scholarly journals miR-155 Promotes ox-LDL-Induced Autophagy in Human Umbilical Vein Endothelial Cells

2017 ◽  
Vol 2017 ◽  
pp. 1-7 ◽  
Author(s):  
Zhaozhi Zhang ◽  
Xudong Pan ◽  
Shaonan Yang ◽  
Aijun Ma ◽  
Kun Wang ◽  
...  

As an evolutionarily conserved metabolic process, autophagy is involved in the process of atherosclerosis (AS). MicroRNA-155 (miR-155), a multifunctional miRNA, plays an important role in many physiological and pathological conditions, including AS and autophagy. However, the effect of miR-155 on the regulation of autophagy in endothelial cells has not been reported to date. Therefore, the objective of our study was to investigate the role of miR-155 in autophagy induced by oxidized low-density lipoprotein (ox-LDL) in human umbilical vein endothelial cells (HUVECs). Our results demonstrated that ox-LDL induced autophagy in HUVECs and increased the expression of miR-155 significantly. Overexpression of miR-155 improved autophagic activity, whereas low expression of miR-155 inhibited autophagic activity. Therefore, the data demonstrated that miR-155 has a modulating effect on the autophagy of vascular endothelial cells.

1996 ◽  
Vol 120 (1-2) ◽  
pp. 93-99 ◽  
Author(s):  
Akihiro Takahashi ◽  
Takahiro Taniguchi ◽  
Yoshio Fujioka ◽  
Yuichi Ishikawa ◽  
Mitsuhiro Yokoyama

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Chengcheng Chang ◽  
Hongli Liu ◽  
Cong Wei ◽  
Liping Chang ◽  
Junqing Liang ◽  
...  

Vascular hyperpermeability resulting from distortion of endothelial junctions is associated with a number of cardiovascular diseases. Endothelial tight junction regulates the paracellular permeability of macromolecules, a function ofHuman Umbilical Vein Endothelial Cells(HUVEC) monolayers that can be regulated byoxidized Low-density Lipoprotein(ox-LDL). However, the understanding of drug regulation of vascular hyperpermeability is so far limited. This study thus aimed to investigate the role ofTongxinluo(TXL) in the maintenance of the vascular endothelial paracellular permeability. Here, changes in permeability were determined by measuring the paracellular flux of FITC-dextran 40000 (FD40), while protein expression and intercellular distribution were examined by western blot and immunofluorescence assay, respectively. We found that TXL alleviated the ox-LDL-induced increase in flux of FD40 and then reduced the hyperpermeability. Moreover, ox-LDL-induced disruptions of ZO-1, occludin, and claudin1 were also restored. This is via the activation of ERK1/2 in the vascular endothelial cells. Our results provide insights into the molecular mechanism by which TXL alleviates ox-LDL-induced hyperpermeability and provide the basis for further investigations of TXL as regulators of vascular barrier function.


Oncotarget ◽  
2017 ◽  
Vol 8 (37) ◽  
pp. 61001-61010 ◽  
Author(s):  
Ming-Ke Qiu ◽  
Song-Cun Wang ◽  
Yong Tang ◽  
Chang Pan ◽  
Yang Wang ◽  
...  

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