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NET formation is a default epigenetic program controlled by PAD4 in apoptotic neutrophils.
Zhu, Yanfang Peipei; Speir, Mary; Tan, ZheHao; Lee, Jamie Casey; Nowell, Cameron J; Chen, Alyce A; Amatullah, Hajera; Salinger, Ari J; Huang, Carolyn J; Wu, Gio; Peng, Weiqi; Askari, Kasra; Griffis, Eric; Ghassemian, Majid; Santini, Jennifer; Gerlic, Motti; Kiosses, William B; Catz, Sergio D; Hoffman, Hal M; Greco, Kimberly F; Weller, Edie; Thompson, Paul R; Wong, Lai Ping; Sadreyev, Ruslan; Jeffrey, Kate L; Croker, Ben A.
  • Zhu YP; Department of Pediatrics, University of California San Diego, La Jolla, CA 92093, USA.
  • Speir M; Immunology Center of Georgia, Augusta University, Augusta, GA 30912, USA.
  • Tan Z; Division of Hematology/Oncology, Boston Children's Hospital, Boston, MA 02115, USA.
  • Lee JC; Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA.
  • Nowell CJ; Department of Pediatrics, University of California San Diego, La Jolla, CA 92093, USA.
  • Chen AA; Department of Pediatrics, University of California San Diego, La Jolla, CA 92093, USA.
  • Amatullah H; Monash Institute of Pharmaceutical Sciences, Parkville, Victoria 3052, Australia.
  • Salinger AJ; Division of Hematology/Oncology, Boston Children's Hospital, Boston, MA 02115, USA.
  • Huang CJ; Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA.
  • Wu G; Department of Medicine, Division of Gastroenterology and the Center for the Study of Inflammatory Bowel Disease, Massachusetts General Hospital, Harvard Medical School, Boston MA 02114, USA.
  • Peng W; Center for Microbiome Informatics and Therapeutics, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
  • Askari K; Program in Chemical Biology and Department of Biochemistry and Molecular Biology, University of Massachusetts Medical School, Worcester, MA 01605, USA.
  • Griffis E; Division of Hematology/Oncology, Boston Children's Hospital, Boston, MA 02115, USA.
  • Ghassemian M; Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA.
  • Santini J; Department of Pediatrics, University of California San Diego, La Jolla, CA 92093, USA.
  • Gerlic M; Department of Pediatrics, University of California San Diego, La Jolla, CA 92093, USA.
  • Kiosses WB; Scripps Research Institute, La Jolla, CA 92037, USA.
  • Catz SD; Nikon Imaging Center, University of California San Diego, La Jolla, CA 92093, USA.
  • Hoffman HM; Biomolecular and Proteomics Mass Spectrometry Facility, University of California San Diego, La Jolla, CA 92093, USA.
  • Greco KF; UCSD School of Medicine Microscopy Core, University of California San Diego, La Jolla 92093, CA, USA.
  • Weller E; Department of Clinical Microbiology and Immunology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv 69978, Israel.
  • Thompson PR; La Jolla Institute for Immunology, La Jolla, CA 92037, USA.
  • Wong LP; Scripps Research Institute, La Jolla, CA 92037, USA.
  • Sadreyev R; Department of Pediatrics, University of California San Diego, La Jolla, CA 92093, USA.
  • Jeffrey KL; Biostatistics and Research Design Center, Institutional Centers for Clinical and Translational Research, Boston Children's Hospital, Boston, 02115, USA.
  • Croker BA; Division of Hematology/Oncology, Boston Children's Hospital, Boston, MA 02115, USA.
Sci Adv ; 9(51): eadj1397, 2023 Dec 22.
Article en En | MEDLINE | ID: mdl-38117877
ABSTRACT
Neutrophil extracellular traps (NETs) not only counteract bacterial and fungal pathogens but can also promote thrombosis, autoimmunity, and sterile inflammation. The presence of citrullinated histones, generated by the peptidylarginine deiminase 4 (PAD4), is synonymous with NETosis and is considered independent of apoptosis. Mitochondrial- and death receptor-mediated apoptosis promote gasdermin E (GSDME)-dependent calcium mobilization and membrane permeabilization leading to histone H3 citrullination (H3Cit), nuclear DNA extrusion, and cytoplast formation. H3Cit is concentrated at the promoter in bone marrow neutrophils and redistributes in a coordinated process from promoter to intergenic and intronic regions during apoptosis. Loss of GSDME prevents nuclear and plasma membrane disruption of apoptotic neutrophils but prolongs early apoptosis-induced cellular changes to the chromatin and cytoplasmic granules. Apoptotic signaling engages PAD4 in neutrophils, establishing a cellular state that is primed for NETosis, but that occurs only upon membrane disruption by GSDME, thereby redefining the end of life for neutrophils.
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Texto completo: 1 Banco de datos: MEDLINE Asunto principal: Trampas Extracelulares / Neutrófilos Idioma: En Año: 2023 Tipo del documento: Article
Texto completo
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Texto completo: 1 Banco de datos: MEDLINE Asunto principal: Trampas Extracelulares / Neutrófilos Idioma: En Año: 2023 Tipo del documento: Article