GPRC5B promotes collagen production in myofibroblasts

Noburo Takizawa, Takanori Hironaka, Kyosuke Mae, Tomoyuki Ueno, Yuma Horii, Akiomi Nagasaka, Michio Nakaya

研究成果: ジャーナルへの寄稿学術誌査読

2 被引用数 (Scopus)

抄録

Fibrosis is a condition characterized by the overproduction of extracellular matrix (ECM) components (e.g., collagen) in the myofibroblasts, causing tissue hardening and eventual organ dysfunction. Currently, the molecular mechanisms that regulate ECM production in the myofibroblasts are still obscure. In this study, we investigated the function of GPRC5B in the cardiac and lung myofibroblasts using real-time RT-PCR and siRNA-mediated knockdown. We discovered a significantly high expression of Gprc5b in the tissues of the fibrosis mice models and confirmed that Gprc5b was consistently expressed in the myofibroblasts of fibrotic hearts and lungs. We also found that Gprc5b expression was associated and may be dependent on the actin-MRTF-SRF signaling pathway. Notably, we observed that Gprc5b knockdown reduced the expression of collagen genes in the cardiac and lung myofibroblasts. Therefore, our findings reveal that GPRC5B enhances collagen production in the myofibroblasts, which directly promotes fibrosis in the tissues.

本文言語英語
ページ(範囲)180-186
ページ数7
ジャーナルBiochemical and Biophysical Research Communications
561
DOI
出版ステータス出版済み - 7月 5 2021

!!!All Science Journal Classification (ASJC) codes

  • 生物理学
  • 生化学
  • 分子生物学
  • 細胞生物学

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