Inducible phospholipid transfer protein deficiency ameliorates atherosclerosis

Zhang, Ke; Zheng, Jiao; Chen, Yunqin; Dong, Jianyu; Li, Zhiqiang; Chiang, Yeunpo; He, Mulin; Huang, Qingzhong; Tang, Huiru

doi:10.1016/j.atherosclerosis.2021.03.011

Cited by 11 publications

(1 citation statement)

References 39 publications

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“…PLTP encodes a protein involved in the transfer of phospholipids and free cholesterol from low-density lipoproteins (LDL) and very low-density lipoproteins (VLDL) into high-density lipoproteins (HDL) and the exchange of phospholipids between LDL and VLDL themselves [ 58 ]. In mouse models, PLTP deficiency reduces VLDL and LDL levels and attenuates atherosclerosis, while PLTP overexpression exerts an opposite effect [ 59 , 60 ]. Thus, lipoprotein metabolism is another pathway involved in the genotoxic stress induced endothelial dysfunction.…”

Section: Discussionmentioning

confidence: 99%

Identification of Key Genes and Pathways in Genotoxic Stress Induced Endothelial Dysfunction: Results of Whole Transcriptome Sequencing

et al. 2022

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Atherosclerosis is a leading cause of cardiovascular morbidity and mortality worldwide. Endothelial disfunction underlying the atherogenesis can be triggered by genotoxic stress in endothelial cells. In the presented research whole transcriptome sequencing (RNA-seq) of human coronary artery (HCAEC) and internal thoracic artery (HITAEC) endothelial cells in vitro exposed to 500 ng/mL mitomycin C (treatment group) or 0.9% NaCl (control group) was performed. Resulting to bioinformatic analysis, 56 upregulated differentially expressed genes (DEGs) and 6 downregulated DEGs with absolute fold change ≥ 2 and FDR p-value < 0.05 were selected in HCAEC exposed to mitomycin C compared to the control group; in HITAEC only one upregulated DEG was found. According to Gene Ontology enrichment analysis, DEGs in HCAEC were classified into 25 functional groups of biological processes, while in HITAEC we found no statistically significant (FDR p-value < 0.05) groups. The four largest groups containing more than 50% DEGs (“signal transduction”, “response to stimulus”, “biological regulation”, and “regulation of biological process”) were identified. Finally, candidate DEGs and pathways underlying the genotoxic stress induced endothelial disfunction have been discovered that could improve our understanding of fundamental basis of atherogenesis and help to justification of genotoxic stress as a novel risk factor for atherosclerosis.

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Section: Discussionmentioning

confidence: 99%