetylase inhibitors on phorbol ester- and TGF-β1 induced murine tissue inhibitor of metalloproteinases-1 gene expression. FEBS J 2005; 272: 1912-1926.
17. Arts J, Angibaud P, Mariën A, et al. R306465 is a novel potent inhibitor of class I histone deacetylases with broad-spectrum antitumoral activity against solid and haematological malignancies. Br J Cancer 2007; 97: 1344-1353.
18. Ghosh AK, Mori Y, Dowling E, et al. Trichostatin A blocks TGF-β-induced collagen gene expression in skin fibroblasts: involvement of Sp1. Biochem Biophys Res Commun 2007; 354: 420-426.
19. Glenisson W, Castronovo V, Waltregny D. Histone deacetylase 4 is required for TGFβ1-induced myofibroblastic differentiation. Biochim Biophys Acta 2007; 1773: 1572-1582.
20. Hubbert C, Guardiola A, Shao R, et al. HDAC6 is a microtubule-associated deacetylase. Nature 2002; 417: 455-458.
21. Tran AD, Marmo TP, Salam AA, et al. HDAC6 deacetylation of tubulin modulates dynamics of cellular adhesions. J Cell Sci 2007; 120: 1469-1479.
22. Wynn TA. Common and unique mechanisms regulate fibrosis in various fibroproliferative diseases. J Clin Invest 2007; 117: 524-529.
23. Bode KA, Schroder K, Hume DA, et al. Histone deacetylase inhibitors decrease Toll-like receptor-mediated activation of proinflammatory gene expression by impairing transcription factor recruitment. Immunology 2007; 122: 596-606.
24. Zhu Z, Homer RJ, Wang Z, et al. Pulmonary expression of interleukin-13 causes inflammation, mucus hypersecretion, subepithelial fibrosis, physiologic abnormalities, and eotaxin production. J Clin Invest 1999; 103: 779-788.
25. Lanone S, Zheng T, Zhu Z, et al. Overlapping and enzyme-specific contributions of matrix metalloproteinases-9 and -12 in IL-13-induced inflammation and remodelling. J Clin Invest 2002; 110: 463-474.
26. Borowski A, Kuepper M, Horn U, et al. Interleukin-13 acts as an apoptotic effector on lung epithelial cells and induces pro-fibrotic gene expression in lung fibroblasts. Clin Exp Allergy 2008; 38: 619-628.
27. Nakagome K, Dohi M, Okunishi K, et al. In vivo IL-10 gene delivery attenuates bleomycin induced pulmonary fibrosis by inhibiting the production and activation of TGF-β in the lung. Thorax 2006; 61: 886-894.
28. Lee CG, Homer RJ, Cohn L, et al. Transgenic overexpression of interleukin (IL)-10 in the lung causes mucus metaplasia, tissue inflammation, and airway remodeling via IL-13-dependent and -independent pathways. J Biol Chem 2002; 277: 35466-35474.
29. Barbarin V, Arras M, Misson P, et al. Characterization of the effect of interleukin-10 on silica-induced lung fibrosis in mice. Am J Respir Cell Mol Biol 2004; 31: 78-85.
30. Barbarin V, Xing Z, Delos M, et al. Pulmonary overexpression of IL-10 augments lung fibrosis and Th2 responses induced by silica particles. Am J Physiol Lung Cell Mol Physiol 2005; 288: L841-L848.