Figure 1 | Scientific Reports

Figure 1

From: Prokineticin receptor-1-dependent paracrine and autocrine pathways control cardiac tcf21+ fibroblast progenitor cell transformation into adipocytes and vascular cells

Figure 1

Microarray analyses of TG-PKR1 hearts. (A) K-means analysis of the microarray data: gene expression is presented as a colored matrix, where each row represents a gene and each column represents a sample. Green, black and red correspond to lower values, median values and higher values, respectively. Left: transcriptome data clustered by K-means (with k = 10). The highlighted cluster 8 clearly distinguishes WT from TG-PKR1 mice (shown by hierarchical clustering on the right). (B) Hierarchical clustering of the samples based on the 46 expression profiles of WT and TG-PKR1 mice (12 weeks old). All n = 3 mice/group. (C) qPCR analyses of the PPARγ signaling pathway-related genes (Fabp4, UCP-1, Scd1, PPARγ, perilipin and adiponectin) involved in adipogenesis (*p < 0.05, n = 4; t-test). (D) Western blot analyses of PPARγ protein levels in cultured CF-like non-cardiomyocytes and cardiomyocytes derived from TG-PKR1 and WT hearts. (E) Histogram shows the quantification of PPARγ protein levels in the CF-like cells and cardiomyocytes (*p < 0.05, n = 4; two way ANOVA). (F) Western blot analyses of PPARγ protein levels in CF-like cells upon prokineticin-2 (PK2) treatment at the indicated times. Histogram shows the quantification of PPARγ protein levels after PK2 exposure in the CF-like cells (*p < 0.05, n = 3; two way ANOVA). All n = 6 mice/group. Original blots are shown in Figure S5.

Back to article page