Hypoxia-inducible factor 1α induces corticosteroid-insensitive inflammation via reduction of histone deacetylase-2 transcription

C.E. Charron, P.-C. Chou, D.J.C. Coutts, V. Kumar, M. To, K. Akashi, L. Pinhu, M. Griffiths, I.M. Adcock, P.J. Barnes, K. Ito

Research output: Contribution to journalArticle

29 Citations (Scopus)

Abstract

Corticosteroids are potent anti-inflammatory agents, but corticosteroid insensitivity is a major barrier for the treatment of some chronic inflammatory diseases. Here, we show that hypoxia induces corticosteroid-insensitive inflammation via reduced transcription of histone deacetylase-2 (HDAC2) in lung epithelial and macrophage cells. HDAC2 mRNA and protein expression was reduced under hypoxic conditions (1% O2). Hypoxia enhanced interleukin-1β-induced interleukin-8 (CXCL8) production in A549 cells and decreased the ability of dexamethasone to suppress the CXCL8 production. Deletion or point mutation studies revealed that binding of the transcription factor hypoxia-inducible factor (HIF) 1a to a HIF response element at position 320, but not HIF-1b or HIF-2a, results in reduced polymerase II binding at the site, leading to reduced promoter activity ofHDAC2.Our results suggest that activation of HIF-1α by hypoxia decreases HDAC2 levels, resulting in amplified inflammation and corticosteroid resistance. © 2009 by The American Society for Biochemistry and Molecular Biology, Inc.
Original languageEnglish
Pages (from-to)36047-36054
Number of pages8
JournalJournal of Biological Chemistry
Volume284
Issue number52
DOIs
Publication statusPublished - Dec 25 2009

Fingerprint

Histone Deacetylase 2
Hypoxia-Inducible Factor 1
Transcription
Adrenal Cortex Hormones
Inflammation
Macrophages
Response Elements
Interleukin-8
Interleukin-1
Dexamethasone
Anti-Inflammatory Agents
Transcription Factors
Chemical activation
Sequence Deletion
Messenger RNA
Hypoxia
Point Mutation
Chronic Disease
Epithelial Cells
Binding Sites

Keywords

  • A549 cells
  • Anti-inflammatory agents
  • Chronic inflammatory disease
  • Dexamethasones
  • Histone deacetylases
  • Hypoxia-inducible factor 1
  • Hypoxia-inducible factors
  • Hypoxic condition
  • Interleukin-1
  • Interleukin-8
  • Macrophage cells
  • Point mutations
  • Polymerase II
  • Promoter activities
  • Protein expressions
  • Response elements
  • Pathology
  • Transcription
  • Transcription factors
  • Drug products
  • corticosteroid
  • dexamethasone
  • DNA directed DNA polymerase alpha
  • histone deacetylase 2
  • hypoxia inducible factor 1alpha
  • hypoxia inducible factor 1beta
  • hypoxia inducible factor 2alpha
  • interleukin 8
  • messenger RNA
  • article
  • binding site
  • cell strain
  • controlled study
  • cytokine production
  • drug resistance
  • gene deletion
  • gene expression
  • gene function
  • human
  • human cell
  • hypoxia
  • inflammation
  • lung alveolus epithelium
  • macrophage
  • mutational analysis
  • point mutation
  • priority journal
  • promoter region
  • protein binding
  • protein degradation
  • protein expression
  • transcription initiation
  • transcription regulation
  • Basic Helix-Loop-Helix Transcription Factors
  • Cell Hypoxia
  • Dexamethasone
  • Drug Resistance
  • Gene Expression Regulation, Enzymologic
  • Glucocorticoids
  • Histone Deacetylase 2
  • Humans
  • Hypoxia-Inducible Factor 1, alpha Subunit
  • Inflammation
  • Interleukin-1beta
  • Macrophages
  • Point Mutation
  • Respiratory Mucosa
  • Response Elements
  • RNA, Messenger
  • U937 Cells

Cite this

Hypoxia-inducible factor 1α induces corticosteroid-insensitive inflammation via reduction of histone deacetylase-2 transcription. / Charron, C.E.; Chou, P.-C.; Coutts, D.J.C.; Kumar, V.; To, M.; Akashi, K.; Pinhu, L.; Griffiths, M.; Adcock, I.M.; Barnes, P.J.; Ito, K.

In: Journal of Biological Chemistry, Vol. 284, No. 52, 25.12.2009, p. 36047-36054.

Research output: Contribution to journalArticle

Charron, CE, Chou, P-C, Coutts, DJC, Kumar, V, To, M, Akashi, K, Pinhu, L, Griffiths, M, Adcock, IM, Barnes, PJ & Ito, K 2009, 'Hypoxia-inducible factor 1α induces corticosteroid-insensitive inflammation via reduction of histone deacetylase-2 transcription', Journal of Biological Chemistry, vol. 284, no. 52, pp. 36047-36054. https://doi.org/10.1074/jbc.M109.025387
Charron, C.E. ; Chou, P.-C. ; Coutts, D.J.C. ; Kumar, V. ; To, M. ; Akashi, K. ; Pinhu, L. ; Griffiths, M. ; Adcock, I.M. ; Barnes, P.J. ; Ito, K. / Hypoxia-inducible factor 1α induces corticosteroid-insensitive inflammation via reduction of histone deacetylase-2 transcription. In: Journal of Biological Chemistry. 2009 ; Vol. 284, No. 52. pp. 36047-36054.
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abstract = "Corticosteroids are potent anti-inflammatory agents, but corticosteroid insensitivity is a major barrier for the treatment of some chronic inflammatory diseases. Here, we show that hypoxia induces corticosteroid-insensitive inflammation via reduced transcription of histone deacetylase-2 (HDAC2) in lung epithelial and macrophage cells. HDAC2 mRNA and protein expression was reduced under hypoxic conditions (1{\%} O2). Hypoxia enhanced interleukin-1β-induced interleukin-8 (CXCL8) production in A549 cells and decreased the ability of dexamethasone to suppress the CXCL8 production. Deletion or point mutation studies revealed that binding of the transcription factor hypoxia-inducible factor (HIF) 1a to a HIF response element at position 320, but not HIF-1b or HIF-2a, results in reduced polymerase II binding at the site, leading to reduced promoter activity ofHDAC2.Our results suggest that activation of HIF-1α by hypoxia decreases HDAC2 levels, resulting in amplified inflammation and corticosteroid resistance. {\circledC} 2009 by The American Society for Biochemistry and Molecular Biology, Inc.",
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note = "引用次數:25 Export Date: 13 September 2018 CODEN: JBCHA 通訊地址: Charron, C.E.; Section of Airway Disease, National Heart and Lung Institute, Imperial College London, London SW3 6LY, United Kingdom; 電子郵件: c.charron@imperial.ac.uk 化學物質/CAS: dexamethasone, 50-02-2; interleukin 8, 114308-91-7; Basic Helix-Loop-Helix Transcription Factors; Dexamethasone, 50-02-2; Glucocorticoids; HDAC2 protein, human, 3.5.1.98; HIF1A protein, human; Histone Deacetylase 2, 3.5.1.98; Hypoxia-Inducible Factor 1, alpha Subunit; IL8 protein, human; Interleukin-1beta; Interleukin-8; RNA, Messenger; endothelial PAS domain-containing protein 1 參考文獻: Lee, K.A., Roth, R.A., LaPres, J.J., (2007) Pharmacol. Ther, 113, pp. 229-246; Wenger, R.H., Stiehl, D.P., Camenisch, G., (2005) Sci. STKE, 2005, pp. re12; Guzy, R.D., Hoyos, B., Robin, E., Chen, H., Liu, L., Mansfield, K.D., Simon, M.C., Schumacker, P.T., (2005) Cell Metab, 1, pp. 401-408; Blouin, C.C., Pag{\'e}, E.L., Soucy, G.M., Richard, D.E., (2004) Blood, 103, pp. 1124-1130; Thornton, R.D., Lane, P., Borghaei, R.C., Pease, E.A., Caro, J., Mochan, E., (2000) Biochem. J, 350, pp. 307-312; Tacchini, L., De Ponti, C., Matteucci, E., Follis, R., Desiderio, M.A., (2004) Carcinogenesis, 25, pp. 2089-2100; Barnes, P.J., Adcock, I.M., Ito, K., (2005) Eur. Respir. J, 25, pp. 552-563; Ito, K., Barnes, P.J., Adcock, I.M., (2000) Mol. Cell. Biol, 20, pp. 6891-6903; Ito, K., Caramori, G., Lim, S., Oates, T., Chung, K.F., Barnes, P.J., Adcock, I.M., (2002) Am. J. Respir. Crit. Care Med, 166, pp. 392-396; Ito, K., Yamamura, S., Essilfie-Quaye, S., Cosio, B., Ito, M., Barnes, P.J., Adcock, I.M., (2006) J. Exp. Med, 203, pp. 7-13; Ito, K., Ito, M., Elliott, W.M., Cosio, B., Caramori, G., Kon, O.M., Barczyk, A., Barnes, P.J., (2005) N. Engl. J. Med, 352, pp. 1967-1976; Smith, S.J., Fenwick, P.S., Nicholson, A.G., Kirschenbaum, F., Finney- Hayward, T.K., Higgins, L.S., Giembycz, M.A., Donnelly, L.E., (2006) Br. J. Pharmacol, 149, pp. 393-404; McDonough, M.A., Li, V., Flashman, E., Chowdhury, R., Mohr, C., Li{\'e}nard, B.M., Zondlo, J., Schofield, C.J., (2006) Proc. Natl. Acad. Sci. U.S.A, 103, pp. 9814-9819; Kim, K.S., Rajagopal, V., Gonsalves, C., Johnson, C., Kalra, V.K., (2006) J. Immunol, 177, pp. 7211-7224; Sengupta, N., Seto, E., (2004) J. Cell. Biochem, 93, pp. 57-67; Komarova, E.A., Krivokrysenko, V., Wang, K., Neznanov, N., Chernov, M.V., Komarov, P.G., Brennan, M.L., Gudkov, A.V., (2005) FASEB J, 19, pp. 1030-1032; Mejlvang, J., Kriajevska, M., Vandewalle, C., Chernova, T., Sayan, A.E., Berx, G., Mellon, J.K., Tulchinsky, E., (2007) Mol. Biol. Cell, 18, pp. 4615-4624; Ebert, B.L., Bunn, H.F., (1998) Mol. Cell. Biol, 18, pp. 4089-4096; Wyrwicz, L.S., Gaj, P., Hoffmann, M., Rychlewski, L., Ostrowski, J., (2007) Acta Biochim. Pol, 54, pp. 89-98; Kim, M.S., Kwon, H.J., Lee, Y.M., Baek, J.H., Jang, J.E., Lee, S.W., Moon, E.J., Kim, K.W., (2001) Nat. Med, 7, pp. 437-443; Pluemsampant, S., Safronova, O.S., Nakahama, K., Morita, I., (2008) Int. J. Cancer, 122, pp. 333-341; Kato, H., Tamamizu-Kato, S., Shibasaki, F., (2004) J. Biol. Chem, 279, pp. 41966-41974; Metzen, E., Zhou, J., Jelkmann, W., Fandrey, J., Br{\"u}ne, B., (2003) Mol. Biol. Cell, 14, pp. 3470-3481; Brindicci, C., Ito, K., Resta, O., Pride, N.B., Barnes, P.J., Kharitonov, S.A., (2005) Eur. Respir. J, 26, pp. 52-59; Nagy, G., Clark, J.M., Buzas, E., Gorman, C., Pasztoi, M., Koncz, A., Falus, A., Cope, A.P., (2008) Immunol. Lett, 118, pp. 55-58; Lim, K.H., Ancrile, B.B., Kashatus, D.F., Counter, C.M., (2008) Nature, 452, pp. 646-649; Gerald, D., Berra, E., Frapart, Y.M., Chan, D.A., Giaccia, A.J., Mansuy, D., Pouyss{\'e}gur, J., Mechta-Grigoriou, F., (2004) Cell, 118, pp. 781-794; Bonello, S., Z{\"a}hringer, C., BelAiba, R.S., Djordjevic, T., Hess, J., Michiels, C., Kietzmann, T., G{\"o}rlach, A., (2007) Arterioscler. Thromb. Vasc. Biol, 27, pp. 755-761; Barnes, P.J., (2007) PLoS Med, 4, pp. e112; Filippin, L.I., Vercelino, R., Marroni, N.P., Xavier, R.M., (2008) Clin. Exp. Immunol, 152, pp. 415-422",
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TY - JOUR

T1 - Hypoxia-inducible factor 1α induces corticosteroid-insensitive inflammation via reduction of histone deacetylase-2 transcription

AU - Charron, C.E.

AU - Chou, P.-C.

AU - Coutts, D.J.C.

AU - Kumar, V.

AU - To, M.

AU - Akashi, K.

AU - Pinhu, L.

AU - Griffiths, M.

AU - Adcock, I.M.

AU - Barnes, P.J.

AU - Ito, K.

N1 - 引用次數:25 Export Date: 13 September 2018 CODEN: JBCHA 通訊地址: Charron, C.E.; Section of Airway Disease, National Heart and Lung Institute, Imperial College London, London SW3 6LY, United Kingdom; 電子郵件: c.charron@imperial.ac.uk 化學物質/CAS: dexamethasone, 50-02-2; interleukin 8, 114308-91-7; Basic Helix-Loop-Helix Transcription Factors; Dexamethasone, 50-02-2; Glucocorticoids; HDAC2 protein, human, 3.5.1.98; HIF1A protein, human; Histone Deacetylase 2, 3.5.1.98; Hypoxia-Inducible Factor 1, alpha Subunit; IL8 protein, human; Interleukin-1beta; Interleukin-8; RNA, Messenger; endothelial PAS domain-containing protein 1 參考文獻: Lee, K.A., Roth, R.A., LaPres, J.J., (2007) Pharmacol. Ther, 113, pp. 229-246; Wenger, R.H., Stiehl, D.P., Camenisch, G., (2005) Sci. STKE, 2005, pp. re12; Guzy, R.D., Hoyos, B., Robin, E., Chen, H., Liu, L., Mansfield, K.D., Simon, M.C., Schumacker, P.T., (2005) Cell Metab, 1, pp. 401-408; Blouin, C.C., Pagé, E.L., Soucy, G.M., Richard, D.E., (2004) Blood, 103, pp. 1124-1130; Thornton, R.D., Lane, P., Borghaei, R.C., Pease, E.A., Caro, J., Mochan, E., (2000) Biochem. J, 350, pp. 307-312; Tacchini, L., De Ponti, C., Matteucci, E., Follis, R., Desiderio, M.A., (2004) Carcinogenesis, 25, pp. 2089-2100; Barnes, P.J., Adcock, I.M., Ito, K., (2005) Eur. Respir. J, 25, pp. 552-563; Ito, K., Barnes, P.J., Adcock, I.M., (2000) Mol. Cell. Biol, 20, pp. 6891-6903; Ito, K., Caramori, G., Lim, S., Oates, T., Chung, K.F., Barnes, P.J., Adcock, I.M., (2002) Am. J. Respir. Crit. Care Med, 166, pp. 392-396; Ito, K., Yamamura, S., Essilfie-Quaye, S., Cosio, B., Ito, M., Barnes, P.J., Adcock, I.M., (2006) J. Exp. Med, 203, pp. 7-13; Ito, K., Ito, M., Elliott, W.M., Cosio, B., Caramori, G., Kon, O.M., Barczyk, A., Barnes, P.J., (2005) N. Engl. J. Med, 352, pp. 1967-1976; Smith, S.J., Fenwick, P.S., Nicholson, A.G., Kirschenbaum, F., Finney- Hayward, T.K., Higgins, L.S., Giembycz, M.A., Donnelly, L.E., (2006) Br. J. Pharmacol, 149, pp. 393-404; McDonough, M.A., Li, V., Flashman, E., Chowdhury, R., Mohr, C., Liénard, B.M., Zondlo, J., Schofield, C.J., (2006) Proc. Natl. Acad. Sci. U.S.A, 103, pp. 9814-9819; Kim, K.S., Rajagopal, V., Gonsalves, C., Johnson, C., Kalra, V.K., (2006) J. Immunol, 177, pp. 7211-7224; Sengupta, N., Seto, E., (2004) J. Cell. Biochem, 93, pp. 57-67; Komarova, E.A., Krivokrysenko, V., Wang, K., Neznanov, N., Chernov, M.V., Komarov, P.G., Brennan, M.L., Gudkov, A.V., (2005) FASEB J, 19, pp. 1030-1032; Mejlvang, J., Kriajevska, M., Vandewalle, C., Chernova, T., Sayan, A.E., Berx, G., Mellon, J.K., Tulchinsky, E., (2007) Mol. Biol. Cell, 18, pp. 4615-4624; Ebert, B.L., Bunn, H.F., (1998) Mol. Cell. Biol, 18, pp. 4089-4096; Wyrwicz, L.S., Gaj, P., Hoffmann, M., Rychlewski, L., Ostrowski, J., (2007) Acta Biochim. Pol, 54, pp. 89-98; Kim, M.S., Kwon, H.J., Lee, Y.M., Baek, J.H., Jang, J.E., Lee, S.W., Moon, E.J., Kim, K.W., (2001) Nat. Med, 7, pp. 437-443; Pluemsampant, S., Safronova, O.S., Nakahama, K., Morita, I., (2008) Int. J. Cancer, 122, pp. 333-341; Kato, H., Tamamizu-Kato, S., Shibasaki, F., (2004) J. Biol. Chem, 279, pp. 41966-41974; Metzen, E., Zhou, J., Jelkmann, W., Fandrey, J., Brüne, B., (2003) Mol. Biol. Cell, 14, pp. 3470-3481; Brindicci, C., Ito, K., Resta, O., Pride, N.B., Barnes, P.J., Kharitonov, S.A., (2005) Eur. Respir. J, 26, pp. 52-59; Nagy, G., Clark, J.M., Buzas, E., Gorman, C., Pasztoi, M., Koncz, A., Falus, A., Cope, A.P., (2008) Immunol. Lett, 118, pp. 55-58; Lim, K.H., Ancrile, B.B., Kashatus, D.F., Counter, C.M., (2008) Nature, 452, pp. 646-649; Gerald, D., Berra, E., Frapart, Y.M., Chan, D.A., Giaccia, A.J., Mansuy, D., Pouysségur, J., Mechta-Grigoriou, F., (2004) Cell, 118, pp. 781-794; Bonello, S., Zähringer, C., BelAiba, R.S., Djordjevic, T., Hess, J., Michiels, C., Kietzmann, T., Görlach, A., (2007) Arterioscler. Thromb. Vasc. Biol, 27, pp. 755-761; Barnes, P.J., (2007) PLoS Med, 4, pp. e112; Filippin, L.I., Vercelino, R., Marroni, N.P., Xavier, R.M., (2008) Clin. Exp. Immunol, 152, pp. 415-422

PY - 2009/12/25

Y1 - 2009/12/25

N2 - Corticosteroids are potent anti-inflammatory agents, but corticosteroid insensitivity is a major barrier for the treatment of some chronic inflammatory diseases. Here, we show that hypoxia induces corticosteroid-insensitive inflammation via reduced transcription of histone deacetylase-2 (HDAC2) in lung epithelial and macrophage cells. HDAC2 mRNA and protein expression was reduced under hypoxic conditions (1% O2). Hypoxia enhanced interleukin-1β-induced interleukin-8 (CXCL8) production in A549 cells and decreased the ability of dexamethasone to suppress the CXCL8 production. Deletion or point mutation studies revealed that binding of the transcription factor hypoxia-inducible factor (HIF) 1a to a HIF response element at position 320, but not HIF-1b or HIF-2a, results in reduced polymerase II binding at the site, leading to reduced promoter activity ofHDAC2.Our results suggest that activation of HIF-1α by hypoxia decreases HDAC2 levels, resulting in amplified inflammation and corticosteroid resistance. © 2009 by The American Society for Biochemistry and Molecular Biology, Inc.

AB - Corticosteroids are potent anti-inflammatory agents, but corticosteroid insensitivity is a major barrier for the treatment of some chronic inflammatory diseases. Here, we show that hypoxia induces corticosteroid-insensitive inflammation via reduced transcription of histone deacetylase-2 (HDAC2) in lung epithelial and macrophage cells. HDAC2 mRNA and protein expression was reduced under hypoxic conditions (1% O2). Hypoxia enhanced interleukin-1β-induced interleukin-8 (CXCL8) production in A549 cells and decreased the ability of dexamethasone to suppress the CXCL8 production. Deletion or point mutation studies revealed that binding of the transcription factor hypoxia-inducible factor (HIF) 1a to a HIF response element at position 320, but not HIF-1b or HIF-2a, results in reduced polymerase II binding at the site, leading to reduced promoter activity ofHDAC2.Our results suggest that activation of HIF-1α by hypoxia decreases HDAC2 levels, resulting in amplified inflammation and corticosteroid resistance. © 2009 by The American Society for Biochemistry and Molecular Biology, Inc.

KW - A549 cells

KW - Anti-inflammatory agents

KW - Chronic inflammatory disease

KW - Dexamethasones

KW - Histone deacetylases

KW - Hypoxia-inducible factor 1

KW - Hypoxia-inducible factors

KW - Hypoxic condition

KW - Interleukin-1

KW - Interleukin-8

KW - Macrophage cells

KW - Point mutations

KW - Polymerase II

KW - Promoter activities

KW - Protein expressions

KW - Response elements

KW - Pathology

KW - Transcription

KW - Transcription factors

KW - Drug products

KW - corticosteroid

KW - dexamethasone

KW - DNA directed DNA polymerase alpha

KW - histone deacetylase 2

KW - hypoxia inducible factor 1alpha

KW - hypoxia inducible factor 1beta

KW - hypoxia inducible factor 2alpha

KW - interleukin 8

KW - messenger RNA

KW - article

KW - binding site

KW - cell strain

KW - controlled study

KW - cytokine production

KW - drug resistance

KW - gene deletion

KW - gene expression

KW - gene function

KW - human

KW - human cell

KW - hypoxia

KW - inflammation

KW - lung alveolus epithelium

KW - macrophage

KW - mutational analysis

KW - point mutation

KW - priority journal

KW - promoter region

KW - protein binding

KW - protein degradation

KW - protein expression

KW - transcription initiation

KW - transcription regulation

KW - Basic Helix-Loop-Helix Transcription Factors

KW - Cell Hypoxia

KW - Dexamethasone

KW - Drug Resistance

KW - Gene Expression Regulation, Enzymologic

KW - Glucocorticoids

KW - Histone Deacetylase 2

KW - Humans

KW - Hypoxia-Inducible Factor 1, alpha Subunit

KW - Inflammation

KW - Interleukin-1beta

KW - Macrophages

KW - Point Mutation

KW - Respiratory Mucosa

KW - Response Elements

KW - RNA, Messenger

KW - U937 Cells

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U2 - 10.1074/jbc.M109.025387

DO - 10.1074/jbc.M109.025387

M3 - Article

VL - 284

SP - 36047

EP - 36054

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JF - Journal of Biological Chemistry

SN - 0021-9258

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