scholarly journals Irradiation influences endothelial cell function in vitro and in vivo: A possible role for IP10

2005 ◽  
Vol 11 (2) ◽  
pp. 45 ◽  
Author(s):  
L. Cannella ◽  
R. Laylor ◽  
F. Marelli-Berg ◽  
F. Dazzi
2009 ◽  
Vol 96 (3) ◽  
pp. 682a
Author(s):  
Aydin Tay ◽  
William G. Mayhan ◽  
Denise Arrick ◽  
Chun-Hong Shao ◽  
Hong Sun ◽  
...  

2008 ◽  
Vol 294 (2) ◽  
pp. R467-R476 ◽  
Author(s):  
Chun Yang ◽  
Bupe R. Mwaikambo ◽  
Tang Zhu ◽  
Carmen Gagnon ◽  
Josiane Lafleur ◽  
...  

Recent studies have demonstrated that lymphocyte-derived microparticles (LMPs) impair endothelial cell function. However, no data currently exist regarding the contribution of LMPs in the regulation of angiogenesis. In the present study, we investigated the effects of LMPs on angiogenesis in vivo and in vitro and demonstrated that LMPs strongly suppressed aortic ring microvessel sprouting and in vivo corneal neovascularization. In vitro, LMPs considerably diminished human umbilical vein endothelial cell survival and proliferation in a concentration-dependent manner. Mechanistically, the antioxidants U-74389G and U-83836E were partially protective against the antiproliferative effects of LMPs, whereas the NADPH oxidase (NOX) inhibitors apocynin and diphenyleneiodonium significantly abrogated these effects. Moreover, LMPs increased not only the expression of the NOX subunits gp91phox, p22phox, and p47phox, but also the production of ROS and NOX-derived superoxide (O2−). Importantly, LMPs caused a pronounced augmentation in the protein expression of the CD36 antiangiogenic receptor while significantly downregulating the protein levels of VEGF receptor type 2 and its downstream signaling mediator, phosphorylated ERK1/2. In summary, LMPs potently suppress neovascularization in vivo and in vitro by augmenting ROS generation via NOX and interfering with the VEGF signaling pathway.


Blood ◽  
2009 ◽  
Vol 114 (5) ◽  
pp. 1123-1130 ◽  
Author(s):  
Guo Wei ◽  
Ruchika Srinivasan ◽  
Carmen Z. Cantemir-Stone ◽  
Sudarshana M. Sharma ◽  
Ramasamy Santhanam ◽  
...  

Abstract The ras/Raf/Mek/Erk pathway plays a central role in coordinating endothelial cell activities during angiogenesis. Transcription factors Ets1 and Ets2 are targets of ras/Erk signaling pathways that have been implicated in endothelial cell function in vitro, but their precise role in vascular formation and function in vivo remains ill-defined. In this work, mutation of both Ets1 and Ets2 resulted in embryonic lethality at midgestation, with striking defects in vascular branching having been observed. The action of these factors was endothelial cell autonomous as demonstrated using Cre/loxP technology. Analysis of Ets1/Ets2 target genes in isolated embryonic endothelial cells demonstrated down-regulation of Mmp9, Bcl-XL, and cIAP2 in double mutants versus controls, and chromatin immunoprecipitation revealed that both Ets1 and Ets2 were loaded at target promoters. Consistent with these observations, endothelial cell apoptosis was significantly increased both in vivo and in vitro when both Ets1 and Ets2 were mutated. These results establish essential and overlapping functions for Ets1 and Ets2 in coordinating endothelial cell functions with survival during embryonic angiogenesis.


2013 ◽  
Author(s):  
Gareth C. Davies ◽  
James A. Harper ◽  
Richard C. Sainson ◽  
Lee Brown ◽  
Grace Opoku-Ansah ◽  
...  

Blood ◽  
2003 ◽  
Vol 101 (8) ◽  
pp. 3014-3020 ◽  
Author(s):  
Jian-Miao Liu ◽  
Françoise Lawrence ◽  
Milica Kovacevic ◽  
Jérôme Bignon ◽  
Evangelia Papadimitriou ◽  
...  

Abstract The tetrapeptide acetyl-Ser-Asp-Lys-Pro (AcSDKP), purified from bone marrow and constitutively synthesized in vivo, belongs to the family of negative regulators of hematopoiesis. It protects the stem cell compartment from the toxicity of anticancer drugs and irradiation and consequently contributes to a reduction in marrow failure. This current work provides experimental evidence for another novel biologic function of AcSDKP. We report that AcSDKP is a mediator of angiogenesis, as measured by its ability to modulate endothelial cell function in vitro and angiogenesis in vivo. AcSDKP at nanomolar concentrations stimulates in vitro endothelial cell migration and differentiation into capillary-like structures on Matrigel as well as enhances the secretion of an active form of matrix metalloproteinase-1 (MMP-1). In vivo, AcSDKP promotes a significant angiogenic response in the chicken embryo chorioallantoic membrane (CAM) and in the abdominal muscle of the rat. Moreover, it induces the formation of blood vessels in Matrigel plugs implanted subcutaneously in the rat. This is the first report demonstrating the ability of AcSDKP to interact directly with endothelial cells and to elicit an angiogenic response in vitro and in vivo.


Angiogenesis ◽  
2013 ◽  
Vol 16 (4) ◽  
pp. 821-836 ◽  
Author(s):  
Aurore Grelier ◽  
Audrey Cras ◽  
Nicole Balitrand ◽  
Catherine Delmau ◽  
Séverine Lecourt ◽  
...  

2008 ◽  
Vol 1136 ◽  
Author(s):  
Jing Lu ◽  
Dongwoo Khang ◽  
Thomas J. Webster

ABSTRACTTo study the contribution of different surface feature properties in improving vascular endothelial cell adhesion, rationally designed nano/sub-micron patterns with various dimensions were created on titanium surfaces in this study. In vitro results indicated that endothelial cell adhesion was improved when the titanium pattern dimensions decreased into the nano-scale. Specifically, endothelial cells preferred to adhere on sub-micron and nano rough titanium substrates compared to flat titanium. Moreover, titanium with nano and sub-micron roughness and with the same chemistry as compared to flat titanium, had significantly greater surface energy. Thus, the present study indicated the strong potential of surface nanotopography and nano/sub-micron roughness for improving current vascular stent design.


2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Chunbo Yang ◽  
Magdalini Eleftheriadou ◽  
Sophia Kelaini ◽  
Thomas Morrison ◽  
Marta Vilà González ◽  
...  

Abstract Vascular endothelial cell (EC) dysfunction plays a key role in diabetic complications. This study discovers significant upregulation of Quaking-7 (QKI-7) in iPS cell-derived ECs when exposed to hyperglycemia, and in human iPS-ECs from diabetic patients. QKI-7 is also highly expressed in human coronary arterial ECs from diabetic donors, and on blood vessels from diabetic critical limb ischemia patients undergoing a lower-limb amputation. QKI-7 expression is tightly controlled by RNA splicing factors CUG-BP and hnRNPM through direct binding. QKI-7 upregulation is correlated with disrupted cell barrier, compromised angiogenesis and enhanced monocyte adhesion. RNA immunoprecipitation (RIP) and mRNA-decay assays reveal that QKI-7 binds and promotes mRNA degradation of downstream targets CD144, Neuroligin 1 (NLGN1), and TNF-α-stimulated gene/protein 6 (TSG-6). When hindlimb ischemia is induced in diabetic mice and QKI-7 is knocked-down in vivo in ECs, reperfusion and blood flow recovery are markedly promoted. Manipulation of QKI-7 represents a promising strategy for the treatment of diabetic vascular complications.


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