| Autor: |
Wang KJ; Division of Vascular Surgery, The First Affiliated Hospital, Sun Yat-sen University.; National-Local Joint Engineering Laboratory of Vascular Diseases Treatment, The First Affiliated Hospital, Sun Yat-sen University.; Guangdong Engineering Laboratoty of Diagnosis and Treatment of Vascular Disease, The First Affiliated Hospital, Sun Yat-sen University., Zhang YX; National-Local Joint Engineering Laboratory of Vascular Diseases Treatment, The First Affiliated Hospital, Sun Yat-sen University.; Division of Hypertension and Vascular Diseases, Department of Cardiology, Heart Center, The First Affiliated Hospital, Sun Yat-sen University., Mo ZW; Division of Vascular Surgery, The First Affiliated Hospital, Sun Yat-sen University.; National-Local Joint Engineering Laboratory of Vascular Diseases Treatment, The First Affiliated Hospital, Sun Yat-sen University.; Guangdong Engineering Laboratoty of Diagnosis and Treatment of Vascular Disease, The First Affiliated Hospital, Sun Yat-sen University., Li ZL; Division of Vascular Surgery, The First Affiliated Hospital, Sun Yat-sen University.; National-Local Joint Engineering Laboratory of Vascular Diseases Treatment, The First Affiliated Hospital, Sun Yat-sen University.; Guangdong Engineering Laboratoty of Diagnosis and Treatment of Vascular Disease, The First Affiliated Hospital, Sun Yat-sen University., Wang M; Division of Vascular Surgery, The First Affiliated Hospital, Sun Yat-sen University.; National-Local Joint Engineering Laboratory of Vascular Diseases Treatment, The First Affiliated Hospital, Sun Yat-sen University.; Guangdong Engineering Laboratoty of Diagnosis and Treatment of Vascular Disease, The First Affiliated Hospital, Sun Yat-sen University., Wang R; Division of Vascular Surgery, The First Affiliated Hospital, Sun Yat-sen University.; National-Local Joint Engineering Laboratory of Vascular Diseases Treatment, The First Affiliated Hospital, Sun Yat-sen University.; Guangdong Engineering Laboratoty of Diagnosis and Treatment of Vascular Disease, The First Affiliated Hospital, Sun Yat-sen University., Wang ZC; Division of Vascular Surgery, The First Affiliated Hospital, Sun Yat-sen University.; National-Local Joint Engineering Laboratory of Vascular Diseases Treatment, The First Affiliated Hospital, Sun Yat-sen University.; Guangdong Engineering Laboratoty of Diagnosis and Treatment of Vascular Disease, The First Affiliated Hospital, Sun Yat-sen University., Chang GQ; Division of Vascular Surgery, The First Affiliated Hospital, Sun Yat-sen University.; National-Local Joint Engineering Laboratory of Vascular Diseases Treatment, The First Affiliated Hospital, Sun Yat-sen University.; Guangdong Engineering Laboratoty of Diagnosis and Treatment of Vascular Disease, The First Affiliated Hospital, Sun Yat-sen University., Wu WB; Division of Vascular Surgery, The First Affiliated Hospital, Sun Yat-sen University.; National-Local Joint Engineering Laboratory of Vascular Diseases Treatment, The First Affiliated Hospital, Sun Yat-sen University.; Guangdong Engineering Laboratoty of Diagnosis and Treatment of Vascular Disease, The First Affiliated Hospital, Sun Yat-sen University. |
| Abstrakt: |
Arteriosclerosis obliterans (ASO) is characterized by arterial narrowing and blockage due to atherosclerosis, influenced by endothelial dysfunction and inflammation. This research focuses on exploring the role of MAGOH-DT, a long noncoding RNA, in mediating endothelial cell dysfunction through endothelial-mesenchymal transition (EndMT) under inflammatory and hyperglycemic stimuli, aiming to uncover potential therapeutic targets for ASO. Differential expression of lncRNAs, including MAGOH-DT, was initially identified in arterial tissues from ASO patients compared to healthy controls through lncRNA microarray analysis. Validation of MAGOH-DT expression in response to tumor necrosis factor-alpha (TNF-α) and high glucose (HG) was performed in human umbilical vein endothelial cells (HUVECs) using RT-qPCR. The effects of MAGOH-DT and HNRPC knockdown on EndMT were assessed by evaluating EndMT markers and TGF-β2 protein expression with Western blot analysis. RNA-immunoprecipitation assays were used to explore the interaction between MAGOH-DT and HNRPC, focusing on their role in regulating TGF-β2 translation. In the results, MAGOH-DT expression is found to be upregulated in ASO and further induced in HUVECs under TNF-α/HG conditions, contributing to the facilitation of EndMT. Silencing MAGOH-DT or HNRPC is shown to inhibit the TNF-α/HG-induced increase in TGF-β2 protein expression, effectively attenuating EndMT processes without altering TGF-β2 mRNA levels. In conclusion, MAGOH-DT is identified as a key mediator in the process of TNF-α/HG-induced EndMT in ASO, offering a promising therapeutic target. Inhibition of MAGOH-DT presents a novel therapeutic strategy for ASO management, especially in cases complicated by diabetes mellitus. Further exploration into the therapeutic implications of MAGOH-DT modulation in ASO treatment is warranted. |
