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      Cellular senescence and senescence-associated secretory phenotype: comparison of idiopathic pulmonary fibrosis, connective tissue disease-associated interstitial lung disease, and chronic obstructive pulmonary disease

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          Abstract

          Background

          The senescence-associated secretory phenotype (SASP) develops due to cellular senescence during conditions such as chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF). However, studies comparing the degree of cellular senescence and SASP between COPD and IPF are limited. Furthermore, to the best of our knowledge, no study has examined cellular senescence and/or SASP in connective tissue disease-associated interstitial lung disease (CTD-ILD).

          Methods

          To compare the degree of cellular senescence among COPD, IPF, and CTD-ILD, tissue samples from surgical lung biopsies or noncancerous tissue from lobectomy specimens of patients with lung cancer were subjected to immunostaining for p16 and p21. Double-staining for p16 and phosphorylated NF-κB was performed to verify the relationship between cellular senescence and SASP.

          Results

          There was a greater degree of enhancement of p16 and p21 expression in patients with IPF than in those with COPD and controls. Immunostaining for p16 revealed an enhanced expression of this marker in patients with COPD compared with that in controls. No significant differences were observed in the phosphorylated NF-κB expression rate of p16-positive and p16-negative cells among patients with IPF, CTD-ILD, and COPD.

          Conclusions

          Epithelial cells in patients with IPF express higher levels of both cellular senescence and SASP than those in patients with COPD or controls.

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          Author and article information

          Journal
          J Thorac Dis
          J Thorac Dis
          JTD
          Journal of Thoracic Disease
          AME Publishing Company
          2072-1439
          2077-6624
          March 2019
          March 2019
          : 11
          : 3
          : 857-864
          Affiliations
          [1 ]Department of Respiratory Medicine, Kanagawa Cardiovascular and Respiratory Center , Yokohama, Japan;
          [2 ]Department of Respiratory Medicine, Tokyo Medical University Ibaraki Medical Center, Inashiki, Japan;
          [3 ]Department of Respiratory Medicine, Saitama Red Cross Hospital , Saitama, Japan;
          [4 ]Department of Pathology, Yokohama City University Graduate School of Medicine , Yokohama, Japan
          Author notes

          Contributions: (I) Conception and design: All authors; (II) Administrative support: All authors; (III) Provision of study materials or patients: R Okuda, K Aoshiba, H Matsushima; (IV) Collection and assembly of data: R Okuda, K Aoshiba, H Matsushima, K Okudela, K Ohashi; (V) Data analysis and interpretation: All authors; (VI) Manuscript writing: All authors; (VII) Final approval of manuscript: All authors.

          Correspondence to: Ryo Okuda. Department of Respiratory Medicine, Kanagawa Cardiovascular and Respiratory Center, 6-16-1 Tomioka-higashi, Kanazawa-ku, Yokohama, Japan. Email: b980013@ 123456yahoo.co.jp .
          Article
          PMC6462683 PMC6462683 6462683 jtd-11-03-857
          10.21037/jtd.2019.02.11
          6462683
          31019774
          d4e0474a-9796-4c07-81c9-cffa3064888f
          2019 Journal of Thoracic Disease. All rights reserved.
          Categories
          Original Article

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