scholarly journals CCAAT/Enhancer-Binding Protein β Mediates Oxygen-Induced Retinal Neovascularization via Retinal Vascular Damage and Vascular Endothelial Growth Factor

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Tingting Li ◽  
Xuan Cai ◽  
Xiangning Wang ◽  
Xueyan Zhang ◽  
Hui Zhang ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Western Blot ◽  
Binding Protein ◽  
Retinal Function ◽  
Vascular Damage ◽  
Vascular Endothelial ◽  
Protein Levels ◽  
Enhancer Binding Protein ◽  
Endothelial Growth Factor

Objective. To evaluate the role of CCAAT/enhancer-binding protein β (C/EBP β) in retinal neovascularization (RNV) in an oxygen-induced retinopathy (OIR) model. Methods. Rats with OIR were exposed to alternating hypoxic and hyperopic conditions for 14 days. Then, the rats with OIR were assigned randomly to groups that received intravitreal injections of either shRNA lentiviral particles targeting C/EBP β (LV.shC/EBP β) or control particles (LV.shScrambled). The effectiveness of transduction using intravitreal injection of C/EBP β shRNA was examined in rats with OIR. The retinal vascular damage and accumulation of RNV were determined by retinal fluorescein-dextran perfusion, retinal ADPase staining, and periodic acid-Schiff (PAS) staining. Retinal function was recorded by electroretinogram responses to full-field light flashes. Reverse transcriptase-polymerase chain reaction (RT-PCR) and western blot analyses were used to measure mRNA and protein levels of C/EBP β and vascular endothelial growth factor (VEGF). The expression of p-C/EBP β was also examined by western blot analyses. The location of C/EBP β expression in the retina was determined by immunohistochemistry. Results. In OIR rats, the expression levels of C/EBP β and VEGF were significantly increased at both the mRNA and protein levels (P<0.01). The p-C/EBP β expression was consistent with the level of C/EBP β. C/EBP β was predominantly localized to the ganglion cell layer (GCL) and the inner nuclear layer (INL). The retinal C/EBP β level was significantly reduced in tissues from rats with OIR transduced with LV.shC/EBP β compared with tissues from those transduced with LV.shScrambled (P<0.01). Compared with those of the rats with OIR in the LV.shScrambled group, nonperfused retinal areas, neovascular tufts, pericyte death, and the ratio of endothelial cells to pericytes in the LV.shC/EBP β group were significantly reduced. In OIR rats, retinal function was impaired. There was no significant change in retinal dysfunction between the LV.shC/EBP β group and the LV.shScrambled group. The levels of VEGF mRNA and protein in the LV.shC/EBP β group were also decreased significantly compared with those of the rats with OIR in the LV.shScrambled group (P<0.01). Conclusions. C/EBP β shRNA inhibits RNV in OIR. A potential mechanism may be that the activity of C/EBP β increases with its overexpression, which in turn aggravates the amount of the retinal vascular damage and promotes transcription of VEGF. C/EBP β might be a new therapeutic target for preventing RNV.

scholarly journals Yangjing capsule attenuates cyclophosphamide-induced deficiency of testicular microcirculation in mice

2020 ◽  
Vol 19 (3) ◽  
pp. 603-608
Author(s):  
Baofang Jin ◽  
Weihang Dong ◽  
Dalin Sun ◽  
Bin Cai ◽  
Weimin Deng ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Western Blot ◽  
Microvascular Density ◽  
Vascular Endothelial ◽  
Protective Effects ◽  
Protein Levels ◽  
Mrna And Protein Expression ◽  
High Concentrations ◽  
Endothelial Growth Factor

Purpose: To explore the protective effects of Yangjing capsule (YC) on testicular microcirculation in a mouse model of deficiency of testicular microcirculation. Methods: Immunohistochemistry was applied to determine the effects of YC on microvascular density of mice. The protein level of CD34 and vascular endothelial growth factor A (VEGF A) was measured by western blot. The viability of Testicular cell line (TM4 cells) was examined by CCK-8 assay. Results: Histopathological changes demonstrated that CP-induced decrease of microvascular density of the mice was rescued by YC dose-dependently (p < 0.5). Western blot data showed that the protein levels of CD34 and VEGF A in CP group were significantly decreased, but dose-dependently increased by YC, respectively, following co-administration of CP + YC, compared with those in CP group (p < 0.5). The results from CCK-8 assay showed that the cell viability of TM4 cells increased with the amount of YC administered, and that high concentrations of YC (0.1 and 1 mg/mL) showed significant effects (p < 0.5). Moreover, YC showed little effect on VEGF A mRNA and protein expression in TM4 cells. Conclusion: YC may be considered an alternative therapeutic agent for the management of testicular microcirculation disease. However, further studies are required to ascertain this. Keywords: Yangjing Capsule, Testicular microcirculation, Cyclophosphamide, Vascular endothelial growth factor A

scholarly journals Expression of vascular endothelial growth factor in response to high glucose in rat mesangial cells

2000 ◽  
Vol 165 (3) ◽  
pp. 617-624 ◽  
Author(s):  
NH Kim ◽  
HH Jung ◽  
DR Cha ◽  
DS Choi
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Diabetic Nephropathy ◽  
Growth Factor ◽  
High Glucose ◽  
Mesangial Cells ◽  
Vascular Endothelial ◽  
Vegf Expression ◽  
Protein Levels ◽  
Calphostin C ◽  
Endothelial Growth Factor

Diabetic nephropathy associated with hyperglycemia is characterized by glomerular hyperfiltration and endothelial dysfunction. Vascular endothelial growth factor (VEGF) is known to be primarily involved in neoangiogenesis and increased endothelial permeability. The purpose of this study was to investigate VEGF expression in response to high glucose in rat cultured mesangial cells and to identify its signal pathway via protein kinase C (PKC). Rat mesangial cells were cultured with different concentrations of glucose: normal (5 mM d-glucose), medium (15 mM d-glucose) and high (30 mm d-glucose). Calphostin-C as a PKC inhibitor and phorbol myristate acetate (PMA) as a PKC downregulator were instillated into culture media to evaluate the role of PKC in mediating the glucose-induced increase in VEGF expression. High glucose increased expression of VEGF at the mRNA and protein levels, identified by semi-quantitative RT-PCR and western blotting, within 3 h and in a time- and glucose concentration-dependent manner. Calphostin-C and PMA inhibited glucose-induced increases in VEGF expression at the mRNA and protein levels. In conclusion, high glucose can directly increase VEGF expression in rat mesangial cells via a PKC-dependent mechanism. These results suggest that VEGF could be a potential mediator of glomerular hyperfiltration and proteinuria in diabetic nephropathy.

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