GSE86569 dataset was performed to explore the potential role of PTX3 in HF. Male C57/BL6J mice were administered with lentiviral vector encoding PTX3 KD or empty vector, and then underwent either coronary ligation or sham surgery. Echocardiography, Masson staining, and immunofluorescence counterstaining were conducted to evaluate the cardiac function and fibrosis. Cardiac fibroblasts were isolated and transfected with lentiviral vector encoding PTX3 KD in vitro to verify the in vivo findings.

Results: Bioinformatics analysis based on GSE86569 revealed the aberrant expression of PTX3 in HF patients. Echocardiography showed that PTX3 KD reversed the HF-induced cardiac dysfunction with better cardiac function parameters. Masson staining demonstrated that the obvious infarct and high fibrosis ratio in HF mice were remarkably improved after PTX3 KD. Immunofluorescence staining indicated that the HF-induced increase expression of α-SMA was significantly suppressed by PTX3 KD. Additionally, both in vivo and in vitro results confirmed that PTX3 KD decreased the fibrosis-related up-regulation of collagen I, collagen III, and p-STAT3. However, the result was opposite after IL-6 treatment.

Conclusions: PTX3 KD protects the cardiac function and counteracts the myocardial fibrosis by down-regulating IL-6/STAT3 pathway in HF." name="description"> Pentraxin 3 depletion (PTX3 KD) inhibited myocardial fibrosis in heart failure after myocardial infarction - Figure f1 | Aging

Research Paper Volume 14, Issue 9 pp 4036—4049

Pentraxin 3 depletion (PTX3 KD) inhibited myocardial fibrosis in heart failure after myocardial infarction


Figure 1. Bioinformatics analysis indicated the potential association between PTX3 and HF progression. (A) Kaplan-Meier analysis in GEO database showed that the up-regulation of PTX3 was associated with a lower overall survival rate. (B) PTX3 in tissues from HF patients was up-regulated compared with that in normal tissues. (C) Volcano plot and (D) heatmap of the PTX3-induced DEGs; red indicates the up-regulated genes and blue indicates the down-regulated genes. (E) Protein-protein interaction network of DEGs. (F) GSEA showed a significant correlation between PTX3 expression and the pathways related to IL-6 production. (G) GO analysis and (H) KEGG analysis revealed the representative enrichment pathways.