SETDB1-Mediated Chromatin Regulation in Intestinal Epithelial Cells During Intestinal Ischemia-Reperfusion Injury

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  • Higuchi Kazuhiro
    Department of Anatomy, Histochemistry and Cell Biology, Faculty of Medicine, University of Miyazaki Department of Surgery, Faculty of Medicine, University of Miyazaki
  • Ikenoue Makoto
    Department of Anatomy, Histochemistry and Cell Biology, Faculty of Medicine, University of Miyazaki Department of Surgery, Faculty of Medicine, University of Miyazaki
  • Ishizuka Takumi
    Department of Anatomy, Histochemistry and Cell Biology, Faculty of Medicine, University of Miyazaki
  • Kai Kengo
    Department of Anatomy, Histochemistry and Cell Biology, Faculty of Medicine, University of Miyazaki Department of Surgery, Faculty of Medicine, University of Miyazaki
  • Takahashi Nobuyasu
    Department of Anatomy, Ultrastructural Cell Biology, Faculty of Medicine, University of Miyazaki
  • Kubota Toshiki
    Department of Anatomy, Histochemistry and Cell Biology, Faculty of Medicine, University of Miyazaki Department of Oral and Maxillofacial Surgery, Faculty of Medicine, University of Miyazaki
  • Shirouzu Shinichiro
    Department of Oral and Maxillofacial Surgery, Faculty of Medicine, University of Miyazaki
  • Lkham-Erdene Baljinnyam
    Department of Anatomy, Histochemistry and Cell Biology, Faculty of Medicine, University of Miyazaki
  • Aung Kham Mo
    Department of Anatomy, Histochemistry and Cell Biology, Faculty of Medicine, University of Miyazaki
  • Nakai Michikazu
    Clinical Research Support Center, University of Miyazaki Hospital
  • Sawaguchi Akira
    Department of Anatomy, Ultrastructural Cell Biology, Faculty of Medicine, University of Miyazaki
  • Nanashima Atsushi
    Department of Surgery, Faculty of Medicine, University of Miyazaki
  • Hishikawa Yoshitaka
    Department of Anatomy, Histochemistry and Cell Biology, Faculty of Medicine, University of Miyazaki Frontier Science Research Center, University of Miyazaki

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<p>SET domain bifurcated 1 (SETDB1), a histone H3K9-specific methyltransferase, is crucial for heterochromatin formation and intestinal homeostasis, but its role in intestinal ischemia-reperfusion injury (IRI) remains unclear. This study investigated changes in SETDB1-mediated nuclear chromatin regulation in intestinal epithelial cells (IECs) using an IRI mouse model. Jejunal samples were collected after 75 min of ischemia followed by 24 hr of reperfusion. Sinefungin was administered as a histone methyltransferase inhibitor. Morphologic changes were evaluated using hematoxylin-eosin staining and electron microscopy, and cell-adhesion molecule expression, including ZO-1, E-cadherin, integrin-β4, and laminin, was evaluated using immunohistochemistry. Super-resolution microscopy analyzed intranuclear SETDB1 localization and heterochromatin formation in IECs. IRI-affected jejunum exhibited massive IEC detachment, dilated intercellular spaces, basement membrane damage, and decreased expression of E-cadherin and integrin-β4. Sinefungin prevented these changes, however. The proportion of IECs expressing nuclear SETDB1 throughout the euchromatin was significantly higher in IRI-affected jejunum (77.8%) than sham-treated (3.0%) or sinefungin-treated, IRI-affected jejunum (2.7%). The proportion of IECs with decreased heterochromatin was significantly higher in sinefungin-treated, IRI-affected jejunum (84.3%) than untreated IRI-affected jejunum (15.6%). These findings suggest that SETDB1-mediated chromatin regulation is pivotal in intestinal IRI and represents a potential therapeutic target.</p>

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