The mechanism of myocardial fibrosis is ameliorated by myocardial infarction-associated transcript through the PI3K/Akt signaling pathway to relieve heart failure

Figures

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  Figure 1.. (a) Cell proliferation activity as measured by the CCK-8 assay in each group. (b) Measurement of collagen content in each group. (c–p) Expression levels of mRNA and protein for various factors in vitro with measurement by real-time reverse transcription polymerase chain reaction and ELISA assays. *p<0.05 versus the NC group; **p<0.01 versus the NC group. #p<0.05 versus the NC+Scramble group; ##p<0.01 versus the NC+Scramble group. ϕp<0.05 versus the NC+si-MIAT group; ϕϕp<0.01 versus the NC+si-MIAT group. NC, negative control; siMIAT, short interfering RNA myocardial infarction-associated transcript; TGF-ß, transforming growth factor-ß; CCK-8, cholecystokinin-8; VEGF, vascular endothelial growth factor; PI3K, phosphoinositide 3-kinase; Akt, protein kinase B; IL, interleukin; TNF-α, tumor necrosis factor-α; Col, collagen; ELISA, enzyme-linked immunosorbent assay; MIAT, myocardial infarction-associated transcript.

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  Figure 2.. Silencing MIAT inhibits the PI3K/Akt signaling pathway in vitro. **p<0.01 versus the NC group; ##p<0.01 versus the NC+Scramble group. ϕϕp<0.01 versus the NC+si-MIAT group. NC, negative control; siMIAT, short interfering RNA myocardial infarction-associated transcript; TGF-ß1, transforming growth factor-ß1; VEGF, vascular endothelial growth factor; p-PI3K, phosphorylated phosphoinositide 3-kinase; PI3K, phosphoinositide 3-kinase; p-Akt, phosphorylated protein kinase B; Akt, protein kinase B; TNF-α, tumor necrosis factor-α; GAPDH, glyceraldehyde-3-phosphate dehydrogenase.

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  Figure 3.. Expression levels of mRNA and protein for various factors in vivo with measurement by real-time reverse transcription polymerase chain reaction and ELISA assays. *p<0.05 versus the NC group; **p<0.01 versus the NC group. #p<0.05 versus the HF group; ##p<0.01 versus the HF group. NC, negative control; HF, heart failure; siMIAT, short interfering RNA myocardial infarction-associated transcript; VEGF, vascular endothelial growth factor; PI3K, phosphoinositide 3-kinase; Akt, protein kinase B; IL, interleukin; TNF-α, tumor necrosis factor-α; Col, collagen; ELISA, enzyme-linked immunosorbent assay; MIAT, myocardial infarction-associated transcript.

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  Figure 4.. (a) Silencing MIAT inhibits the PI3K/Akt signaling pathway (protein expression). (b) Hematoxylin and eosin staining in in vivo experiments. *p<0.05 versus the NC group; #p<0.05 versus the HF group. NC, negative control; HF, heart failure; siMIAT, short interfering RNA myocardial infarction-associated transcript; VEGF, vascular endothelial growth factor; p-PI3K, phosphorylated phosphoinositide 3-kinase; PI3K, phosphoinositide 3-kinase; p-Akt, phosphorylated protein kinase B; Akt, protein kinase B; TNF-α, tumor necrosis factor-α; GAPDH, glyceraldehyde-3-phosphate dehydrogenase.