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DIA proteomics reveals the regulatory process of Sacubitril in the treatment of myocardial infarction reperfusion

ABSTRACT: As one of the major cardiovascular diseases, myocardial infarction is the most serious manifestation of coronary artery disease, which has attracted wide attention due to its high morbidity and mortality. The left anterior descending artery(LAD) of 6-8 weeks old male KM mice was ligated for 40min, followed by perfusion to establish an ischemia-reperfusion(I/R) model. After 3 days of monitoring, 60 mg/kg sacubitril/valsartan sodium was given for a week. Hematoxylin-eosin(HE) staining, 2, 3, 5-triphenyl-tetrazolium chloride(TTC) staining and echocardiography were used to evaluate the therapeutic effect of sacubitril/valsartan sodium on I/R.The proteomics information of heart tissue was obtained by data-independent acquisition(DIA) proteomics. The analysis results showed that sacubitril/valsartan sodium may mediate the treatment of I/R injury by regulating enzyme activity and immune-related biological processes, up-regulating fatty acid degradation metabolic pathway, PPAR pathway, peroxisome pathway, and down-regulating complement system and ribosome pathway.The results showed that sacubitril/valsartan sodium had a good therapeutic effect on I/R injury.

ORGANISM(S): Mus Musculus

SUBMITTER: Xia Chen

PROVIDER: PXD045090 | iProX | Mon Sep 04 00:00:00 BST 2023

REPOSITORIES: iProX

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Project description:We adopted a transcriptome-wide microarray analysis approach to determine the extent to which vascular gene expression is altered as a result of juvenile obesity and identify obesity-responsive mRNAs. We examined transcriptional profiles in the left anterior descending coronary artery (LAD), perivascular fat adjacent to the LAD, and descending thoracic aorta between obese (n=5) and lean (n=6) juvenile Ossabaw pigs (age=22 weeks). Obesity was experimentally induced by feeding the animals a high-fat/high fructose corn syrup/high-cholesterol diet for 16 weeks. We found that expression of 189 vascular cell genes in the LAD and expression of 165 genes in the thoracic aorta were altered with juvenile obesity (FDRM-bM-^IM-$10%) with an overlap of only 28 genes between both arteries. Notably, a number of genes found to be markedly up-regulated in the LAD of obese pigs are implicated in atherosclerosis, including ACP5, LYZ, CXCL14, APOE, PLA2G7, LGALS3, SPP1, ITGB2, CYBB, and P2RY12. Furthermore, pathway analysis revealed the induction of pro-inflammatory and pro-oxidant pathways with obesity primarily in the LAD. Gene expression in the LAD perivascular fat was minimally altered with juvenile obesity. Together, we provide new evidence that obesity produces artery-specific changes in pre-translational regulation with a clear up-regulation of pro-atherogenic genes in the LAD. Our data may offer potential viable drug targets and mechanistic insights regarding the molecular precursors involved in the origins of over-nutrition and obesity-associated vascular disease. In particular, our results suggest that the oxLDL-LOX-1-NFM-NM-:B signaling axis may be involved in the early initiation of a juvenile obesity-induced pro-atherogenic coronary artery phenotype. We examined transcriptional profiles in the left anterior descending coronary artery (LAD), perivascular fat adjacent to the LAD, and descending thoracic aorta between obese (n=5) and lean (n=6) juvenile Ossabaw pigs (age= 22 weeks). All three tissue types were taken from each animal, and each was applied to one and only one array array except a single Thoracic aorta (Animal ID 63 because there were not enough arrays), so there were 32 total arrays (11 unique pigs).

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DIA proteomics reveals the regulatory process of Sacubitril in the treatment of myocardial infarction reperfusion

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