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Miscellaneous

Airway smooth muscle: new targets for asthma pharmacotherapy

Pages 447-459 | Published online: 25 Feb 2005

Bibliography

  • AMRANI Y, PANETTIERI RA JR: Cytokines induce airway smooth muscle cell hyperresponsiveness to contractile agonists. Thorax (1998) 53:713–716.
  • COBURN RF, BARON CB: Coupling mechanisms in airway smooth muscle. Am.Physiol. (1990) 258:L119–L133.
  • GIEMBYCZ MA, RAEBURN D: Current concepts on mechanisms of force generation and maintenance in airway smooth muscle. Palm. Pharmacol. (1992) 5:279–297.
  • SCHMIDT D, RUEHLMANN E, BRANSCHEID D, MAGNUSSEN H, RABE KF: Passive sensitization of human airways increases responsiveness to leukotriene C4. Eur: Respir: 1 (1999) 14:315-319.
  • BLACK JL, MARTHAN R, ARMOUR CL, JOHNSON PRSensitization alters contractile responses and calcium influx in human airway smooth muscle. J. Aller. Clin. Immunol. (1989) 84:440–447.
  • MARTHAN R, CREVEL H,GUENARD H, SAVINEAU JP: Responsiveness to histamine in human sensitized airway smooth muscle. Respir: Physiol. (1992) 90:239–250.
  • KIPS JC, TAVERNIER JH,PAUWELS RA: Tumor necrosis factor (TNF) causes bronchial hyperresponsivenessin rats. Am. Rev Resp. Dis. (1992) 145:332–336.
  • TSUKAGOSHI H, SAKAMOTO T, XU W, BARNES PJ, CHUNG KF: Effect of interleukin-113 on airway hyperresponsiveness and inflammation in sensitized and nonsensitized Brown-Norway rats. Aller: Clin. Immunol. (1994) 93:464–469.
  • THOMAS PS, YATES DH, BARNES JP: Tumor necrosis factor-a increases airway responsiveness and sputum neutrophilia in normal human subjects. Am. Respir: Crit. Care Med. (1995) 152:76–80.
  • PENNINGS HJ, KRAMER K, BAST A, BUURMAN W, WOUTERS E: Tumour necrosis factor causes hyperresponsiveness in tracheal smooth muscle of the guinea-pig model M vitro. Eur. Respir. J. (1993) 70:325s.
  • HAKONARSON H, HERRICK DJ, SERRANO PG, GRUNSTEIN MM: Autocrine role of interleukin 113 in altered responsiveness of atopic asthmatic sensitized airway smooth muscle. Clin. Invest. (1997) 99:117–124.
  • TOEWS ML, USTINOVA EE, SCHULTZ HD: Lysophosphatidic acidenhances contractility of isolated airway smooth muscle. J. Appl. Physiol. (1997) 83:1216–1222.
  • TAKATA Y, NISHIMURA Y, MAEDA H, YOKOYAMA M: Phospholipase A2 augments contraction and intracellular calcium mobilization through thromboxaneA2 in bovine tracheal smooth muscle. Eur. Respir. J. (1999) 14:396–404.
  • REYNOLDS AM, HOLMES MD, SCICCHITANO R: Cytokines enhance airway smooth muscle contractility in response to acetylcholine and neurokinin A. Respirology (2000) 5:153–160.
  • SETOGUCHI H, NISHIMURA J, HIRANO K, TAKAHASHI S,KANAIDE H: Leukotriene C(4) enhances the contraction of porcine tracheal smooth muscle through the activation of Y-27632, a rho kinase inhibitor, sensitive pathway. Br. J. Pharmacol. (2001) 132:111–118.
  • AMRANI Y, MARTINET N,BRONNER C: Potentiation by tumour necrosis factor-a of calcium signals induced by bradykinin and carbachol in human tracheal smooth muscle cells. Br. J. Pharmacol. (1995) 114:4–5.
  • SCHMIDLIN F, SCHERRER D, DAEFFLER L, BERTRAND C,LANDRY Y, GIES JP: Interleukin-1I3 induces bradykinin B2 receptor gene expression through a prostanoid cyclic AMP dependent pathway in human bronchial smooth muscle cells. Mol. Pharm. (1998) 53:1009–1015.
  • WYLAM ME, GUNGOR N, MITCHELL RW, UMANS JG:Eosinophils, major basic protein, and polycationic peptides augment bovine airway myocyte Ca2+ mobilization. Am. J. Physiol. (1998) 274:L997–L1005.
  • SCHMIDT D, RABE KF: Immune mechanisms of smooth muscle hyperreactivity in asthma. j All. Clin. Immunol. (2000) 105:673–682.
  • PARRIS JR, COBBAN HJ, LITTLEJOHN AF, MACEWAN DJ, NIXON GF: Tumor necrosis factor-a activates a calcium sensitization pathway in guinea-pig bronchial smooth muscle.Physiol (1999) 518:561–569.
  • NAKATANI Y, NISHIMURA Y, NISHIUMUA T, MAEDA H, YOKOYAMA M: Tumor necrosis factor-a augments contraction and cytosolic Ca2+ through phospholipase A2 in bovine tracheal smooth muscle. Eut: Pharmacol(2000) 392:175–182.
  • AMMIT AJ, ARMOUR CL, BLACK JL: Smooth-muscle myosin light-chain kinase content is increased in human sensitized airways. Am. I Respit Grit. Care Med. (2000) 161:257–263.
  • JIANG H, RAO K, LIU X, LIU G, STEPHENS NL: Increased Ca2+ andmyosin phosphorylation, but not calmodulin activity in sensitized airway smooth muscles. Am. J. Physic] (1995) 268:L739–L746.
  • PANETTIERI RA JR, KOTLIKOFF MI:Cellular and molecular mechanisms regulating airway smooth muscle cell physiology and pharmacology. In:Pulmonary Diseases and Disorders (Third Edition). Fishman AP, Elias JA, Fishman JA, Grippi MA, Kaiser LR, Senior RM (Eds), McGraw-Hill, New York, USA (1998) 107–117.
  • HOTTA K, EMALA CW,HIRSHMAN CA: TNF-a upregulates Ga and Gga protein expression and function in human airway smooth muscle cells. Am. J. Physiol (1999) 276:L405–L411.
  • EMALA CW, KUHL J,HUNGERFORD CL, HIRSHMAN CA: TNFa inhibits isoproterenol-stimulated adenylyl cyclase activity in cultured airway smooth muscle cells. Am. Physiol (1997) 272:L644–L650.
  • SHORE SA, LAPORTE J, HALL IP, HARDY E, PANETTIERI RA JR: Effect of IL-1I3 on responses of cultured human airway smooth muscle cells to bronchodilator agonists. Am. J. Respir. Cell MM. Biol. (1997) 16:702–712.
  • MOORE PE, LAHIRI T, LAPORTE JD,CHURCH T, PANETTIERI RA JR, SHORE SA: Synergism between TNF-a and IL-1I3 in airway smooth muscle cells: implications for beta-adrenergicresponsiveness. J. Appl. Physic] (2001) 91:1467–1474.
  • LAPORTE JD, MOORE PE,BARALDO S et al.: Direct effects of interleukin-13 on signaling pathways for physiological responses in cultured human airway smooth muscle cells. Am. J. Respir. Grit. Care Med. (2001) 164:141–148.
  • LAZAAR AL, AMRANI Y,PANETTIERI RA JR: The role of inflammation in the regulation of airway smooth muscle cell function and growth. In: Asthma and Rhinitts Busse W,Holgate S, (Eds), Blackwell Science, Ltd., Oxford, UK (2000) 1402–1413.
  • BERKMAN N, KRISHNAN VL, GILBEY T et al.: Expression of RANTES mRNA and protein in airways of patients with mild asthma. Am. I Respit Grit. Care Med. (1996) 154:1804–1811.
  • JOHN M, HIRST SJ, JOSE PJ et al.: Human airway smooth muscle cells express and release RANTES in response to T helper 1 cytokines. Immunol (1997) 158: 1841-1847.
  • PYPE JL, DUPONT LJ,MENTEN P et al.: Expression of monocyte chemotactic protein (MCP)-1, MCP-2, and MCP-3 by human airway smooth-muscle cells. Modulation by corticosteroids and T-helper 2 cytokines. Am. I Respit: Cell Ma Biol. (1999) 21:528–536.
  • AMMIT AJ, HOFFMAN RK,AMRANI Y et al.: Tumor necrosis factor-a-induced secretion of RANTES and interleukin-6 from human airway smooth-muscle cells. Modulation by cyclic adenosine monophosphate. Am. I Respir. Cell MM. Biol. (2000) 23:794–802.
  • JOHN M, AU B-T, JOSE PJ et al.: Expression and release of interleukin-8 by human airway smooth muscle cells: inhibition by Th-2 cytokines and corticosteroids. Am. Respir. Cell Ma Biol. (1998) 18:84–90.
  • PANG L, KNOX AJ: Bradyldnin stimulates IL-8 production in cultured human airway smooth muscle cells: role of cyclooxygenase products. Immunol (1998) 161:2509–2515.
  • HEDGES JC, SINGER CA,GERTHOFFER WT: Mitogen-activatedprotein kinases regulate cytokine gene expression in human airway myocytes. Am. Respir. Cell Ma Biol. (2000) 23:86–94.
  • GHAFFAR 0, HAMID Q, RENZI PM et al.: Constitutive andcytokine-stimulated expression of eotaxin by human airway smooth muscle cells. Am. Respit Cell MM. Biol. (1999) 159:1933–1942.
  • CHUNG KF, PATEL HJ,FADLON EJ et al.: Induction of eotaxin expression and release from human airway smooth muscle cells by IL-1I3 and TNFa: effects of IL-10 and corticosteroids. Br. J. Pharmacol (1999) 127:1145–1150.
  • MOORE PE, CHURCH TL,CHISM DD, PANETTIERI RA JR, SHORE SA: IL-13 and IL-4 cause eotaxin release in human airway smooth muscle cells: a role for ERK. Am. J. Physiol (2002) 282:L847–L853.
  • SOUSA AR, LANE SJ,NAKHOSTEEN JA, YOSHIMURA T, LEE TH, POSTON RN: Increased expression of the monocyte chemoattractant protein-1 in bronchial tissue from asthmatic subjects. Am. I Respir. Cell MM. Biol. (1994) 10:142–147.
  • DE S, ZELAZNY ET, SOUHRADA JF, SOUHRADA M: IL-1I3 and IL-6 induce hyperplasia and hypertrophy of cultured guinea pig airway smooth muscle cells.Appl. Physic] (1995) 78:1555–1563.
  • ELIAS JA, WU Y, ZHENG T, PANETTIERI R: Cytokine- and virus-stimulated airway smooth muscle cells produce IL-11 and other IL-6-type cytokines. Am. J. Physic] (1997) 273:L648–L655.
  • MCKAY S, HIRST SJ,BERTRAND-DE HAAS M et al.: Tumor necrosis factor-a enhances mRNA expression and secretion of interleukin-6 in cultured human airway smooth muscle cells. Am. J. Respir. Cell Ma Biol. (2000) 23:103–111.
  • AMMIT AJ, HASTIE AT,EDSALL LC et al.: Sphingosine 1-phosphate modulates human airway smooth muscle cell functions that promote inflammation and airway remodeling in asthma. FASEB (2001) 15:1212–1214.
  • DICOSMO BE GEBA GP,PICARELLA D et al.: Airway epithelial cell expression of interleukin-6 transgenic mice: uncoupling of airway inflammation and bronchial hyperreactivity. I Clin. Invest.(1994) 94:2028–2035.
  • WANG J, HOMER RJ, CHEN Q, ELIAS JA: Endogenous and exogenous IL-6 inhibit aeroallergen-induced Th2 inflammation. I Immunol (2000) 165:4051–4061.
  • SAUNDERS MA, MITCHELL JA, SELDON PM et al.: Release of granulocyte-macrophage colony stimulating factor by human cultured airway smooth muscle cells: suppression by dexamethasone. Br. J. Pharm. (1997) 120:545–546.
  • HALLSWORTH MP, SOH CPC, TWORT CHC, LEE TH, HIRST SJ: Cultured human airway smooth muscle cell stimulated by interleultin-l3 enhance eosinophil survival. Am. I Respir. Cell Mal. Biol. (1998) 19:910–919.
  • HAKONARSON H, MASKERI N, CARTER C, CHUANG S,GRUNSTEIN MM: Autocrine interaction between IL-5 and IL-1I3 mediates altered responsiveness of atopic asthmatic sensitized airway smooth muscle. J. Clin. Invest. (1999) 104:657–667.
  • KASSEL 0, SCHMIDLIN F, DUVERNELLE C, GASSER B, MASSARD G, FROSSARD N: Human bronchial smooth muscle cells in culture produce stem cell factor. Ear: Respir. (1999) 13:951–954.
  • RIZZO CA, YANG R, GREENFEDER S, EGAN RW, PAUWELS RA, HEY IA: The IL-5 receptor on human bronchus selectively primes for hyperresponsiveness.Clin. Immune] (2002) 109:404–409.
  • VENKAYYA R, LAM M, WILLKOM M, GRUNIG G, CORRY DB, ERLE DJ: The Th2 lymphocyte products IL-4 and IL-13 rapidly induce airway hyperresponsiveness through direct effects on resident airway cells. Am. J. Respir. Cell MM. Biol. (2002) 26:202–208.
  • KNIGHT DA, LYDELL CP,ZHOU D, VVEIR TD,SCHELLENBERG RR, BAI TR: Leukemia inhibitory factor (LIE) and LIF receptor in human lung: distribution and regulation of LIF release. Am. I Respir. Cell MM. Biol. (1999) 20:834–841.
  • HAKONARSON H, CARTER C, MASKERI N, HODINKA R, GRUNSTEIN MM: Rhinovirus-mediated changes in airway smooth muscle responsiveness: induced autocrine role of interleukin-l3. Am.j Physiol (1999) 277:L13–L21.
  • RODEL J, ASSEFA S,PROCHNAU D et al.: Interferon-I3 induction by Chlamydia pneumoniae in human smooth muscle cells. FEMS Immunol Med. Microbic] (2001) 32:9–15.
  • KUHN C, HOMER RJ, ZHU Z, WARD N, ELIAS JA: Morphometryexplains variation in airway responsiveness in transgenic mice overexpressing interleultin-6 and interleukin-11 in the lung. Chest (2000) 117:260S–262S.
  • LAHIRI T, LAPORTE JD, MOORE PE,PANETTIERI RA JR, SHORE SA: Interleultin-6 family cytokines: signaling and effects in human airway smooth muscle cells. Am. J. Physiol (2001) 280:L1225–L1232.
  • SPRINGER TA: Adhesion receptors of the immune system. Nature (1990) 46:425–434.
  • ••Seminal review of adhesion receptors andtheir function.
  • LAZAAR AL, ALBELDA SM,PILEWSKI JM, BRENNAN B, PURE E, PANETTIERI RA JR: T lymphocytes adhere to airway smooth muscle cells via integrins and CD44 and induce smooth muscle cell DNA synthesis. I Exp. Med. (1994) 180:807–816.
  • •First description of adhesion receptors on ASM cells.
  • FREYER AM, JOHNSON SR, HALL IP: Effects of growth factors and extracellular matrix on survival of human airway smooth muscle cells. Am. Respir. Cell Ma Biol. (2001) 25:569–576.
  • DUSTIN ML, SPRINGER TA: Role of lymphocyte adhesion receptors in transient interactions and cell locomotion. Ann. Rev. Immunol (1991) 9:27–66.
  • VAN SEVENTER GA, NEWMAN W, SHIMUZU Y et al.: Analysis of T cell stimulation by superantigen plus major histocompatibility complex class II molecules or by CD3 monoclonal antibody: costimultion by purified adhesion ligands VCAM-1, ICAM-1, but not ELAM-1. Exp. Med. (1991) 174:901–913.
  • LAZAAR AL, REITZ HE,PANETTIERI RA JR, PETERS T,PURE E: Antigen-receptor stimulated peripheral blood and bronchoalveolar lavage-derived T cells induce MHC class II and ICAM-1 expression of human airway smooth muscle. Am. I Respir. Cell Ma Biol. (1997) 16:38–45.
  • LAZAAR AL, AMRANI Y, HSU J et al: CD40-mediated signal transduction in human airway smooth muscle. I Immunol (1998) 161:3120–3127.
  • HAKONARSON H, KIM C, WHELAN R, CAMPBELL D, GRUNSTEIN MM: Bi-directional activation between human airway smooth muscle cells and T lymphocytes: role ininduction of altered airway responsiveness. J. Immune] (2001) 166:293–303.
  • LAZAAR AL, KRYMSKAYA VP, DAS SKP: VCAM-1 activates phosphatidylinositol 3-kinase and induces p120aiphosphorylation in human airway smooth muscle cells. Immunol (2001) 166:155–161.
  • HAMANN KJ, VIEIRA JE,HALAYKO Al et al.: Fas cross-linking induces apoptosis in human airway smooth muscle cells. Ain. Physiol (2000) 278:L618–L624.
  • GASTON B, DRAZEN JM,LOSCALZO J, STAMLERJS: The biologyof nitrogen oxides in the airways. Am. Respir. Crit. Care Med. (1994) 149:538–551.
  • HAMAD AM, JOHNSON SR,KNOX AJ: Antiproliferative effects of NO and ANP in cultured human airway smooth muscle. Am. J. Physic] (1999) 277:L910–L918.
  • PATEL HJ, BELVISI MG,DONNELLY LE, YACOUB MH, CHUNG KF, MITCHELL JA: Constitutive expressions of Type I NOS in human airway smooth muscle cells: evidence for an antiproliferative role. FASEB 1. (1999) 13: 1810-1816.
  • GOW AJ, CHEN Q, HESS DT, DAY BJ,ISCHIROPOULOS H, STAMLER JS: Basal and stimulated protein S-nitrosylation in multiple cell types and tissues. Biol. Chem. (2002) 277:9637–9640.
  • BELVISI MG, SAUNDERS MA, HADDAD E-B et al.: Induction of cyclo-oxygenase-2 by cytokines in human cultured airway smooth muscle cells: novel inflammatory role of this cell type. Br. Pharmacol (1997) 120:910–916.
  • •One of the earliest reports of COX-2 induction in ASM cells.
  • HAKONARSON H, GRUNSTEIN MM: Autologously up-regulated Fc receptor expression and action in airway smooth muscle mediates its altered responsiveness in the atopic asthmatic sensitized state. Proc. Nat] Acad. Sci. USA (1998) 95:5257–5262.
  • CERNADAS M, DE SANCTIS GT, KRINZMAN SJ et al: CD23 and allergic pulmonary inflammation: potential role as an inhibitor. Am. I Respir. Cell Ma Biol. (1999) 20:1–8.
  • DASIC G, JUILLARD P, GRABER P et al.:Critical role of CD23 in allergen-induced bronchoconstriction in a murine model of
  • ••allergic asthma. Ear: J Immunol (1999) 29:2957–2967.
  • HACZKU A, TAKEDA K,HAMELMANN E et al.: CD23 exhibits negative regulatory effects on allergic sensitization and airway hyperresponsiveness. Am. J. Respir. Grit. Care Med. (2000) 161:952–960.
  • LAZZERI N, BELVISI MG, PATEL HJ, YACOUB MH, FAN CHUNG K, MITCHELL JA: Effects of prostaglandin E2 and cAMP elevating drugs on GM-CSF release by cultured human airway smooth muscle cells. Relevance to asthma therapy. Am. J. Respir. Cell MM. Biol. (2001) 24:44–48.
  • HARTERT TV, DWORSKIRT, MELLEN BG, OATES JA, MURRAY JJ, SHELLER JR: Prostaglandin E2 decreases allergen-stimulated release of prostaglandin D2 in airways of subjects with asthma. Am. Respir. Grit. Care Med. (2000) 162:637–640.
  • KAPSENBERG ML, HILKENS CM, WIERENGA EA, KALINSKI P: The paradigm of Type 1 and Type 2 antigen-presenting cells. Implications for atopic allergy. Clin. Exp. Allergy (1999)29\(Suppl. 2):33–36.
  • ROPER RL, CONRAD DH,BROWN DM, WARNER GL,PHIPPS RP: Prostaglandin E2 promotes IL-4-induced IgE and IgG1 synthesis. J. Immunol (1990) 145:2644–2651.
  • LYNCH KR, O'NEILL GP, LIU Q et al:Characterization of the human cysteinyl leukotriene CysLT1 receptor. Nature (1999) 399:789–793.
  • HEISE CE, O'DOWD BEFIGUEROA DJ et al.: Characterization of the human cysteinyl leukotriene 2 receptor. Biol Chem. (2000) 275:30531–30536.
  • AMRANI Y, MOORE PE, HOFFMAN R, SHORE SA, PANETTIERI RA JR: Interferon-7 modulates cysteinyl leukotriene receptor-1 expression and function in human airway myocytes. Am. J. Respir. Grit. Care Med. (2001) 164:2098–2101.
  • HUMBLES AA, LU B,NILSSON CA et al.: A role for the C3a anaphylatwdn receptor in the effector phase of asthma. Nature (2000) 406:998–1001.
  • KARP CL, GRUPE A, SCHADT E et al: Identification of complement factor 5 as a susceptibility locus for experimental allergic asthma. Nat. Immune] (2000) 1:221–226.
  • DE S, ZELAZNY ET, SOUHRADA JF, SOUHRADA M: Interleuldn-i3 stimulates the proliferation of cultured airway smooth muscle cells via platelet-derived growth factor. Am. J. Respir. Cell MM. Biol. (1993) 9:645–651.
  • BLACK PN, YOUNG PG, SKINNER SJ: Response of airway smooth muscle cells to TGF-beta 1: effects on growth and synthesis of glycosaminoglycans. Am. J. Physic] (1996) 271:L910–L917.
  • MCKAY S, DE JONGSTE JC,SAXENA PR, SHARMA HS: Angiotensin II induces hypertrophy of human airway smooth muscle cells: expression of transcription factors and transforming growth factor-13i. Am. J. Respir. Cell MM. Biol. (1998) 18:823–833.
  • COUTTS A, CHEN G,STEPHENS N et al.: Release of biologically active TGF-I3 from airway smooth muscle cells induces autocrine synthesis of collagen. Am. J. Physiol (2001) 280:L999–L1008.
  • KNOX AJ, CORBETT L, STOCKS J, HOLLAND E, ZHU YM, PANG L: Human airway smooth muscle cells secrete vascular endothelial growth factor: up-regulation by bradykinin via a protein kinase C and prostanoid-dependent mechanism. FASEB (2001) 15:2480–2488.
  • HOSHINO M, NAKAMURA Y, HAMID QA: Gene expression of vascular endothelial growth factor and its receptors and angiogenesis in bronchial asthma.' All. Clin. Immunol (2001) 107:1034–1038.
  • ROBERTS CR, BURKE AK: Remodelling of the extracellular matrix in asthma: proteoglycan synthesis and degradation. Can. Respir. J. (1998) 5:48–50.
  • LAITINEN A, ALTRAJA A, KAMPE M, LINDEN M, VIRTANEN I,LAITINEN LA: Tenascin is increased in airway basement membrane of asthmatics and decreased by an inhaled steroid. Am. J. Respir. Grit. Care Med. (1997) 156:951–958.
  • JOHNSON PR, BLACK JL, CARLIN S, GE Q, UNDERWOOD PA: The production of extracellular matrix proteins by human passively sensitized airway smooth-muscle cells in culture: the effect of beclomethasone. Am. J. Respir. Grit. Care Med. (2000) 162:2145–2151.
  • LAITINEN LA, LAITINEN A: Inhaled corticosteroid treatment and extracellular matrix in the airways in asthma. Int. Arch. All. Immunol (1995) 107:215–216.
  • MAUTINO G, CAPONY F,BOUSQUET J, VIGNOLA AM: Balance in asthma between matrix etalloproteinases and their inhibitors. " All. Clin. Immunol (1999) 104:530–533.
  • RAJAH R, NUNN SE, HERRICK DJ, GRUNSTEIN MM, COHEN P: Leukotriene D4 induces MMP-1, which functions as an IGFBP protease in human airway smooth muscle cells. Am. J. Physic] (1996) 271:L1014–L1022.
  • YU A, STAMENKOVIC I: Cell surface-localized matrix metalloproteinase-9 proteolytically activates TGF-I3 and promotes tumor invasion and angiogenesis. Genes Dev. (2000) 14:163–176.
  • ••Excellent paper describing the role ofMMP-9 in the activation of TGF-P.
  • FODA HD, GEORGE S, ROLLO E et al: Regulation of gelatinases in human airway smooth muscle cells: mechanism of progelatinase A activation. Am. J. Physic] (1999) 277:L174–L182.
  • KAJITA M, ITOH Y, CHIBA T et al: Membrane-type 1 matrix metalloproteinase cleaves CD44 and promotes cell migration. J. Cell. Biol. (2001) 153:893–904.
  • CORRY DB, RISHI K, KANELLIS J et al: Decreased allergic lung inflammatory cell egression and increased susceptibility to asphyxiation in MMP2-deficiency. Nat. Immunol (2002) 3:347–353.
  • GUNST SJ, TANG DD: The contractile apparatus and mechanical properties of airway smooth muscle. Ear: Respir. J. (2000) 15:600–616.
  • HALAYKO AJ, SOLWAY J: Molecular mechanisms of phenotypic plasticity in smooth muscle cells. J. Appl. Physic] (2001) 90:358–368.
  • HIRST SJ, TWORT CH, LEE TH: Differential effects of extracellular matrix proteins on human airway smooth muscle cell proliferation and phenotype. Am. J. Respir. Cell MM. Biol. (2000) 23:335–434.
  • HAKONARSON H, HALAPI E, WHELAN R, GULCHER J, STEFANSSON K, GRUNSTEIN MM: Association between IL-1 P/TNF-a-induced glucocorticoid-sensitive changes in multiple gene expression and altered responsiveness in airway smooth muscle. Am. J. Respir. Cell MM. Biol. (2001) 25:761–771.
  • HALL IP, WIDDOP S, TOWNSEND P, DAYKIN K: Control of cyclic AMP levels in primary cultures of human trachealsmooth muscle cells. Br. J. Pharmacol(1992) 107:422–428.
  • PANG L, KNOX AJ: Regulation of TNF-a-induced eotaxin release from cultured human airway smooth muscle cells byl32-agonists and corticosteroids. FASEB (2001) 115:261–269.
  • HALLSWORTH MP, TWORT CH, LEE TH, HIRST SJ: I32-adrenoceptor agonists inhibit release of eosinophil-activating cytokines from human airway smooth muscle cells. Br. J. Pharmacol (2001) 132:729–741.
  • PANG L, KNOX AJ: Synergistic inhibition by I32-agonists and corticosteroids on tumor necrosis factor-a-induced interleukin-8 release from cultured human aiway smooth-muscle cells. Am. J. Respir. Cell MM. Biol (2000) 23:79–85.
  • KANEHIRO A, IKEMURA T, MAKELA MJ et al.: Inhibition of phosphodiesterase 4 attenuates airway hyperresponsiveness and airway inflammation in a model of secondary allergen challenge. Am. J. Respir. Grit. Care Med. (2001) 163:173–184.
  • BONAZZI A, BOLLA M,BUCCELLATI C et al.: Effect of endogenous and exogenous prostaglandin E2 on interleukin- 113- induced cyclooxygenase-2 expression in human airway smooth-muscle cells. Am. J. Respir. Grit. Care Med. (2000) 162:2272–2277.
  • STOKES PEEBLES R, HASHIMOTO K, MORROW JD et al.: Selective cyclooxygenase-1 and -2 inhibitors each increase allergic inflammation and airway hyperresponsiveness in mice. Am. J. Respir. Grit. Care Med. (2002) 165:1154–1160.
  • AMMIT AJ, LAZAAR AL, IRANI C et al: Tumor necrosis factor-a-induced secretion of RANTES and interleukin-6 from human airway smooth muscle cells: modulation by glucocorticoids and I3-agonists. Am. J. Respir. Cell Ma Biol. (2002) 26:465–474.
  • OPPENHEIMER-MARKS N,KAVANAUGH AF, LIPSKY PE: Inhibition of the transendothelial migration of human T lymphocytes by prostgandin E2. Immunol (1994) 152:5703–5713.
  • TO SS, SCHREIBER L: Effect of leukotriene B4 and prostaglandin E2 on the adhesion of lymphocytes to endothelial cells. Clin. Exp. Immunol (1990) 81:160–165.
  • PANETTIERI RA JR, LAZAAR AL, PURE E, ALBELDA SM: Activation ofcAMP-dependent pathways in human airway smooth muscle cells inhibits TNF-a-induced ICAM-1 and VCAM-1 expression and T lymphocyte adhesion. J. Immunol. (1995) 154:2358–2365.
  • STEWART AG, FERNANDES D, TOMLINSON PR: The effect of glucocorticoids on proliferation of human cultured airway smooth muscle. Br. J. Pharmacol (1995) 116:3219–3226.
  • PANG L, KNOX AJ: Effect of interleukin-113, tumour necrosis factor-a and interferon-y on the induction of cyclo-oxygenase-2 in cultured human airway smooth muscle cells. Br. J. Pharmacol (1997) 121:579–587.
  • AMRANI Y, LAZAAR A,PANETTIERI RA JR: Up-regulation of ICAM-1 by cytokines in human tracheal smooth muscle cells involves an NF-icB-dependent signaling pathway that is only partially sensitive to dexamethasone. Immunol (1999) 163:2128–2134.
  • JOHNSON EN, DRUEY KM:Heterotrimeric G protein signaling: role in asthma and allergic inflammation. All. Chit. Immunol (2002) 109:592–602.
  • •Thorough review of G proteins.
  • AMMIT AJ, PANETTIERI RA JR: Invited review: the circle of life: cell cycle regulation in airway smooth muscle. J. Appl. Physic] (2001) 91:1431–1437.
  • FERNANDES D, GUIDA E,KOUTSOUBOS V et al.: Glucocorticoids inhibit proliferation, cyclin D1 expression, and retinoblastoma protein phosphorylation, but not activity of the extracellular-regulated kinases in human cultured airway smooth muscle. Am. J. Respir. Cell MM. Biol. (1999) 21:77–88.
  • COOK SJ, MCCORMICK F: Inhibition by cAMP of Ras-dependent activation of Raf. Science (1993) 262:1069–1072.
  • MUSA NL, RAMAKRISHNAN M, LI J et al.: Forskolin inhibits cyclin D1 expression in cultured airway smooth-muscle cells. Am. J. Respir. Cell Ma Biol. (1999) 20:352–358.
  • STEWART AG, HARRIS T, FERNANDES DJ et al.: I32-adrenergic receptor agonists and cAMP arrest human cultured airway smooth muscle cells in the G(1) phase of the cell cycle: role of proteasome degradation of cyclin Dl. Pharm. (1999) 56:1079–1086.
  • HAMAD AM, KNOX AJ: Mechanisms mediating the antiproliferative effects ofnitric oxide in cultured human airway smooth muscle cells. FEBS Lett. (2001) 506:91–96.
  • WANG CG, DU T, XU LJ, MARTIN JG: Role of leukotriene D4 in allergen-induced increases in airway smooth muscle in the rat. Am. Rev Resp. Dis. (1993) 148:413–417.
  • SALMON M, WALSH DA,HUANG TJ et al: Involvement of cysteinyl leukotrienes in airway smooth muscle cell DNA synthesis after repeated allergen exposure in sensitized Brown Norway rats. Br. J. Pharmacol (1999) 127:1151–1158.
  • HENDERSON WR JR, TANG LO, CHU SJ et al.: A role for cysteinyl leukotrienes in airway remodeling in a mouse asthma model. Am. J. Respir. Grit. Care Med. (2002) 165:108–116.
  • BERGER P, PERNG DW,THABREW H et al.: Tryptase and agonists of PAR-2 induce the proliferation of human airway smooth muscle cells. J. Appl. Physiol (2001) 91:1372–1379.
  • CHAMBERS LS, BLACK JL, PORONNIK P, JOHNSON PR: Functional effects of protease-activated receptor-2 stimulation on human airway smooth muscle. Am. J. Physiol (2001) 281:L1369–L1378.
  • CLARK JM, ABRAHAM WM, FISHMAN CE et al.: Tryptase inhibitors block allergen-induced airway and inflammatory responses in allergic sheep. Am. J. Respir. Grit. Care Med. (1995) 152:2076–2083.
  • OH SW, PAE CI, LEE DK et al: Tryptase inhibition blocks airway inflammation in a mouse asthma model. Inununol. (2002) 168:1992–2000.
  • KRISHNA MT, CHAUHAN A, LITTLE L et al.: Inhibition of mast cell tryptase by inhaled APC 366 attenuates allergen-induced late-phase airway obstruction in asthma. I. All. Clin. kununol. (2001) 107:1039–1045.
  • •Early clinical trial demonstrating the potential efficacy of inhaled tryptase inhibitors in asthma.
  • BRAUN-DULLAEUS RC, MANN MJ, DZAU VJ: Cell cycle progression: new therapeutic target for vascular proliferative disease. Circulation (1998) 98:82–89.
  • SCOTT PH, BELHAM CM,AL-HAFIDH J et al: A regulatory role for cAMP in phosphatidylinositol 3-kinase/p70 ribosomal S6 kinase-mediated DNAsynthesis in platelet-derived-growth-factor-stimulated bovine airway smooth-musclecells. Biochem. J. (1996) 318:965–971.
  • HALLSWORTH MP, MOIR LM, LAI D, HIRST SJ: Inhibitors of mitogen-activated protein kinases differentially regulate eosinophil-activating cytokine release from human airway smooth muscle. Am. J. Respir: Crit. Care Med. (2001) 164:688–697.
  • AMRANI Y, AMMIT AJ,PANETTIERI RA JR: Tumor necrosis factor receptor (TNFR) 1, but not TNFR2, mediates tumor necrosis factor-a-induced interleukin-6 and RANTES in human airway smooth muscle cells: role of p38 and p42/44 mitogen-activated protein kinases. MM. Pharm. (2001) 60:646–655.
  • UNDERWOOD DC, OSBORN RR, KOTZER CJ et al.: SB 239063, a potent p38 MAP kinase inhibitor, reduces inflammatory cytokine production, airways eosinophil infiltration, and persistence. J. Pharm. Exp. Ther. (2000) 293:281–288.
  • •Predinical study illustrating the potential benefit of p38 inhibitors in asthma.
  • ESCOTT KJ, BELVISI MG,BIRRELL MA, WEBBER SE,FOSTER ML, SARGENT CA: Effect of the p38 kinase inhibitor, SB 203580, on allergic airway inflammation in the rat. Br.Pharmacol (2000) 131:173–176.
  • IRUSEN E, MATTHEWS JG, TAKAHASHI A, BARNES PJ, CHUNG KF, ADCOCK IM: p38 mitogen-activated protein kinase-induced glucocorticoid receptor phosphorylation reduces its activity: role in steroid-insensitive asthma. J. A//. Immunol(2002) 109:649–657.
  • FUJIHARA SM, CLEAVELAND JS, GROSMAIRE LS et al: A D-amino acid peptide inhibitor of NF-icB nuclear localization is efficacious in models of inflammatory disease. .I. Immunol (2000) 165:1004–1012.
  • ELLIOTT PJ, PIEN CS,MCCORMACK TA, CHAPMAN ID, ADAMS J: Proteasome inhibition: A novel mechanism to combat asthma. J. A//. Chu. Immunol (1999) 104:294–300.
  • HUANG TJ, AD COCK IM,CHUNG KF: A novel transcription factor inhibitor, 5P100030, inhibits cytokine gene expression, but not airway eosinophilia or hyperresponsiveness in sensitized and allergen-exposed rat. Br. J. Pharmacol(2001) 134:1029–1036.
  • CLARK RB: The role of PPARs in inflammation and immunity. j. Leak. Biol.(2002) 71:388–400.
  • BENAYOUN L, LETUVE S,DRUILHE A et al.: Regulation of peroxisome proliferator-activated receptorgamma expression in human asthmatic airways: relationship with proliferation, apoptosis, and airway remodeling. Am. Respir: Crit. Care Med. (2001) 164:1487–1494.
  • DEVCHAND PR, KELLER H,PETERS JM, VAZQUEZ M,GONZALEZ FJ, WAHLI W: The PPARa-leukotriene B4 pathway to inflammation control. Nature (1996) 384:39–43.
  • NYCE JVV, METZGER WJ: DNA antisense therapy for asthma in an animal model. Nature (1997) 385:721–725.
  • •Predinical study illustrating the potential benefit of antisense therapy in asthma.
  • FINOTTO S, BUERKE M, LINGNAU K, SCHMITT E, GALLE PR,NEURATH MF: Local administration of antisense phosphorothioate oligonucleotides to the c-kit ligand, stem cell factor, suppresses airway inflammation and IL-4 production in a murine model of asthma. .1 All. Chu. Immunol. (2001) 107:279–286.

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