Fig. 3
Stimulation of LPAR1/Gi by LPA and S1PR1/3/Gi by S1P are critical for stem cell protection. a The expression profiles of LPAR subtypes were determined in cDNAs from hADMSCs (labelled as MSC) or neonatal rat cardiac myocytes for each set of LPAR primers. b Changes in cell viability and caspase-3/7 activity of hADMSCs after LPS/H2O2/LPA treatments, with or without the AM966 (LPAR1 inhibitor), or PTX (Gi inhibitor) co-treatment (n = 4). c The expression profiles of S1PR subtypes were determined in cDNAs from hADMSCs (labelled as MSC) for each set of S1PR primers (n = 4). d Changes in cell viability and caspase-3/7 activity of hADMSCs after LPS/H2O2/S1P treatments, with or without the W146 (S1PR1 inhibitor), JTE013 (S1PR2 inhibitor), or CAY10444 (S1PR3 inhibitor) co-treatment (n = 4). e Changes in cell viability and caspase-3/7 activity of hADMSCs after LPS/H2O2/LPA/S1P treatments, with or without the PTX (Gi inhibitor) co-treatment (n = 4). f Knockdown efficiency verification of G12/13 shRNA transfection using G12- and G13-specific antibodies. g Changes in cell viability and caspase-3/7 activity of hADMSCs after LPS/H2O2/LPA/S1P treatments, with or without the G12/13 shRNA co-treatment (n = 4). h The signalling pathway concluded from this figure. Data from each group are expressed as means ± SEM. Statistical comparison between groups was performed with the Kruskal–Wallis test followed by Dunn’s post-hoc test to detect differences in all groups. ***p < 0.001 versus control group; #p < 0.05 versus LPS/H2O2 group; ##p < 0.01 versus LPS/H2O2 group; ###p < 0.001 versus LPS/H2O2 group; @p < 0.05 versus LPS/H2O2 + LPA or S1P group; @@@p < 0.001 versus LPS/H2O2 + LPA or S1P group. Ctrl, control; LPA(R), lysophosphatidic acid (receptor); LPS, lipopolysaccharide; S1P(R), sphingosine-1-phosphate (receptor)