LncRNA MALAT1 inhibits hypoxia/reoxygenation-induced human umbilical vein endothelial cell injury via targeting the microRNA-320a/RAC1 axis

2020 ◽  
Vol 401 (3) ◽  
pp. 349-360 ◽  
Author(s):  
Rongrong Zhu ◽  
Xiao Hu ◽  
Wei Xu ◽  
Zhourui Wu ◽  
Yanjing Zhu ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Injury ◽  
Umbilical Vein ◽  
Tube Formation ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Human Umbilical Vein ◽  
Rna Immunoprecipitation ◽  
Reporter Assays ◽  
Hypoxia Reoxygenation

AbstractAngiogenesis is believed to protect against hypoxia/reoxygenation (H/R)-induced cell injury. MALAT1 and microRNA-320a (miR-320a) are involved in cancer angiogenesis. To investigate the function of the MALAT1/miR-320a axis in H/R-induced cell injury, human umbilical vein endothelial cell (HUVEC) angiogenesis was detected using the Cell Counting Kit-8 (CCK-8), Transwell migration, cell adhesion and tube formation assays. The expression of MALAT1 and miR-320a was revealed by quantitative reverse transcription polymerase chain reaction (qRT-PCR). The direct binding relationship between miR-320a and MALAT1 was detected by RNA immunoprecipitation (RIP) and dual luciferase reporter assays. The data indicated that H/R induces angiogenesis injury and that the expression of MALAT1 was augmented in H/R-stimulated HUVECs. Overexpression of MALAT1 alleviated H/R-stimulated HUVEC dysfunction, whereas silencing of MALAT1 exerted the opposite effects. MALAT1 also reduced miR-320a levels in HUVECs. Overexpression of miR-320a repressed the function of MALAT1 on H/R-stimulated HUVECs, whereas inhibition of miR-320a exerted the opposite effect. Additionally, miR-320a inhibition alleviated H/R-stimulated HUVEC injury via RAC1. Taken together, this investigation concluded that MALAT1 represses H/R-stimulated HUVEC injury by targeting the miR-320a/RAC1 axis.

Circulating miR-3656 induces human umbilical vein endothelial cell injury by targeting eNOS and ADAMTS13

2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Jikang Shi ◽  
Yaxuan Ren ◽  
Sainan Liu ◽  
Qian Zhao ◽  
Fei Kong ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Injury ◽  
Umbilical Vein ◽  
Endothelial Cell Injury ◽  
Human Umbilical Vein

Curculigoside attenuates human umbilical vein endothelial cell injury induced by H2O2

2010 ◽  
Vol 132 (1) ◽  
pp. 233-239 ◽  
Author(s):  
Yun Kai Wang ◽  
Ya Jun Hong ◽  
Mao Wei ◽  
Ye Wu ◽  
Zhao Quan Huang ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Injury ◽  
Umbilical Vein ◽  
Endothelial Cell Injury ◽  
Human Umbilical Vein

scholarly journals Omentin-1 Ameliorated Free Fatty Acid-Induced Impairment in Proliferation, Migration, and Inflammatory States of HUVECs

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Yubin Chen ◽  
Fen Liu ◽  
Fei Han ◽  
Lizhi Lv ◽  
Can-e Tang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Fatty Acid ◽  
Endothelial Cell ◽  
Free Fatty Acid ◽  
Cell Injury ◽  
Umbilical Vein ◽  
Quantitative Polymerase Chain Reaction ◽  
Cell Counting ◽  
Endothelial Cell Injury ◽  
Umbilical Vein Endothelial Cells

Objectives. Endothelial cell injury is a critical pathological change during the development of atherosclerosis. Here, we explored the effect of omentin-1 on free fatty acid- (FFA-) induced endothelial cell injury. Methods. An FFA-induced endothelial cell injury model was established to investigate the role of omentin-1 in this process. Cell proliferation was analyzed with the Cell Counting Kit assay and flow cytometry. Scratch and transwell assays were used to evaluate cell migration. Factors secreted by endothelial cells after injury were detected by western blotting, reverse-transcription quantitative polymerase chain reaction, and cellular fluorescence assay. Results. Omentin-1 rescued the FFA-induced impaired proliferation and migration capabilities of human umbilical vein endothelial cells (HUVECs). It decreased the number of THP-1 cells attached to HUVECs in response to injury and inhibited the FFA-induced proinflammatory state of HUVECs. Conclusion. Omentin-1 could partly ameliorate FFA-induced endothelial cell injury.

scholarly journals Secoisolariciresinol Diglucoside Exerts Anti-Inflammatory and Antiapoptotic Effects through Inhibiting the Akt/IκB/NF-κB Pathway on Human Umbilical Vein Endothelial Cells

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Shaoyang Zhang ◽  
Meili Cheng ◽  
Zhen Wang ◽  
Yuzhi Liu ◽  
Yuhua Ren ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Ischemia Reperfusion ◽  
Tube Formation ◽  
Cell Counting ◽  
Enzyme Linked Immunosorbent Assay ◽  
Secoisolariciresinol Diglucoside ◽  
Human Umbilical Vein ◽  
No Release ◽  
Umbilical Vein Endothelial Cells

Inflammation is a key regulator in the progression of atherosclerosis (AS) which extremely affects people’s health. Secoisolariciresinol diglucoside (SDG), a plant lignan, is relevant to angiogenesis and cardioprotection against ischemia-reperfusion injury and improves vascular disorders. However, the effect of SDG on cardiovascular disorder is not clear. In the present study, we aimed to investigate the effects of SDG on lipopolysaccharide- (LPS-) stimulated Human Umbilical Vein Endothelial Cells (HUVECs) and elucidate the underlying mechanism. The LPS-stimulated HUVEC cellular model was established. The cell viability, the cell tube formation activity, the nitric oxide (NO) release, the levels of inflammatory cytokine interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), the activation of nuclear factor kappa-B (NF-κB) pathway, and the expression of protein kinase B (Akt) were determined using Cell Counting Kit-8, cell tube-formation assay, western blotting, and enzyme-linked immunosorbent assay. Our results revealed that SDG reduces the angiogenic capacity of HUVECs and inhibited LPS-mediated HUVEC injury and apoptosis. In addition, SDG increased NO release and decreased the levels of IL-1β, IL-6, and TNF-α in LPS-treated HUVECs. Meanwhile, SDG inhibited the NF-κB pathway and downregulated Akt expression in LPS-induced HUVECs. Our results indicated that SDG relieves LPS-mediated HUVEC injury by inhibiting the NF-κB pathway which is partly dependent on the disruption of Akt activation. Therefore, SDG exerts its cytoprotective effects in the context of LPS-treated HUVECs via regulation of the Akt/IκB/NF-κB pathway and may be a potential treatment drug for cardiovascular disease.

scholarly journals MiR-375-3p regulates rat pulmonary microvascular endothelial cell activity by targeting Notch1 during hypoxia

2020 ◽  
Vol 48 (7) ◽  
pp. 030006052092685
Author(s):  
Yuan An ◽  
Ziquan Liu ◽  
Hui Ding ◽  
Qi Lv ◽  
Haojun Fan ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Cell Activity ◽  
Tube Formation ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Microvascular Endothelial Cell ◽  
Adaptation To Hypoxia ◽  
Pulmonary Microvascular Endothelial Cell ◽  
Reporter Assays ◽  
Microvascular Endothelial

Objective Pulmonary microvascular endothelial cells (PMECs) exhibit specific responses in adaptation to hypoxia. However, the mechanisms regulating PMEC activities during hypoxia remain unclear. This study investigated the potential involvement of a microRNA, miR-375-3p, in the regulation of PMEC activities. Methods Primary PMECs were isolated from rats. The expression levels of miR-375-3p and Notch1 in the PMECs were detected by quantitative PCR and western blotting. Luciferase reporter assays were performed to explore the transcriptional regulation of Notch1 by miR-375-3p. The proliferation and chemotaxis of the PMECs were measured with the Cell Counting Kit-8 and Transwell invasion assays, respectively. Additionally, the capacity of hypoxia-treated PMECs for angiogenesis and inflammatory response was determined with tube formation assays and ELISA, respectively. Results The expression of miR-375-3p and Notch1 in the PMECs was significantly down-regulated and up-regulated during hypoxia, respectively. The results demonstrated that miR-375-3p directly targets Notch1 in PMECs, thereby suppressing the transcriptional expression of Notch1. It was further revealed that miR-375-3p regulates the proliferation, chemotaxis, angiogenesis, and inflammatory response of PMECs. Conclusions Our findings revealed the important role of miR-375-3p in the regulation of PMEC function and suggest the potential involvement of miR-375-3p in the development of lung diseases.

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