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LncRNA DIGIT Accelerates Tube Formation of Vascular Endothelial Cells by Sponging miR-134.
Int Heart J. 2018 Sep 26; 59(5):1086-1095.IH

Abstract

Atherosclerosis is one of the most prevalent and important cardiac diseases, involving the heart and brain. This study aimed to explore the impacts of lncRNA Divergent to GSC induced by TGF-b family signaling (DIGIT) on vascular endothelial cells tube-formation capacity so as to reveal the potentials of DIGIT in atherosclerosis therapy. DIGIT expression in human microvascular endothelial HMEC-1 cells was silenced by transfection with shRNAs-targeted DIGIT. The effects of DIGIT silence on cell viability, migration, apoptosis, and tube formation were then assessed. Additionally, the cross-regulation between DIGIT and miR-134, and between miR-134 and Bmi-1 was detected to further reveal through which mechanism (s) DIGIT mediated HMEC-1 cells. The results showed that DIGIT silence significantly reduced cell viability, migration, tube-like structures formation, and induced apoptosis in HMEC-1 cells. DIGIT worked as a sponge for miR-134, and the anti-growth, anti-migratory, and anti-tube-formation functions of DIGIT silence on HMEC-1 cells were abolished by miR-134 suppression. Bmi-1 was a target of miR-134, and Bmi-1 upregulation abolished miR-134 overexpression-diminished cell growth, migration, and tube formation of HMEC-1 cells. Furthermore, Bmi-1 upregulation activated PI3K/AKT and Notch signaling pathways. In conclusion, our study demonstrated that lncRNA DIGIT accelerated tube formation of vascular endothelial cells through sponging miR-134. Our findings suggest that DIGIT and miR-134 may be promising molecular targets for atherosclerosis therapy.

Authors+Show Affiliations

Department of Vascular Surgery, The Frist Affiliated Hospital of Zhengzhou University.Department of Hematology, The Frist Affiliated Hospital of Zhengzhou University.Department of Vascular Surgery, The Frist Affiliated Hospital of Zhengzhou University.Department of Vascular Surgery, The Frist Affiliated Hospital of Zhengzhou University.Department of Vascular Surgery, The Frist Affiliated Hospital of Zhengzhou University.Department of Pediatric Surgery, The Frist Affiliated Hospital of Zhengzhou University.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

30158376

Citation

Miao, Chaofeng, et al. "LncRNA DIGIT Accelerates Tube Formation of Vascular Endothelial Cells By Sponging MiR-134." International Heart Journal, vol. 59, no. 5, 2018, pp. 1086-1095.
Miao C, Cao H, Zhang Y, et al. LncRNA DIGIT Accelerates Tube Formation of Vascular Endothelial Cells by Sponging miR-134. Int Heart J. 2018;59(5):1086-1095.
Miao, C., Cao, H., Zhang, Y., Guo, X., Wang, Z., & Wang, J. (2018). LncRNA DIGIT Accelerates Tube Formation of Vascular Endothelial Cells by Sponging miR-134. International Heart Journal, 59(5), 1086-1095. https://doi.org/10.1536/ihj.17-290
Miao C, et al. LncRNA DIGIT Accelerates Tube Formation of Vascular Endothelial Cells By Sponging MiR-134. Int Heart J. 2018 Sep 26;59(5):1086-1095. PubMed PMID: 30158376.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - LncRNA DIGIT Accelerates Tube Formation of Vascular Endothelial Cells by Sponging miR-134. AU - Miao,Chaofeng, AU - Cao,Haixia, AU - Zhang,Yonggan, AU - Guo,Xueli, AU - Wang,Zifan, AU - Wang,Jiaxiang, Y1 - 2018/08/29/ PY - 2018/8/31/pubmed PY - 2018/10/10/medline PY - 2018/8/31/entrez KW - Atherosclerosis KW - Divergent to GSC SP - 1086 EP - 1095 JF - International heart journal JO - Int Heart J VL - 59 IS - 5 N2 - Atherosclerosis is one of the most prevalent and important cardiac diseases, involving the heart and brain. This study aimed to explore the impacts of lncRNA Divergent to GSC induced by TGF-b family signaling (DIGIT) on vascular endothelial cells tube-formation capacity so as to reveal the potentials of DIGIT in atherosclerosis therapy. DIGIT expression in human microvascular endothelial HMEC-1 cells was silenced by transfection with shRNAs-targeted DIGIT. The effects of DIGIT silence on cell viability, migration, apoptosis, and tube formation were then assessed. Additionally, the cross-regulation between DIGIT and miR-134, and between miR-134 and Bmi-1 was detected to further reveal through which mechanism (s) DIGIT mediated HMEC-1 cells. The results showed that DIGIT silence significantly reduced cell viability, migration, tube-like structures formation, and induced apoptosis in HMEC-1 cells. DIGIT worked as a sponge for miR-134, and the anti-growth, anti-migratory, and anti-tube-formation functions of DIGIT silence on HMEC-1 cells were abolished by miR-134 suppression. Bmi-1 was a target of miR-134, and Bmi-1 upregulation abolished miR-134 overexpression-diminished cell growth, migration, and tube formation of HMEC-1 cells. Furthermore, Bmi-1 upregulation activated PI3K/AKT and Notch signaling pathways. In conclusion, our study demonstrated that lncRNA DIGIT accelerated tube formation of vascular endothelial cells through sponging miR-134. Our findings suggest that DIGIT and miR-134 may be promising molecular targets for atherosclerosis therapy. SN - 1349-3299 UR - https://www.unboundmedicine.com/medline/citation/30158376/LncRNA_DIGIT_Accelerates_Tube_Formation_of_Vascular_Endothelial_Cells_by_Sponging_miR_134_ L2 - https://dx.doi.org/10.1536/ihj.17-290 DB - PRIME DP - Unbound Medicine ER -