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Coronary alarmins as residual risk markers of atherosclerosis under hypolipidemic therapy

ABSTRACT: Increased levels of low-density lipoproteins are the main risk factor in the initiation and progression of atherosclerosis. Although statin treatment can effectively lower these levels, there is still a residual risk of cardiovascular events. A more recent therapy, with encouraging results, to regulate the low-density lipoproteins levels, has been represented by the proprotein convertase subtilisin/kexin type 9 inhibition, a protein with critical role in lipid metabolism.Alarmins are endogenous danger signals that are released or secreted from damaged or dead/dying cells as a result of various insults. These stress-sensing molecules have been correlated with various inflammatory states or diseases. We hypothesize that a specific panel of alarmins could indicate the persistence of silent atherosclerosis residual risk.

INSTRUMENT(S): LTQ Orbitrap Velos

ORGANISM(S): Oryctolagus Cuniculus (rabbit)

TISSUE(S): Fibroblast

DISEASE(S): Cardiovascular System Disease

SUBMITTER: Felicia Antohe

LAB HEAD: Felicia Antohe

PROVIDER: PXD035692 | Pride | 2022-10-03

REPOSITORIES: Pride

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			Action	DRS
	Miocard_ERA_CVD_9_11_2020.msf	Msf
	Miocard_ERA_CVD_9_11_2020.mzML	Mzml
	Miocard_ERA_CVD_9_11_2020.pdResult	Other
	Miocard_ERA_CVD_Ae_24_1_201026083200.raw	Raw
	Miocard_ERA_CVD_Ae_24_2_201026103101.raw	Raw

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Project description:Background---For decades, plasma lipid levels have been known risk factors of atherosclerosis. Recently, inflammation has gained acceptance as a crucial event in the pathogenesis and development of atherosclerosis. A number of studies have provided some insights into the relationships between the two aspects of atherosclerosis: plasma lipids --- the risk factors, and circulating leukocytes --- the effectors of inflammation. In this study, we investigate the relationships between plasma lipids and leukocytes. Methods and Results---No significant correlation was found between leukocyte counts and plasma lipid levels in 74 individuals. Profiling and analyzing the leukocyte gene expression of 32 individuals revealed distinctive patterns in response to plasma lipid levels: 1) genes involved in lipid metabolism and in the electron transport chain were positively correlated with triglycerides and low-density lipoprotein cholesterol levels, and negatively correlated with high-density lipoprotein cholesterol levels; 2) genes involved in platelet activation were negatively correlated with high-density lipoprotein cholesterol levels; 3) transcription factors regulating lipidgenesis-related genes were correlated with plasma lipid levels; 4) a number of genes correlated to plasma lipid levels were found located in the regions of known QTLs associated with hyperlipemia. Conclusions--- We discovered interesting patterns of leukocyte gene expression in response to plasma lipid levels. Most importantly, genes involved in lipid metabolism, the electron transportation chain, and platelet activation were found correlated with plasma lipid levels. We suggest that leukocytes respond to changing plasma lipid levels by regulating a network of genes, including genes involved in lipid and fatty acid metabolism, through the activation of key transcription factors, such as sterol regulatory element binding transcription factors and peroxisome proliferative activated receptors. Keywords: Atherosclerosis, leukocyte, lipid, gene expression

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Coronary alarmins as residual risk markers of atherosclerosis under hypolipidemic therapy

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