scholarly journals Proteome-scale profiling reveals MAFF and MAFG as two novel key transcription factors involved in palmitic acid-induced umbilical vein endothelial cell apoptosis

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Mangyuan Wang ◽  
Fen Liu ◽  
Binbin Fang ◽  
Qiang Huo ◽  
Yining Yang

Abstract Background Vascular endothelial cell apoptosis is the leading risk factor of atherosclerosis (AS). The purpose of our study was to use a new generation high-throughput transcription factor (TF) detection method to identify novel key TFs in vascular endothelial cell apoptosis induced by palmitic acid (PA). Methods Human umbilical vein endothelial cells (HUVECs) were treated with 0, 300, or 500 µM PA. Candidate TFs in the three groups were identified by differential expression, pathway enrichment, Western Blot (WB), and RT-qPCR analyses. Apoptosis was assessed by fluorescence-activated cell sorting (FACS) using FITC-annexin V and propidium iodide staining. Results We established a HUVEC apoptosis model to simulate the process of atherosclerosis onset and identified 51 significant TFs. of the 51 TFs, v-maf musculoaponeurotic fibrosarcoma oncogene family protein G (MAFG) and v-maf musculoaponeurotic fibrosarcoma oncogene family protein F (MAFF), were matched to known AS signalling pathways and were validated by WB and RT-qPCR analyses in our study. Overexpression of MAFG or MAFF in HUVECs significantly inhibited PA-induced early apoptosis. Conclusions We identified MAFF and MAFG as novel key TFs in vascular endothelial cell apoptosis.

2020 ◽  
Author(s):  
Mangyuan Wang ◽  
Fen Liu ◽  
Binbin Fang ◽  
Qiang Huo ◽  
Yining Yang

Abstract Backgrounds: Vascular endothelial cell apoptosis is the first risk factor of atherosclerosis (AS), and it can be induced by high doses of glucose and palmitic acid (PA). The purpose of our study is to use a new generation of high-throughput transcription factors (TFs) detecting method to identify novel candidate key TFs involved in PA-induced vascular endothelial cell apoptosis.Methods: Human umbilical vein endothelial cells (HUVECs) were treated with 0µM PA (control group), 250µM PA (group 1), or 500µM PA (group 2). Candidate TFs among the three groups were determined by significant changes according to t-test, and pathway enrichment, western blot (WB) and RT-qPCR were then performed.Results: Fifty-one TFs showing with significant p value were identified, and 24 TFs with significant p value plus fold change > 2 and with dose-dependence were identified with 12 TFs biologically validated in former studies. Two of the remaining 12 novel TFs, v-maf musculoaponeurotic fibrosarcoma oncogene family protein G (MAFG) and v-maf musculoaponeurotic fibrosarcoma oncogene family protein F (MAFF), were matched to AS known signalling pathways and were validated by WB and RT-qPCR in our study.Conclusions: We identified MAFG and MAFF as novel candidate key TFs in vascular endothelial cell apoptosis, which is the key initial process of AS.


2018 ◽  
Vol 38 (3) ◽  
Author(s):  
Chengfu Song ◽  
Xiangdong Zhao

In patients with cerebral infarction (CI), elevated serum uric acid (UA) level may exacerbate the occurrence and development of carotid atherosclerosis (AS). Our study intended to explore the underlying mechanism. We enrolled 86 patients with CI, and divided them into four groups: Non-AS, AS-mild, AS-moderate, and AS-severe groups; the levels of UA and oxidative stress-related factors in serum were detected. The middle cerebral artery occlusion (MCAO) model was used to stimulate CI in rats, and different doses of UA were administrated. The levels of oxidative stress-related factors in serum were detected. Hematoxylin & eosin (H&E) staining was used to observe the morphological alterations, and the apoptotic cell death detection kit was used to detect apoptotic cells. Increased UA concentration and enhanced oxidative stress were found in AS patients. H&E staining results showed that UA treatment exacerbated morphological damage in rats with MCAO, promoted oxidative stress, and enhanced vascular endothelial cell apoptosis in rats with MCAO.


2006 ◽  
Vol 54 (4) ◽  
pp. 268-274 ◽  
Author(s):  
Min Xiang ◽  
Min Yang ◽  
Chenghua Zhou ◽  
Juan Liu ◽  
Wenna Li ◽  
...  

2000 ◽  
Vol 35 (7) ◽  
pp. 1785-1790 ◽  
Author(s):  
Atsushi Iwakura ◽  
Masatoshi Fujita ◽  
Koji Hasegawa ◽  
Tatsuya Sawamura ◽  
Ryuji Nohara ◽  
...  

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