scholarly journals Lipocalin-2 enhances angiogenesis in rat brain endothelial cells via reactive oxygen species and iron-dependent mechanisms

2015 ◽  
Vol 132 (6) ◽  
pp. 622-628 ◽  
Author(s):  
Limin Wu ◽  
Yang Du ◽  
Josephine Lok ◽  
Eng H. Lo ◽  
Changhong Xing
Keyword(s):  
Reactive Oxygen Species ◽  
Endothelial Cells ◽  
Rat Brain ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Brain Endothelial Cells ◽  
Lipocalin 2 ◽  
Rat Brain Endothelial Cells

scholarly journals Methylglyoxal-Induced Dysfunction in Brain Endothelial Cells via the Suppression of Akt/HIF-1α Pathway and Activation of Mitophagy Associated with Increased Reactive Oxygen Species

Antioxidants ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 820 ◽  
Author(s):  
Donghyun Kim ◽  
Kyeong-A Kim ◽  
Jeong-Hyeon Kim ◽  
Eun-Hye Kim ◽  
Ok-Nam Bae
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Endothelial Cells ◽  
Tight Junction ◽  
Reactive Oxygen ◽  
Mitochondrial Damage ◽  
Oxygen Species ◽  
Brain Endothelial Cells ◽  
Tight Junction Proteins ◽  
Junction Proteins

Methylglyoxal (MG) is a dicarbonyl compound, the level of which is increased in the blood of diabetes patients. MG is reported to be involved in the development of cerebrovascular complications in diabetes, but the exact mechanisms need to be elucidated. Here, we investigated the possible roles of oxidative stress and mitophagy in MG-induced functional damage in brain endothelial cells (ECs). Treatment of MG significantly altered metabolic stress as observed by the oxygen-consumption rate and barrier-integrity as found in impaired trans-endothelial electrical resistance in brain ECs. The accumulation of MG adducts and the disturbance of the glyoxalase system, which are major detoxification enzymes of MG, occurred concurrently. Reactive oxygen species (ROS)-triggered oxidative damage was observed with increased mitochondrial ROS production and the suppressed Akt/hypoxia-inducible factor 1 alpha (HIF-1α) pathway. Along with the disturbance of mitochondrial bioenergetic function, parkin-1-mediated mitophagy was increased by MG. Treatment of N-acetyl cysteine significantly reversed mitochondrial damage and mitophagy. Notably, MG induced dysregulation of tight junction proteins including occludin, claudin-5, and zonula occluden-1 in brain ECs. Here, we propose that diabetic metabolite MG-associated oxidative stress may contribute to mitochondrial damage and autophagy in brain ECs, resulting in the dysregulation of tight junction proteins and the impairment of permeability.

Delivery of Human Fibroblast Growth Factor-1 Gene to Brain by Modified Rat Brain Endothelial Cells

2002 ◽  
Vol 67 (4) ◽  
pp. 1643-1652 ◽  
Author(s):  
P. Johnston ◽  
M. Nam ◽  
M. A. Hossain ◽  
R. R. Indurti ◽  
J. L. Mankowski ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Growth Factor ◽  
Rat Brain ◽  
Fibroblast Growth Factor ◽  
Human Fibroblast ◽  
Fibroblast Growth ◽  
Brain Endothelial Cells ◽  
Rat Brain Endothelial Cells

scholarly journals Sodium Glucose Co-Transporter 2 Inhibitors Ameliorate Endothelium Barrier Dysfunction Induced by Cyclic Stretch through Inhibition of Reactive Oxygen Species

2021 ◽  
Vol 22 (11) ◽  
pp. 6044
Author(s):  
Xiaoling Li ◽  
Gregor Römer ◽  
Raphaela P. Kerindongo ◽  
Jeroen Hermanides ◽  
Martin Albrecht ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Endothelial Cells ◽  
Reactive Oxygen ◽  
Cyclic Stretch ◽  
Cell Permeability ◽  
Ros Production ◽  
Oxygen Species ◽  
Barrier Dysfunction ◽  
Human Coronary Artery ◽  
Oxidative Effect

SGLT-2i’s exert direct anti-inflammatory and anti-oxidative effects on resting endothelial cells. However, endothelial cells are constantly exposed to mechanical forces such as cyclic stretch. Enhanced stretch increases the production of reactive oxygen species (ROS) and thereby impairs endothelial barrier function. We hypothesized that the SGLT-2i’s empagliflozin (EMPA), dapagliflozin (DAPA) and canagliflozin (CANA) exert an anti-oxidative effect and alleviate cyclic stretch-induced endothelial permeability in human coronary artery endothelial cells (HCAECs). HCAECs were pre-incubated with one of the SGLT-2i’s (1 µM EMPA, 1 µM DAPA and 3 µM CANA) for 2 h, followed by 10% stretch for 24 h. HCAECs exposed to 5% stretch were considered as control. Involvement of ROS was measured using N-acetyl-l-cysteine (NAC). The sodium-hydrogen exchanger 1 (NHE1) and NADPH oxidases (NOXs) were inhibited by cariporide, or GKT136901, respectively. Cell permeability and ROS were investigated by fluorescence intensity imaging. Cell permeability and ROS production were increased by 10% stretch; EMPA, DAPA and CANA decreased this effect significantly. Cariporide and GKT136901 inhibited stretch-induced ROS production but neither of them further reduced ROS production when combined with EMPA. SGLT-2i’s improve the barrier dysfunction of HCAECs under enhanced stretch and this effect might be mediated through scavenging of ROS. Anti-oxidative effect of SGLT-2i’s might be partially mediated by inhibition of NHE1 and NOXs.

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