scholarly journals Intermittent Hypoxia Activates Duration-Dependent Protective and Injurious Mechanisms in Mouse Lung Endothelial Cells

2018 ◽  
Vol 9 ◽  
Author(s):  
Peter Wohlrab ◽  
Lourdes Soto-Gonzales ◽  
Thomas Benesch ◽  
Max Paul Winter ◽  
Irene Marthe Lang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Intermittent Hypoxia ◽  
Mouse Lung ◽  
Lung Endothelial Cells

scholarly journals A simple protocol for isolating mouse lung endothelial cells

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Jinping Wang ◽  
Niu Niu ◽  
Suowen Xu ◽  
Zheng Gen Jin
Keyword(s):  
Endothelial Cells ◽  
Mouse Lung ◽  
Simple Protocol ◽  
Lung Endothelial Cells

HISTONE ACETYLATION MODULATES DNA DAMAGE IN BACTERIAL ENDOTOXIN-TREATED MOUSE LUNG ENDOTHELIAL CELLS

2004 ◽  
Vol 13 (3) ◽  
pp. 150
Author(s):  
Jane Rose ◽  
Scott Wray ◽  
Hong Huang ◽  
Rostislav Likhotvorik ◽  
Dale Hoyt
Keyword(s):  
Dna Damage ◽  
Endothelial Cells ◽  
Histone Acetylation ◽  
Treated Mouse ◽  
Bacterial Endotoxin ◽  
Mouse Lung ◽  
Lung Endothelial Cells

scholarly journals Targeted Delivery of Oligodeoxynucleotides to Mouse Lung Endothelial Cells in Vitro and in Vivo

2005 ◽  
Vol 12 (3) ◽  
pp. 510-518 ◽  
Author(s):  
Annette Wilson ◽  
Wen Zhou ◽  
Hunter C. Champion ◽  
Sean Alber ◽  
Zhi-Lue Tang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Targeted Delivery ◽  
Mouse Lung ◽  
Lung Endothelial Cells

scholarly journals Diminished metastasis in tetraspanin CD151–knockout mice

Blood ◽  
2011 ◽  
Vol 118 (2) ◽  
pp. 464-472 ◽  
Author(s):  
Yoshito Takeda ◽  
Qinglin Li ◽  
Alexander R. Kazarov ◽  
Mathieu Epardaud ◽  
Kutlu Elpek ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cell Activation ◽  
Immune Cell ◽  
Critical Role ◽  
Mouse Lung ◽  
Null Mouse ◽  
Host Animal ◽  
Lung Endothelial Cells

Abstract Tetraspanin protein CD151 on tumor cells supports invasion and metastasis. In the present study, we show that host animal CD151 also plays a critical role. CD151-null mice showed markedly diminished experimental lung metastasis after injection of Lewis lung carcinoma or B16F10 melanoma cells. Diminished tumor cell residence in the lungs was evident 6-24 hours after injection. Consistent with an endothelial cell deficiency, isolated CD151-null mouse lung endothelial cells showed diminished support for B16F10 adhesion and transendothelial migration, diminished B16F10-induced permeability, and diminished B16F10 adhesion to extracellular matrix deposited by CD151-null mouse lung endothelial cells. However, CD151 deletion did not affect the size of metastatic foci or subcutaneous primary B16F10 tumors, tumor aggregation, tumor clearance from the blood, or tumor-induced immune cell activation and recruitment. Therefore, the effects of host CD151 on metastasis do not involve altered local tumor growth or immune surveillance. VEGF-induced endothelial cell signaling through Src and Akt was diminished in CD151-null endothelial cells. However, deficient signaling was not accompanied by reduced endothelial permeability either in vitro (monolayer permeability assay) or in vivo (VEGF-stimulated Miles assay). In summary, diminished metastasis in CD151-null host animals may be due to impaired tumor-endothelial interactions, with underlying defects in mouse lung endothelial cell extracellular matrix production.

Pulmonary Irradiation Fibrosis Is Preceded By Increased Endothelial Cell Gene Expression

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 5569-5569
Author(s):  
Ronny Kalash ◽  
Jeremiah Au ◽  
Michael W. Epperly ◽  
Julie P. Goff ◽  
Tracy M. Dixon ◽  
...  
Keyword(s):  
Gene Expression ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Conflicts Of Interest ◽  
The Body ◽  
Mouse Lung ◽  
Alveolar Cells ◽  
Cell Gene Expression ◽  
Lung Endothelial Cells ◽  
Endothelial Genes

Abstract Irradiation of the C57BL/6NHsd mouse lung results in pulmonary fibrosis. An acute phase (days 1 to 28) following irradiation recognized by an inflammatory response is followed by a latent phase (day 28 to day 125) where lung appears normal. Fibrosis occurs from day 125 till death characterized by bone marrow stromal cell migration to and proliferation in lung and increased collagen deposition. To investigate the role of endothelial cells, C57BL/6NHsd female mice were irradiated to 20 Gy to the pulmonary cavity shielding the rest of the body. Lung was excised at serial times, endothelial cells separated and tested for expression of endothelial genes vWF, VEGF, FGF1, CCL13 and CTGF; inflammatory genes IL-6; IGFbp7 and genes associated with fibrosis including MnSOD, Nrf2, NfkB, TLR4 and TGF-B. Endothelial cells were separated by using antibodies to CD45, or PECAM and sorting using flow cytometry. RNA was extracted using Triazol and gene expression determined using Real Time Polymerase Chain Reaction (RT-PCR). In irradiated total lung there was significant increase in endothelial cell markers at all times, compared to nonirradiated lung. Transcripts for vWF increased by 474.1 ± 388.5% (p = 0.017) by 2 days after irradiation, 520 ± 55.4% (p < 0.0001) at day 50, and 484.8 ± 26.8% (p < 0.0001) by day 200. VEGF and CTGF also remained elevated. In contrast, total lung MnSOD gene expression increased by 140.6 ± 46.1% at day 2 (p = 0.0185), decreased at day 50 to 17.9 ± 11.2% (p = 0.2808), and increased to 31.5 ± 11.4% by day 200 (p = 0.023). However, purified endothelial cells compared to alveolar cells, showed increased expression of not only the endothelial cell genes but also MnSOD, Nrf2, NfkB, and TGF-B. MnSOD expression in endothelial compared to alveolar cells at day 28 after irradiation was higher at 244.5 ± 7.8 vs 80.5 ± 4.9 (p = 0.0016), at day 150 expression was 140.1 ± 25.0 vs 5.4 ± 1.2 (p < 0.0001) and day 200 expression was 368.5 ± 6.4 vs 51.8 ± 10.3 (p = 0.0007). Lung endothelial cells display critical biomarkers of irradiation injury leading to fibrosis. Disclosures: No relevant conflicts of interest to declare.

Targeted gene delivery to pulmonary endothelium by anti-PECAM antibody

2000 ◽  
Vol 278 (3) ◽  
pp. L504-L511 ◽  
Author(s):  
Song Li ◽  
Yadi Tan ◽  
Ekapop Viroonchatapan ◽  
Bruce R. Pitt ◽  
Leaf Huang
Keyword(s):  
Endothelial Cells ◽  
Gene Delivery ◽  
Mouse Lung ◽  
Pulmonary Endothelium ◽  
Targeted Gene Delivery ◽  
Platelet Endothelial Cell Adhesion ◽  
Charge Interaction ◽  
Cytokine Tumor Necrosis Factor ◽  
Lung Endothelial Cells ◽  
Factor Α

To achieve efficient systemic gene delivery to the lung with minimal toxicity, a vector was developed by chemically conjugating a cationic polymer, polyethylenimine (PEI), with anti-platelet endothelial cell adhesion molecule (PECAM) antibody (Ab). Transfection of mouse lung endothelial cells with a plasmid expression vector with cDNA to luciferase (pCMVL) complexed with anti-PECAM Ab-PEI conjugate was more efficient than that with PEI-pCMVL complexes. Furthermore, the anti-PECAM Ab-PEI conjugate mediated efficient transfection at lower charge plus-to-minus ratios. Conjugation of PEI with a control IgG (hamster IgG) did not enhance transfection of mouse lung endothelial cells, suggesting that the cellular uptake of anti-PECAM Ab-PEI-DNA complexes and subsequent gene expression were governed by a receptor-mediated process rather than by a nonspecific charge interaction. Conjugation of PEI with anti-PECAM Ab also led to significant improvement in lung gene transfer to intact mice after intravenous administration. The increase in lung transfection was associated with a decrease compared with PEI-pCMVL with respect to circulating proinflammatory cytokine (tumor necrosis factor-α) levels. These results indicate that targeted gene delivery to the lung endothelium is an effective strategy to enhance gene delivery to the pulmonary circulation while simultaneously reducing toxicity.

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