TFAP2C inhibits cell autophagy to alleviate myocardial ischemia/reperfusion injury by regulating miR‐23a‐5p/SFRP5/Wnt5a axis

Abstract

Myocardial ischemia/reperfusion (MI/R) injury contributes to severe injury for cardiomyocytes. In this study, we aimed to explore the underlying mechanism of TFAP2C on cell autophagy in MI/R injury. MTT assay measured cell viability.The cells injury was evaluated by commercial kits. IF detected the level of LC3B.Dual luciferase reporter gene assay, ChIP or RIP assay were performed to verify the interactions between crucial molecules. We found that TFAP2C and SFRP5 expression were decreased while miR-23a-5p and Wnt5a increased in AC16 cells in response to H/R condition. H/R induction led to cell injury and induced autophagy, which were reversed by TFAP2C overexpression or 3-MA treatment (an autophagy inhibitor). Mechanistically, TFAP2C suppressed miR-23a expression through binding to miR-23a promoter, and SFRP5 was a target gene of miR-23a-5p. Moreover, miR-23a-5p overexpression or rapamycin reversed the protective impacts of TFAP2C overexpression on cells injury and autophagy upon H/R condition. In conclusion, TFAP2C inhibited autophagy to improve H/R-induced cells injury by mediating miR-23a-5p/SFRP5/Wnt5a axis.

Identification of candidate biomarkers and pathways associated with multiple sclerosis using bioinformatics and next generation sequencing data analysis

“…IKZF3 [69], hsa-mir-146a-5p [607], BRCA1 [608] and NFKB1 [609] can participate in the occurrence and development of MS. IKZF3 [239], TAB2 [256], CCR4 [231], LTF (lactotransferrin) [249], CDH1 [266], BRCA1 [610], NFKB1 [611] and FOXO3 [612] might play an important role in the occurrence and development of autoimmune disease. TAB2 [131], CCR4 [112], LTF (lactotransferrin) [126], hsa-mir-146a-5p [613], hsa-mir-8485 [614], BRCA1 [615], NFKB1 [616], TEAD1 [617], TFAP2C [618], FOXO3 [619 and NRF1 [620] risk factors have been shown to increase susceptibility to cardiovascular diseases. Several studies have shown that TAB2 [131], LTF (lactotransferrin) [487], BRCA1 [621], NFKB1 [622], TEAD1 [623], FOXO3 [624] and NRF1 [625] can be involved in the disease progression of obesity ., Altered expression of CCR4 [280], LTF (lactotransferrin) [295], CDH1 [313], CFTR (CF transmembrane conductance regulator) [317], hsa-mir-146a-5p [626], hsa-mir-195-5p [627], hsa-mir-4739 [628], HNF4A [629], NFKB1 [630], NR2F1 [631], FOXO3 [632] and NRF1 [633] are observed in diabetes mellitus.…”

Cardiomyocyte Autophagy: A Novel Therapeutic Target by LncRNA PART1

“…In this issue of the Korean Circulation Journal , Zeng et al 1) demonstrated that long non-coding RNA (lncRNA) prostate androgen regulated transcript 1 (PART1) was responsible for inducing cardiomyocyte autophagy in the myocardial ischemia-reperfusion injury model. LncRNA PART1 was downregulated by ischemic stress in cardiomyocytes, resulting in significant autophagy and apoptosis.…”