論文 - 詳細
| RRC ID | 78335 |
|---|---|
| 著者 | Jo-Watanabe A, Inaba T, Osada T, Hashimoto R, Nishizawa T, Okuno T, Ihara S, Touhara K, Hattori N, Oh-Hora M, Nureki O, Yokomizo T. |
| タイトル | Bicarbonate signalling via G protein-coupled receptor regulates ischaemia-reperfusion injury. |
| ジャーナル | Nat Commun |
| Abstract |
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. |
| 巻・号 | 15(1) |
| ページ | 1530 |
| 公開日 | 2024-2-27 |
| DOI | 10.1038/s41467-024-45579-3 |
| PII | 10.1038/s41467-024-45579-3 |
| PMID | 38413581 |
| PMC | PMC10899177 |
| MeSH | Animals Bicarbonates Brain Ischemia* Calcium / metabolism Male Mice Receptors, Estrogen / metabolism Receptors, G-Protein-Coupled / genetics Receptors, G-Protein-Coupled / metabolism Reperfusion Injury* Stroke* |
| IF | 12.121 |
| オルトメトリクス指標 |
オルトメトリクス指標項目
|
| 最多言及媒体 | X(Twitter) |
| 各媒体での言及数の合計 | 49 |
| 過去6か月間でのオルトメトリクス指標の変動値 | 0.0 |
| リソース情報 | |
| ヒト・動物細胞 | C2C12(RCB0987) |