Emerging Themes on Pulmonary Microvascular Endothelial Cell Microtubules and Microtubule Associated Proteins

2013 ◽  
Keyword(s):  
Endothelial Cell ◽  
Microvascular Endothelial Cell ◽  
Microtubule Associated Proteins ◽  
Pulmonary Microvascular Endothelial Cell ◽  
Associated Proteins ◽  
Emerging Themes ◽  
Microvascular Endothelial

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 ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Lines ◽  
Microvascular Endothelial Cell ◽  
Pulmonary Microvascular Endothelial Cell ◽  
Microvascular Endothelial

Novel HIF-1-target gene isthmin1 contributes to hypoxia-induced hyperpermeability of pulmonary microvascular endothelial cells monolayers

2021 ◽  
Author(s):  
Junxia Li ◽  
Yiming Xia ◽  
Zhizhong Huang ◽  
Yan Zhao ◽  
Renping Xiong ◽  
...  
Keyword(s):  
Gene Expression ◽  
Endothelial Cell ◽  
Culture System ◽  
Target Gene ◽  
Regulatory Elements ◽  
Alveolar Epithelial Cells ◽  
Microvascular Endothelial Cell ◽  
Pulmonary Microvascular Endothelial Cell ◽  
Microvascular Endothelial

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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