Metabolic changes induced by TGF-β1 via reduced expression of phosphatidylserine decarboxylase during myofibroblast transition

• Uchida Nobuhiko

  Department of Pulmonary Medicine and Clinical Immunology, Dokkyo Medical University School of Medicine

• Shimizu Yasuo

  Department of Pulmonary Medicine and Clinical Immunology, Dokkyo Medical University School of Medicine

• Fujimaki Mio

  Department of Pulmonary Medicine and Clinical Immunology, Dokkyo Medical University School of Medicine

• Horibata Yasuhiro

  Department of Biochemistry, Dokkyo Medical University School of Medicine

• Nakamura Yusuke

  Department of Pulmonary Medicine and Clinical Immunology, Dokkyo Medical University School of Medicine

• Horigane Yukiko

  Department of Pulmonary Medicine and Clinical Immunology, Dokkyo Medical University School of Medicine

• Chibana Kazuyuki

  Department of Pulmonary Medicine and Clinical Immunology, Dokkyo Medical University School of Medicine

• Takemasa Akihiro

  Department of Pulmonary Medicine and Clinical Immunology, Dokkyo Medical University School of Medicine

• Sugimoto Hiroyuki

  Department of Biochemistry, Dokkyo Medical University School of Medicine

• Niho Seiji

  Department of Pulmonary Medicine and Clinical Immunology, Dokkyo Medical University School of Medicine

抄録

Metabolic alteration is increasingly recognized as an important pathogenic process that underlies fibrosis across many organ types, and metabolically targeted therapies could become important strategies for reducing fibrosis. In present study, target enzymes that are involved in changes in phospholipid metabolism during fibroblast-to-myofibroblast transition induced by trans­forming growth factor beta 1 (TGF-β1) were examined. Different amounts of phospholipids were found in the 2 groups. In response to TGF-β1 stimulation, 17 lipids decreased and 17 increased. The latter included the phospholipids phosphatidylcholine (PC), phosphatidylserine (PS), and phosphatidylethanolamine (PE). Furthermore, among the rate-limiting enzymes that regulate these phospholipids, phosphatidylserine decarboxylase (PISD), which controls conversion of PS to PE and is localized in mitochondria, decreased in response to TGF-β1. Knockdown of PISD alone without TGF-β1 stimulation increased expression of α-smooth muscle actin mRNA and production of total collagen. Taken together, these results indicate that PISD is involved in the mechanism of fibrogenesis by regulating phospholipid metabolism.

収録刊行物

• Ｊｏｕｒｎａｌ　ｏｆ　Ｃｌｉｎｉｃａｌ　Ｂｉｏｃｈｅｍｉｓｔｒｙ　ａｎｄ　Ｎｕｔｒｉｔｉｏｎ

  Ｊｏｕｒｎａｌ　ｏｆ　Ｃｌｉｎｉｃａｌ　Ｂｉｏｃｈｅｍｉｓｔｒｙ　ａｎｄ　Ｎｕｔｒｉｔｉｏｎ 70 (2), 108-116, 2022

  一般社団法人　日本酸化ストレス学会

キーワード

• phosphatidylserine decarboxylase
• myofibroblasts
• fibrosis
• lung
• mitochondria
• phospholipids

詳細情報

• CRID: 1390291767485189248
• NII論文ID: 130008165943
• DOI: 10.3164/jcbn.21-121
• ISSN: 18805086
• ISSN: 09120009
• Web Site: https://www.jstage.jst.go.jp/article/jcbn/70/2/70_21-121/_pdf
• Web Site: https://search.jamas.or.jp/link/ui/2023170028
• 本文言語コード: en
• データソース種別:
  • JaLC
  • Crossref
  • CiNii Articles
  • KAKEN
• 抄録ライセンスフラグ: 使用不可