Fig. 5

nCTRP9 promotes cardiac fibrosis through upregulation of Rap1. A. Heatmap of the different genes after nCTRP9 treated immortalized cardiac fibroblasts (iCF) activated with Tgf-β. B KEGG pathway enrichment of differentially expressed genes. C. ESI-05, an inhibitor of Rap1, down-regulated the transcription of fibrosis-related genes in iCF. n = 4. D. nCTRP9 increased MEK 1/2 and ERK 1/2 phosphorylation in fibroblasts. n = 4. E. nCTRP9 increased MEK 1/2 and ERK 1/2 phosphorylation in mice heart post MI surgery. n = 4. F. Rap1 knockdown efficiency in iCF. n = 4. G. Down-regulation of Rap1 attenuated the promoting effect of nCTRP9 on the transcription of fibrosis-related genes in iCF. n = 4. H. Rap1 knockdown attenuated α-smooth muscle actin (α-SMA) expression increased by nCTRP9 in iCF. n = 6. I. Rap1 knockdown attenuated the promoting effect of nCTRP9 on cell proliferation of iCF. n = 6. * p < 0.05, ** p < 0.01