scholarly journals MRI and fluorescence microscopy of the acute vascular response to VEGF165: vasodilation, hyper-permeability and lymphatic uptake, followed by rapid inactivation of the growth factor

2002 ◽  
Vol 15 (2) ◽  
pp. 120-131 ◽  
Author(s):  
Hagit Dafni ◽  
Limor Landsman ◽  
Bilha Schechter ◽  
Fortune Kohen ◽  
Michal Neeman
Keyword(s):  
Growth Factor ◽  
Fluorescence Microscopy ◽  
Vascular Response ◽  
Lymphatic Uptake ◽  
Rapid Inactivation

scholarly journals Myocardin Regulates Vascular Response to Injury Through miR-24/-29a and Platelet-Derived Growth Factor Receptor-β

2013 ◽  
Vol 33 (10) ◽  
pp. 2355-2365 ◽  
Author(s):  
Amarnath Talasila ◽  
Haixiang Yu ◽  
Matthew Ackers-Johnson ◽  
Martine Bot ◽  
Theo van Berkel ◽  
...  
Keyword(s):  
Growth Factor ◽  
Growth Factor Receptor ◽  
Platelet Derived Growth Factor ◽  
Vascular Response

scholarly journals Re-expression of DIRAS3 and p53 induces apoptosis and impaired autophagy in head and neck squamous cell carcinoma

2020 ◽  
Vol 7 (1) ◽  
Author(s):  
Zhe Liu ◽  
Douglas R. Hurst ◽  
Xing Qu ◽  
Li-Guang Lu ◽  
Chen-Zhou Wu ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Growth Factor ◽  
Fluorescence Microscopy ◽  
Mouse Model ◽  
Cell Carcinoma ◽  
Head And Neck ◽  
Western Blotting ◽  
Flow Cytometric Analysis ◽  
Akt Phosphorylation ◽  
Flow Cytometric

Abstract Background p53 and DIRAS3 are tumor suppressors that are frequently silenced in tumors. In this study, we sought to determine whether the concurrent re-expression of p53 and DIRAS3 could effectively induce head and neck squamous cell carcinoma (HNSCC) cell death. Methods CAL-27 and SCC-25 cells were treated with Ad-DIRAS3 and rAd-p53 to induce re-expression of DIRAS3 and p53 respectively. The effects of DIRAS3 and p53 re-expression on the growth and apoptosis of HNSCC cells were examined by TUNEL assay, flow cytometric analysis and MTT. The effects of DIRAS3 and p53 re-expression on Akt phosphorylation, oncogene expression, and the interaction of 4E-BP1 with eIF4E were determined by real-time PCR, Western blotting and immunoprecipitation analysis. The ability of DIRAS3 and p53 re-expression to induce autophagy was evaluated by transmission electron microscopy, LC3 fluorescence microscopy and Western blotting. The effects of DIRAS3 and p53 re-expression on HNSCC growth were evaluated by using an orthotopic xenograft mouse model. Results TUNEL assay and flow cytometric analysis showed that the concurrent re-expression of DIRAS3 and p53 significantly induced apoptosis (P < 0.001). MTT and flow cytometric analysis revealed that DIRAS3 and p53 re-expression significantly inhibited proliferation and induced cell cycle arrest (P < 0.001). Mechanistically, the concurrent re-expression of DIRAS3 and p53 down-regulated signal transducer and activation of transcription 3 (STAT3) and up-regulated p21WAF1/CIP1 and Bax (P < 0.001). DIRAS3 and p53 re-expression also inhibited Akt phosphorylation, increased the interaction of eIF4E with 4E-BP1, and reduced the expression of c-Myc, cyclin D1, vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF), epidermal growth factor receptor (EGFR) and Bcl-2 (P < 0.001). Moreover, the concurrent re-expression of DIRAS3 and p53 increased the percentage of cells with GFP-LC3 puncta compared with that in cells treated with control adenovirus (50.00% ± 4.55% vs. 4.67% ± 1.25%, P < 0.001). LC3 fluorescence microscopy and Western blotting further showed that DIRAS3 and p53 re-expression significantly promoted autophagic activity but also inhibited autophagic flux, resulting in overall impaired autophagy. Finally, the concurrent re-expression of DIRAS3 and p53 significantly decreased the tumor volume compared with the control group in a HNSCC xenograft mouse model [(3.12 ± 0.75) mm3 vs. (189.02 ± 17.54) mm3, P < 0.001]. Conclusions The concurrent re-expression of DIRAS3 and p53 is a more effective approach to HNSCC treatment than current treatment strategies.

scholarly journals Substantial Dysregulation of miRNA Passenger Strands Underlies the Vascular Response to Injury

Cells ◽  
2019 ◽  
Vol 8 (2) ◽  
pp. 83 ◽  
Author(s):  
Karine Pinel ◽  
Louise Diver ◽  
Katie White ◽  
Robert McDonald ◽  
Andrew Baker
Keyword(s):  
Growth Factor ◽  
Signaling Cascades ◽  
Cytokine Signaling ◽  
Vascular Response ◽  
Vein Grafts ◽  
Individual Mirnas ◽  
Vessel Injury ◽  
Non Coding Rnas

Vascular smooth muscle cell (VSMC) dedifferentiation is a common feature of vascular disorders leading to pro-migratory and proliferative phenotypes, a process induced through growth factor and cytokine signaling cascades. Recently, many studies have demonstrated that small non-coding RNAs (miRNAs) can induce phenotypic effects on VSMCs in response to vessel injury. However, most studies have focused on the contribution of individual miRNAs. Our study aimed to conduct a detailed and unbiased analysis of both guide and passenger miRNA expression in vascular cells in vitro and disease models in vivo. We analyzed 100 miRNA stem loops by TaqMan Low Density Array (TLDA) from primary VSMCs in vitro. Intriguingly, we found that a larger proportion of the passenger strands was significantly dysregulated compared to the guide strands after exposure to pathological stimuli, such as platelet-derived growth factor (PDGF) and IL-1α. Similar findings were observed in response to injury in porcine vein grafts and stent models in vivo. In these studies, we reveal that the miRNA passenger strands are predominantly dysregulated in response to vascular injury.

Sign in / Sign up

Export Citation Format

Share Document