scholarly journals Generation of Human Pulmonary Microvascular Endothelial Cell Lines

2001 ◽  
Vol 81 (12) ◽  
pp. 1717-1727 ◽  
Author(s):  
Vera Krump-Konvalinkova ◽  
Fernando Bittinger ◽  
Ronald E Unger ◽  
Kirsten Peters ◽  
Hans-Anton Lehr ◽  
...  
2020 ◽  
Vol 21 (15) ◽  
pp. 5249 ◽  
Author(s):  
Anne-Claire Lagrée ◽  
Fabienne Fasani ◽  
Clotilde Rouxel ◽  
Marine Pivet ◽  
Marie Pourcelot ◽  
...  

Microvascular endothelial cells constitute potential targets for exogenous microorganisms, in particular for vector-borne pathogens. Their phenotypic and functional variations according to the organs they are coming from provide an explanation of the organ selectivity expressed in vivo by pathogens. In order to make available relevant tools for in vitro studies of infection mechanisms, our aim was to immortalize bovine organospecific endothelial cells but also to assess their permissivity to viral infection. Using transfection with SV40 large T antigen, six bovine microvascular endothelial cell lines from various organs and one macrovascular cell line from an umbilical cord were established. They display their own panel of endothelial progenitor/mature markers, as assessed by flow cytometry and RT-qPCR, as well as the typical angiogenesis capacity. Using both Bluetongue and foot-and-mouth disease viruses, we demonstrate that some cell lines are preferentially infected. In addition, they can be transfected and are able to express viral proteins such as BTV8-NS3. Such microvascular endothelial cell lines bring innovative tools for in vitro studies of infection by viruses or bacteria, allowing for the study of host-pathogen interaction mechanisms with the actual in vivo target cells. They are also suitable for applications linked to microvascularization, such as anti-angiogenic and anti-tumor research, growing fields in veterinary medicine.


2012 ◽  
Vol 37 (2) ◽  
pp. 89-100 ◽  
Author(s):  
Masaaki Abe ◽  
Yasuteru Sano ◽  
Toshihiko Maeda ◽  
Fumitaka Shimizu ◽  
Yoko Kashiwamura ◽  
...  

2013 ◽  
Vol 4 (3) ◽  
pp. 326-338 ◽  
Author(s):  
Toshihiko Maeda ◽  
Yasuteru Sano ◽  
Masaaki Abe ◽  
Fumitaka Shimizu ◽  
Yoko Kashiwamura ◽  
...  

Author(s):  
Junxia Li ◽  
Yiming Xia ◽  
Zhizhong Huang ◽  
Yan Zhao ◽  
Renping Xiong ◽  
...  

Hypoxia-induced pulmonary microvascular endothelial cell (PMVEC) monolayers hyperpermeability is vital for vascular leakage, which participates in vascular diseases, such as acute lung injury (ALI) and high altitude pulmonary edema (HAPE). We previously observed PMVEC permeability was markedly elevated in hypoxia when cocultured with primary type II alveolar epithelial cells (AECII) in which isthmin1(ISM1) was highly upregulated. However, whether the upregulation of ISM1 plays a role in hypoxia-induced PMVEC hyperpermeability is unclear. In this study, we assessed the role of AECII-derived ISM1 in hypoxia-induced PMVEC hyperpermeability with an AECII/PMVEC co-culture system and uncovered the underlying mechanism whereby hypoxia stimulates ISM1 gene expression. We found that ISM1 gene expression was upregulated in cultured AECII cells exposed to hypoxia (3% O2), and that AECII-derived ISM1 participated in hypoxia-induced hyperpermeability of PMVEC monolayers since siRNA-mediated knockdown of ISM1 in AECII markedly attenuated the increasement of PMVEC permeability in co-culture system under hypoxia. Additionally, we confirmed that ISM1 was regulated by hypoxia-inducible factor-1α (HIF1α) according to the evidence that silencing of HIF1α inhibited the hypoxia-mediated upregulation of ISM1. Mechanismly, overexpression of HIF1α transcriptionally activated ISM1 gene expression by directly binding to the conserved regulatory elements upstream of the ism1 locus. We identified a novel HIF-1-target gene ISM1, which involves in hyperpermeability of pulmonary microvascular endothelial cell monolayers under hypoxia. Our in vitro cell experiments implied that the upregulated ISM1 derived from alveolar epithelium might be a vital modulator in hypoxia-induced endothelial hyperpermeability and thereby implicates with hypoxic pulmonary-related diseases.


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