Fig 1: IGF-1 and RELN as potential mediators in the crosstalk between LECs and cardiomyocytes. (A) Western blot for IGF-1 in heart tissues from control and swim mice (n = 6); (B) RT-qPCR for IGF-1 and RELN in heart tissues from control and swim mice (n = 6); (C) Western blot for IGF-1 in heart tissues from control and swim mice treated with SAR131675 (100 mg/kg/d) or vehicle controls (n = 6); (D) RT-qPCR for IGF-1 and RELN in heart tissues from control and swim mice treated with SAR131675 (100 mg/kg/d) or vehicle controls (n = 6); and ELISA for (E) IGF-1 and (F) RELN levels in LEC-conditioned medium pre-treated with VEGFR3 inhibitor SAR131675 (100 nM) or not (n = 4). Independent-sample t test (two-tailed) was used for statistical comparisons between 2 groups. One-way ANOVA test was used for statistical comparisons among 3 groups. Two-way ANOVA followed by Tukey post hoc test was used for statistical comparisons among 4 groups. * p < 0.05; ** p < 0.01; *** p < 0.001. ANOVA = analysis of variance; GAPDH = glyceraldehyde-3-phosphate dehydrogenase; IGF-1 = insulin-like growth factor-1; LEC = lympathic endothelial cell; OD = optical density; RELN = the extracellular protein Reelin; RT-qPCR = reverse transcription quantitative polymerase chain reaction.
Fig 2: Cardiac lymphangiogenesis is required for exercise-induced physiological cardiac growth by VEGFR3 activation. LEC-conditioned medium promotes both physiological hypertrophy and proliferation of cardiomyocytes through AKT activation and the C/EBPß–CITED4 axis. AKT = protein kinase B; C/EBPß = CCAAT enhancer-binding protein beta; CITED4 = CBP/p300-interacting transactivators with E (glutamic acid)/D (aspartic acid)-rich-carboxylterminal domain4; IGF-1 = insulin-like growth factor-1; LEC = lymphatic endothelial cell; LYVE-1 = lymphatic vessel endothelial hyaluronic acid receptor 1; RELN = the extracellular protein Reelin; VEGFR3 = vascular endothelial growth factor receptor 3.
Supplier Page from Abcam for Human Insulin like Growth Factor 1 ELISA Kit (IGF1)