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LC-MS/MS of thoracic aorta and perivascular adipose tissue following short-term dietary methionine restriction

ABSTRACT: We are exploring pathways influenced by short-term dietary methionine restriction (MR) in thoracic aorta and associated perivascular adipose tissue (PVAT) from obese C57BL/6J male mice around 26 weeks of age. Mice were fed 60% high fat diet (HFD) until they were obese, experimental mice were given 60% HFD with 0.12% methionine for 3, 5, and 10 days while the control group maintained a 60% HFD with 0.86% methionine. All mice were euthanized on the same day, then thoracic aorta was harvested, the PVAT was removed, and both sample types were prepared and analyzed separately. Three mice per group were assessed with LC-MS/MS. MR diet induced lean phenotype in PVAT, which was observed histologically, and we hypothesized that changes in lipid metabolism and mitochondrial bioenergetics mediated this response.

INSTRUMENT(S): LTQ FT

ORGANISM(S): Arachis Hypogaea (peanut)

TISSUE(S): Blood Plasma, Early Embryonic Cell

DISEASE(S): Polycystic Kidney

SUBMITTER: Carlos Gartner

LAB HEAD: Marissa McGilvrey

PROVIDER: PXD051504 | Pride | 2025-04-07

REPOSITORIES: Pride

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			Action	DRS
	2019-06-03_Bethany_PVATSW_10_1.wiff	Wiff
	2019-06-03_Bethany_PVATSW_10_1.wiff.scan	Wiff
	2019-06-03_Bethany_PVATSW_10_2.wiff	Wiff
	2019-06-03_Bethany_PVATSW_10_2.wiff.scan	Wiff
	2019-06-03_Bethany_PVATSW_10_3.wiff	Wiff

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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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LC-MS/MS of thoracic aorta and perivascular adipose tissue following short-term dietary methionine restriction

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