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Connective tissue diseases and related disorders

The involvement of leucine-rich α-2 glycoprotein in the progression of skin and lung fibrosis in bleomycin-induced systemic sclerosis model

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Pages 1120-1128 | Received 08 Oct 2020, Accepted 25 Jan 2021, Published online: 17 Feb 2021

References

  • Denton CP, Khanna D. Systemic sclerosis. Lancet. 2017;390(10103):1685–99.
  • Varga J, Abraham D. Systemic sclerosis: a prototypic multisystem fibrotic disorder. J Clin Invest. 2007;117(3):557–67.
  • Verrecchia F, Mauviel A, Farge D. Transforming growth factor-beta signaling through the Smad proteins: role in systemic sclerosis . Autoimmun Rev. 2006;5(8):563–9.
  • Tsai C-Y, Hsieh S-C, Wu T-H, Li K-J, Shen C-Y, Liao H-T, et al. Pathogenic roles of autoantibodies and aberrant epigenetic regulation of immune and connective tissue cells in the tissue fibrosis of patients with systemic sclerosis. IJMS. 2020;21(9):3069.
  • Serada S, Fujimoto M, Ogata A, Terabe F, Hirano T, Iijima H, et al. iTRAQ-based proteomic identification of leucine-rich alpha-2 glycoprotein as a novel inflammatory biomarker in autoimmune diseases. Ann Rheum Dis. 2010;69(4):770–4.
  • Nakajima H, Serada S, Fujimoto M, Naka T, Sano S. Leucine-rich α-2 glycoprotein is an innovative biomarker for psoriasis. J Dermatol Sci. 2017;86(2):170–4.
  • Takahashi N, Takahashi Y, Putnam FW. Periodicity of leucine and tandem repetition of a 24-amino acid segment in the primary structure of leucine-rich alpha 2-glycoprotein of human serum. Proc Natl Acad Sci U S A. 1985;82(7):1906–10.
  • Wang X, Abraham S, McKenzie JA, Jeffs N, Swire M, Tripathi VB, et al. LRG1 promotes angiogenesis by modulating endothelial TGF-β signalling. Nature 2013;499(7458):306–11.
  • Takemoto N, Serada S, Fujimoto M, Honda H, Ohkawara T, Takahashi T, et al. Leucine-rich α-2-glycoprotein promotes TGFβ1-mediated growth suppression in the Lewis lung carcinoma cell lines. Oncotarget 2015;6(13):11009–22.
  • Urushima H, Fujimoto M, Mishima T, Ohkawara T, Honda H, Lee H, et al. Leucine-rich alpha 2 glycoprotein promotes Th17 differentiation and collagen-induced arthritis in mice through enhancement of TGF-β-Smad2 signaling in naïve helper T cells. Arthritis Res Ther. 2017;19(1):137.
  • Honda H, Fujimoto M, Serada S, Urushima H, Mishima T, Lee H, et al. Leucine-rich α-2 glycoprotein promotes lung fibrosis by modulating TGF-β signaling in fibroblasts. Physiol Rep. 2017;5(24):e13556.
  • Takahashi T, Asano Y, Ichimura Y, Toyama T, Taniguchi T, Noda S, et al. Amelioration of tissue fibrosis by toll-like receptor 4 knockout in murine models of systemic sclerosis. Arthritis Rheumatol. 2015;67(1):254–65.
  • Lok SS, Haider Y, Howell D, Stewart JP, Hasleton PS, Egan JJ. Murine gammaherpes virus as a cofactor in the development of pulmonary fibrosis in bleomycin resistant mice. Eur Respir J. 2002;20(5):1228–32.
  • Okamoto Y, Hasegawa M, Matsushita T, Hamaguchi Y, Huu DL, Iwakura Y, et al. Potential roles of interleukin-17A in the development of skin fibrosis in mice. Arthritis Rheum. 2012;64(11):3726–35.
  • Nakajima K, Kanda T, Takaishi M, Shiga T, Miyoshi K, Nakajima H, et al. Distinct roles of IL-23 and IL-17 in the development of psoriasis-like lesions in a mouse model. J Immunol. 2011;186(7):4481–9.
  • Yamamoto M, Nakajima K, Takaishi M, Kitaba S, Magata Y, Kataoka S, et al. Psoriatic inflammation facilitates the onset of arthritis in a mouse model. J Invest Dermatol. 2015;135(2):445–53.
  • Brown RL, Ormsby I, Doetschman TC, Greenhalgh DG. Wound healing in the transforming growth factor-β1-deficient mouse. Wound Repair Regen. 1995;3(1):25–36.
  • Takagi N, Kawakami K, Kanno E, Tanno H, Takeda A, Ishii K, et al. IL-17A promotes neutrophilic inflammation and disturbs acute wound healing in skin. Exp Dermatol. 2017;26(2):137–44.
  • Shirai R, Hirano F, Ohkura N, Ikeda K, Inoue S. Up-regulation of the expression of leucine-rich alpha(2)-glycoprotein in hepatocytes by the mediators of acute-phase response . Biochem Biophys Res Commun. 2009;382(4):776–9.
  • Serada S, Fujimoto M, Terabe F, Iijima H, Shinzaki S, Matsuzaki S, et al. Serum leucine-rich alpha-2 glycoprotein is a disease activity biomarker in ulcerative colitis. Inflamm Bowel Dis 2012;18:2169–79.
  • Sun C, Chen SY. RGC32 promotes bleomycin-induced systemic sclerosis in a murine disease model by modulating classically activated macrophage function. J Immunol. 2018;200(8):2777–85.
  • Zhou Y, Schneider DJ, Morschl SE, Song L, Pedroza M, Karmouty-Quintana H, et al. Distinct roles for the A2B adenosine receptor in acute and chronic stages of bleomycin-induced lung injury. J Immunol. 2011;186(2):1097–106.
  • Zhang J, Zhu L, Fang J, Ge Z, Li X. LRG1 modulates epithelial-mesenchymal transition and angiogenesis in colorectal cancer via HIF-1α activation. J Exp Clin Cancer Res. 2016;35:29.
  • Kasai H, Allen JT, Mason T, Kamimura T, Zhang Z. TGF-beta1 induces human alveolar epithelial to mesenchymal cell transition (EMT) ). Respir Res. 2005;6:56.
  • O'Reilly S, Cant R, Ciechomska M, van Laar JM. Interleukin-6: a new therapeutic target in systemic sclerosis? Clin Transl Immunology. 2013;2(4):e4.
  • Huang X-L, Wang Y-J, Yan J-W, Wan Y-N, Chen B, Li B-Z, et al. Role of anti-inflammatory cytokines IL-4 and IL-13 in systemic sclerosis. Inflamm Res. 2015;64(3-4):151–9.
  • Chizzolini C, Dufour AM, Brembilla NC. Is there a role for IL-17 in the pathogenesis of systemic sclerosis? Immunol Lett. 2018;195:61–7.

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