Fig. 5: GPR30 is expressed in brain mural cells.
From: Bicarbonate signalling via G protein-coupled receptor regulates ischaemia-reperfusion injury
a Design of the Gpr30-Venus-KI construct. The coding sequence of Gpr30 was replaced in frame with that of Venus. b Confocal microscopy image of a heterozygous Gpr30-Venus-KI (Gpr30+/Venus) mouse brain. Slices (50 µm) of the brains were stained with an antibody for collagen type IV (Col-IV) and DAPI. Scale bars, 100 µm. c, d Quantitative RT-PCR analyses of marker genes for neurons, astrocytes, oligodendrocytes, oligodendrocyte progenitor cells, pericytes, and endothelial cells. Relative expression levels of the genes in Venus+ cells compared with those in the whole brain cortex are shown in (d). e In situ hybridisation analyses of brain sections from wild-type (Gpr30+/+) mice. Gpr30 mRNA is visualised as magenta dots. Scale bars, 50 µm. f Visualisation of Gpr30 (green), the vascular smooth muscle cell (SMC) marker Acta2 (red), and the mural cell marker Pdgfrb (magenta) using multiple in situ hybridisation. Scale bar, 50 µm. g Visualisation of Gpr30 (green), endothelial marker Pecam1 (red), and pericyte marker Pdgfrb (magenta) using multiple in situ hybridisation. Scale bars, 10 µm. h, i Quantitative RT-PCR analyses of the marker genes for neurons, astrocytes, oligodendrocytes, oligodendrocyte progenitor cells, pericytes, and endothelial cells. CD41−CD45−CD31+CD13− and CD41−CD45−CD31−CD13+ microvascular cells were isolated from the brain cortex of Gpr30+/+ mice. Relative expression levels of the genes compared with those in the whole brain cortex are shown in (i). Statistical analysis: two-tailed unpaired t-test with Holm-Šídák’s correction (i). Data are presented as mean values ± SEM. P values are shown if significant. N.D. indicates not detected. Source data are provided as a Source Data file.
