論文

国際誌
2024年2月27日

Bicarbonate signalling via G protein-coupled receptor regulates ischaemia-reperfusion injury.

Nature communications
  • Airi Jo-Watanabe
  • Toshiki Inaba
  • Takahiro Osada
  • Ryota Hashimoto
  • Tomohiro Nishizawa
  • Toshiaki Okuno
  • Sayoko Ihara
  • Kazushige Touhara
  • Nobutaka Hattori
  • Masatsugu Oh-Hora
  • Osamu Nureki
  • Takehiko Yokomizo
  • 全て表示

15
1
開始ページ
1530
終了ページ
1530
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1038/s41467-024-45579-3

Homoeostatic regulation of the acid-base balance is essential for cellular functional integrity. However, little is known about the molecular mechanism through which the acid-base balance regulates cellular responses. Here, we report that bicarbonate ions activate a G protein-coupled receptor (GPCR), i.e., GPR30, which leads to Gq-coupled calcium responses. Gpr30-Venus knock-in mice reveal predominant expression of GPR30 in brain mural cells. Primary culture and fresh isolation of brain mural cells demonstrate bicarbonate-induced, GPR30-dependent calcium responses. GPR30-deficient male mice are protected against ischemia-reperfusion injury by a rapid blood flow recovery. Collectively, we identify a bicarbonate-sensing GPCR in brain mural cells that regulates blood flow and ischemia-reperfusion injury. Our results provide a perspective on the modulation of GPR30 signalling in the development of innovative therapies for ischaemic stroke. Moreover, our findings provide perspectives on acid/base sensing GPCRs, concomitantly modulating cellular responses depending on fluctuating ion concentrations under the acid-base homoeostasis.

リンク情報
DOI
https://doi.org/10.1038/s41467-024-45579-3
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/38413581
PubMed Central
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10899177
ID情報
  • DOI : 10.1038/s41467-024-45579-3
  • PubMed ID : 38413581
  • PubMed Central 記事ID : PMC10899177

エクスポート
BibTeX RIS