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01-04-2018 | Original Article

ADAM-17 is expressed in the inflammatory myopathy and is involved with interstitial lung disease

Authors: Airi Nishimi, Takeo Isozaki, Shinichiro Nishimi, Sho Ishii, Takahiro Tokunaga, Hidekazu Furuya, Kuninobu Wakabayashi, Tsuyoshi Kasama

Published in: Clinical Rheumatology | Issue 4/2018

Abstract

The “A disintegrin and metalloprotease” (ADAM) family is thought to play an important role in tissue destruction and inflammatory reactions. ADAM-17 was first described as the protease responsible for tumor necrosis factor (TNF)-α shedding. Here, we have shown the expression of ADAM-17 in inflammatory myopathy and demonstrated the role of inflammation in interstitial lung diseases (ILD). ADAM-17 in inflammatory myopathy serum [polymyositis (n = 26), dermatomyositis (n = 34), and clinically amyopathic dermatomyositis (n = 10)] and healthy control (n = 19) was measured using enzyme-linked immunosorbent assay. The relationship between ADAM-17 and clinical data was examined. Finally, we performed immunohistological analysis to investigate the expression of ADAM-17 on the muscles of the inflammatory myopathy patients. ADAM-17 in inflammatory myopathy was significantly higher than that in healthy control (mean ± SEM, 1048 ± 312 and 36 ± 18 pg/ml, respectively; p < 0.05). ADAM-17 in post-treatment with corticosteroid and/or immunosuppressant serum was significantly decreased compared with that in pre-treatment serum (1465 ± 562 and 1059 ± 503 pg/ml, respectively; p < 0.01). ADAM-17 was significantly positively correlated with fractalkine/CX3CL1 and CXCL16. In addition, ADAM-17 in inflammatory myopathy with ILD patients (n = 46) was significantly higher than that in non-ILD patients (n = 24) (1379 ± 454 and 413 ± 226 pg/ml, respectively; p < 0.05). We found the expression of ADAM-17 on muscle biopsy tissue. ADAM-17 is expressed in inflammatory myopathies especially ILD, suggesting that ADAM-17 plays a role in lung fibrosis. ADAM-17 may be a potential target in inflammatory myopathies with ILD.

Dalakas MC, Hohlfeld R (2003) Polymyositis and dermatomyositis. Lancet 362(9388):971–982. https://doi.org/10.1016/S0140-6736(03)14368-1 CrossRefPubMed

Callen JP (2000) Dermatomyositis. Lancet 355(9197):53–57. https://doi.org/10.1016/S0140-6736(99)05157-0 CrossRefPubMed

Malik A, Hayat G, Kalia JS, Guzman MA (2016) Idiopathic inflammatory myopathies: clinical approach and management. Front Neurol 7:64CrossRefPubMedPubMedCentral

Sun WC, Sun YC, Lin H, Yan B, Shi GX (2012) Dysregulation of the type I interferon system in adult-onset clinically amyopathic dermatomyositis has a potential contribution to the development of interstitial lung disease. Br J Dermatol 167(6):1236–1244. https://doi.org/10.1111/j.1365-2133.2012.11145.x CrossRefPubMed

Marie I, Hatron PY, Dominique S, Cherin P, Mouthon L, Menard JF (2011) Short-term and long-term outcomes of interstitial lung disease in polymyositis and dermatomyositis: a series of 107 patients. Arthritis Rheum 63(11):3439–3447. https://doi.org/10.1002/art.30513 CrossRefPubMed

Kang EH, Lee EB, Shin KC, Im CH, Chung DH, Han SK, Song YW (2005) Interstitial lung disease in patients with polymyositis, dermatomyositis and amyopathic dermatomyositis. Rheumatology 44(10):1282–1286. https://doi.org/10.1093/rheumatology/keh723 CrossRefPubMed

Sakamoto N, Mukae H, Fujii T, Yoshioka S, Kakugawa T, Yamaguchi H et al (2004) Nonspecific interstitial pneumonia with poor prognosis associated with amyopathic dermatomyositis. Intern Med 43(9):838–842. https://doi.org/10.2169/internalmedicine.43.838 CrossRefPubMed

Suda T, Fujisawa T, Enomoto N, Nakamura Y, Inui N, Naito T, Hashimoto D, Sato J, Toyoshima M, Hashizume H, Chida K (2006) Interstitial lung diseases associated with amyopathic dermatomyositis. Eur Respir J 28(5):1005–1012. https://doi.org/10.1183/09031936.06.00038806 CrossRefPubMed

Ye S, Chen XX, Lu XY, Wu MF, Deng Y, Huang WQ, Guo Q, Yang CD, Gu YY, Bao CD, Chen SL (2007) Adult clinically amyopathic dermatomyositis with rapid progressive interstitial lung disease: a retrospective cohort study. Clin Rheumatol 26(10):1647–1654. https://doi.org/10.1007/s10067-007-0562-9 CrossRefPubMed

10.

Isozaki T, Ishii S, Nishimi S, Nishimi A, Oguro N, Seki S, Miura Y, Miwa Y, Oh K, Toyoshima Y, Nakamura M, Inagaki K, Kasama T (2015) A disintegrin and metalloprotease-10 is correlated with disease activity and mediates monocyte migration and adhesion in rheumatoid arthritis. Transl Res 166(3):244–253. https://doi.org/10.1016/j.trsl.2015.02.005 CrossRefPubMed

11.

Dreymueller D, Uhlig S, Ludwig A (2015) ADAM-family metalloproteinases in lung inflammation: potential therapeutic targets. Am J Physiol Lung Cell Mol Physiol 308(4):L325–L343. https://doi.org/10.1152/ajplung.00294.2014 CrossRefPubMed

12.

Charbonneau M, Harper K, Grondin F, Pelmus M, McDonald PP, Dubois CM (2007) Hypoxia-inducible factor mediates hypoxic and tumor necrosis factor alpha-induced increases in tumor necrosis factor-alpha converting enzyme/ADAM17 expression by synovial cells. J Biol Chem 282(46):33714–33724. https://doi.org/10.1074/jbc.M704041200 CrossRefPubMed

13.

Lorenzen I, Trad A, Grotzinger J (2011) Multimerisation of A disintegrin and metalloprotease protein-17 (ADAM17) is mediated by its EGF-like domain. Biochem Biophys Res Commun 415(2):330–336. https://doi.org/10.1016/j.bbrc.2011.10.056 CrossRefPubMed

14.

Ermert M, Pantazis C, Duncker HR, Grimminger F, Seeger W, Ermert L (2003) In situ localization of TNFalpha/beta, TACE and TNF receptors TNF-R1 and TNF-R2 in control and LPS-treated lung tissue. Cytokine 22(3–4):89–100. https://doi.org/10.1016/S1043-4666(03)00117-0 CrossRefPubMed

15.

Moss ML, Sklair-Tavron L, Nudelman R (2008) Drug insight: tumor necrosis factor-converting enzyme as a pharmaceutical target for rheumatoid arthritis. Nat Clin Pract Rheumatol 4(6):300–309CrossRefPubMed

16.

Umemura M, Isozaki T, Ishii S, Seki S, Oguro N, Miura Y, Miwa Y, Nakamura M, Inagaki K, Kasama T (2014) Reduction of serum ADAM17 level accompanied with decreased cytokines after abatacept therapy in patients with rheumatoid arthritis. Int J Biomed Sci IJBS 10(4):229–235PubMed

17.

Suzuki F, Kubota T, Miyazaki Y, Ishikawa K, Ebisawa M, Hirohata S et al (2014) Serum level of soluble CX3CL1/fractalkine is elevated in patients with polymyositis and dermatomyositis, which is correlated with disease activity. Arthritis Res Ther 14(2):R48CrossRef

18.

Cao H, Parikh TN, Zheng J (2009) Amyopathic dermatomyositis or dermatomyositis-like skin disease: retrospective review of 16 cases with amyopathic dermatomyositis. Clin Rheumatol 28(8):979–984. https://doi.org/10.1007/s10067-009-1152-9 CrossRefPubMed

19.

Gerami P, Schope JM, McDonald L, Walling HW, Sontheimer RD (2006) A systematic review of adult-onset clinically amyopathic dermatomyositis (dermatomyositis sine myositis): a missing link within the spectrum of the idiopathic inflammatory myopathies. J Am Acad Dermatol 54(4):597–613. https://doi.org/10.1016/j.jaad.2005.10.041 CrossRefPubMed

20.

Ohta S, Harigai M, Tanaka M, Kawaguchi Y, Sugiura T, Takagi K, Fukasawa C, Hara M, Kamatani N (2001) Tumor necrosis factor-alpha (TNF-alpha) converting enzyme contributes to production of TNF-alpha in synovial tissues from patients with rheumatoid arthritis. J Rheumatol 28(8):1756–1763PubMed

21.

Sisto M, Lisi S, Lofrumento DD, Ingravallo G, Mitolo V, D'Amore M (2010) Expression of pro-inflammatory TACE-TNF-alpha-amphiregulin axis in Sjogren’s syndrome salivary glands. Histochem Cell Biol 134(4):345–353. https://doi.org/10.1007/s00418-010-0735-5 CrossRefPubMed

22.

Lundberg I, Ulfgren AK, Nyberg P, Andersson U, Klareskog L (1997) Cytokine production in muscle tissue of patients with idiopathic inflammatory myopathies. Arthritis Rheum 40(5):865–874. https://doi.org/10.1002/art.1780400514 CrossRefPubMed

23.

Gono T, Kaneko H, Kawaguchi Y, Hanaoka M, Kataoka S, Kuwana M, Takagi K, Ichida H, Katsumata Y, Ota Y, Kawasumi H, Yamanaka H (2014) Cytokine profiles in polymyositis and dermatomyositis complicated by rapidly progressive or chronic interstitial lung disease. Rheumatology 53(12):2196–2203. https://doi.org/10.1093/rheumatology/keu258 CrossRefPubMed

Title: ADAM-17 is expressed in the inflammatory myopathy and is involved with interstitial lung disease
Authors: Airi Nishimi
Takeo Isozaki
Shinichiro Nishimi
Sho Ishii
Takahiro Tokunaga
Hidekazu Furuya
Kuninobu Wakabayashi
Tsuyoshi Kasama
Publication date: 01-04-2018
Publisher: Springer London
Published in: Clinical Rheumatology / Issue 4/2018
Print ISSN: 0770-3198
Electronic ISSN: 1434-9949
DOI: https://doi.org/10.1007/s10067-018-4014-5

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