Baseline serum syndecan-4 predicts prognosis after the onset of acute exacerbation of idiopathic interstitial pneumonia

Sato, Yuki; Tanino, Yoshinori; Wang, Xintao; Nikaido, Takefumi; Sato, Suguru; Misa, Kenichi; Togawa, Ryuichi; Frevert, Charles W.; Munakata, Mitsuru

doi:10.1371/journal.pone.0176789

Cited by 20 publications

(17 citation statements)

References 57 publications

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“…Axial and coronal images show a) baseline computed tomography 1 year before presentation showing reticulation and honeycombing in a definite usual interstitial pneumonia pattern; b) presentation of acute exacerbation of interstitial lung disease with new onset bilateral ground-glass opacities on background of usual interstitial pneumonia and c) follow-up computed tomography 1 week after treatment with high-dose steroids showing some improvement in ground-glass opacification. https://doi.org/10.1183/16000617.0071-2018dehydrogenase, C-reactive protein, Krebs von den Lungen-6, pro-calcitonin, circulating fibrocytes, elevated interleukin-17 and anti-heat shock protein 70 autoantibodies, syndecan-4), only a limited number have been validated in prospective studies[51,59,60].…”

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confidence: 99%

Acute exacerbations of progressive-fibrosing interstitial lung diseases

et al. 2018

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Acute exacerbation of interstitial lung disease (ILD) is associated with a poor prognosis and high mortality. Numerous studies have documented acute exacerbation in idiopathic pulmonary fibrosis (IPF), but less is known about these events in other ILDs that may present a progressive-fibrosing phenotype. We propose defining acute exacerbation as an acute, clinically significant respiratory deterioration, typically less than 1 month in duration, together with computerised tomography imaging showing new bilateral glass opacity and/or consolidation superimposed on a background pattern consistent with fibrosing ILDs. Drawing on observations in IPF, it is suspected that epithelial injury or proliferation and autoimmunity are risk factors for acute exacerbation in ILDs that may present a progressive-fibrosing phenotype, but further studies are required. Current acute exacerbation management strategies are based on recommendations in IPF, but no randomised controlled trials of acute exacerbation management have been performed. Although there are no formal strategies to prevent the development of acute exacerbation, possible approaches include antifibrotic drugs (such as nintedanib and pirfenidone), and minimising exposure to infection, airborne irritants and pollutants. This review discusses the current knowledge of acute exacerbation of ILDs that may present a progressive-fibrosing phenotype and acknowledges limitations of the data available.

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Acute exacerbations of progressive-fibrosing interstitial lung diseases

et al. 2018

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“…The diagnosis of IPF was made in accordance with the 2011 ATS/ERS/JRS/ALAT joint statement (Sato et al. ). Midkine concentrations in serum and BAL fluid were measured using the Human Midkine DuoSet ELISA kit (R&D; Minneapolis, MN) and were examined for associations with the clinical characteristics of the IPF patients (Tables and 4a).…”

Section: Methodsmentioning

confidence: 99%

Involvement of midkine in the development of pulmonary fibrosis

et al. 2017

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Midkine is a low‐molecular‐weight heparin‐binding protein that is strongly expressed mainly in the midgestation period and has various physiological activities such as in development and cell migration. Midkine has been reported to be strongly expressed in cancer cells and in inflammation and repair processes, and to be involved in the pathogenesis of various diseases. However, its role in the lung is poorly understood. In this study, we analyzed the clinical characteristics of idiopathic pulmonary fibrosis patients in relation to midkine expression and used a mouse bleomycin‐induced pulmonary fibrosis model to investigate the role of midkine in pulmonary fibrosis. In the idiopathic pulmonary fibrosis patients, the serum midkine level was significantly higher than in healthy subjects, and midkine levels in the serum and bronchoalveolar lavage (BAL) fluid correlated positively with the percentage of inflammatory cells in the BAL fluid. In wild‐type mice, intratracheal bleomycin administration increased midkine expression in lung tissue. Additionally, compared with wild‐type mice, midkine‐deficient mice showed low expression of both collagen and α‐smooth muscle actin, as well as a low value for the pathological lung fibrosis score after bleomycin administration. Furthermore, the total cell count and lymphocyte percentage in the BAL fluid, as well as TNF‐α and transforming growth factor‐β expression in lung tissue, were significantly lower in the midkine‐deficient mice compared with wild‐type mice. These results suggest that midkine is involved in the development of pulmonary fibrosis by regulating inflammatory cell migration into the lung, and TNF‐α and transforming growth factor‐β expression.

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“…The same research group showed that Sdc4 levels were increased in patients with idiopathic interstitial pneumonia. Again, the authors propose that baseline serum Sdc4 levels were indicative for the prognosis, showing that higher serum levels of Sdc4 were associated with a worse prognosis than lower baseline levels (Sato et al ., ). Sdc4 serum levels were also associated with severe community‐acquired pneumonia, and these increased serum levels were linked to a higher mortality rate (Luo et al ., ).…”

Section: Shed Syndecans As Biomarkers For Different Diseasesmentioning

confidence: 97%

Soluble syndecans: biomarkers for diseases and therapeutic options

Bertrand

Bollmann

2018

British J Pharmacology

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Syndecans are important mediators of signalling by transmitting external stimuli into the cells. This role in signal transduction has been attributed mainly to the membrane-bound syndecans. In the last years, however, the soluble ectodomain of syndecans generated by shedding has come into the focus of research as this process has been show to modulate the syndecan-dependent signalling pathways, as well as other pathways. This review summarizes the current knowledge about the induction of syndecan shedding and the different pathways modulated by shed syndecan proteins. This review summarizes the known and putative sheddases for each syndecan and describes the exemplary conditions of sheddase activity for some syndecans. This review summarizes the proposed use of shed syndecans as biomarkers for various diseases, as the shedding process of syndecans depends crucially on tissue- and disease-specific activation of the sheddases. Furthermore, the potential use of soluble syndecans as a therapeutic option is discussed, on the basis of the current literature. LINKED ARTICLES: This article is part of a themed section on Translating the Matrix. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v176.1/issuetoc.

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Baseline serum syndecan-4 predicts prognosis after the onset of acute exacerbation of idiopathic interstitial pneumonia

Cited by 20 publications

References 57 publications

Acute exacerbations of progressive-fibrosing interstitial lung diseases

Acute exacerbations of progressive-fibrosing interstitial lung diseases

Involvement of midkine in the development of pulmonary fibrosis

Soluble syndecans: biomarkers for diseases and therapeutic options

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