Monocrotaline pyrrole targets proteins with and without cysteine residues in the cytosol and membranes of human pulmonary artery endothelial cells

PROTEOMICS ◽  
2005 ◽  
Vol 5 (17) ◽  
pp. 4398-4413 ◽  
Author(s):  
Michael W. Lamé ◽  
A. Daniel Jones ◽  
Dennis W. Wilson ◽  
H. J. Segall
Keyword(s):  
Endothelial Cells ◽  
Pulmonary Artery ◽  
Cysteine Residues ◽  
Human Pulmonary Artery ◽  
Monocrotaline Pyrrole

scholarly journals Fenfluramine-Induced Gene Dysregulation in Human Pulmonary Artery Smooth Muscle and Endothelial Cells

2011 ◽  
Vol 1 (3) ◽  
pp. 405-418 ◽  
Author(s):  
Weijuan Yao ◽  
Wenbo Mu ◽  
Amy Zeifman ◽  
Michelle Lofti ◽  
Carmelle V. Remillard ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Pulmonary Artery ◽  
Gene Dysregulation ◽  
Pulmonary Artery Smooth Muscle ◽  
Human Pulmonary Artery

Abstract 218: Fibrinolytic Reactivity of Venous Endothelial Cells from Different Vascular Beds

2012 ◽  
Vol 32 (suppl_1) ◽  
Author(s):  
Neil G Kumar ◽  
Elisa Roztocil ◽  
John P Cullen ◽  
David L Gillespie
Keyword(s):  
Endothelial Cells ◽  
Pulmonary Artery ◽  
Cell Types ◽  
Iliac Vein ◽  
Vein Thrombosis ◽  
Cellular Expression ◽  
Artery Embolism ◽  
Vascular Beds ◽  
Human Pulmonary Artery ◽  
Pai 1

Objective: Little is known about the molecular biology of endothelial cells from different venous vascular beds. As a result, our treatment of deep vein thrombosis (DVT) and pulmonary artery embolism (PE) remain identical. PAI-1 and tPA are important regulators of thrombosis and fibrinolysis, while ICAM-1 is known to bind fibrinogen. Here, we aim to investigate differences in fibrinolytic reactivity between human iliac vein endothelial cells (HIVECs) and human pulmonary artery endothelial cells (HPAECs). Methods: Confluent HIVECs and HPAECs, passages 3 - 6, were cultured in the absence or presence of TNFα (10 ng/mL) for 24 hours. Cellular expression of tPA and PAI-1 as analyzed by Western blot analysis and ICAM-1 as analyzed by flow cytometry were compared to controls. Results: Following TNFα stimulation, PAI-1 was upregulated in both HPAECs and HIVECs, however the upregulation observed in HPAECs was approximately 9-fold the increase observed in HIVECs (relative expression: 3.23 ± 0.52 vs 1.26 ± 0.27, n = 3, p < 0.05). While TNFα had no effect on tPA expression in HIVECs, tPA expression in HPAECS was upregulated by 33% (n = 3, p < 0.05). Although TNFα stimulation increased the number of ICAM-1 positive to approximately 100% in both cell types, a 3-fold greater increase in the Mean Fluorescence Intensity (MFI) was observed in HIVECs when compared to HPAECs (relative MFI: 69.28 ± 13.58 vs 21.92 ± 7.22, n = 3, p <0.05). Conclusions: HPAECs and HIVECs react differently in terms of fibrinolytic potential when challenged with a cytokine associated with systemic inflammation, such as in DVT and PE. These findings suggest that endothelial cells from distinct venous vascular beds may differentially regulate the fibrinolytic pathway, thus demonstrating unique properties of the deep veins and the pulmonary artery to respond to thromboembolism.

Isolation and maintenance of human pulmonary artery endothelial cells in culture isolated from transplant donors

1994 ◽  
Vol 267 (4) ◽  
pp. L406-L413 ◽  
Author(s):  
G. A. Visner ◽  
E. D. Staples ◽  
S. E. Chesrown ◽  
E. R. Block ◽  
D. S. Zander ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Pulmonary Artery ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Immunofluorescent Staining ◽  
Northern Analysis ◽  
Pulmonary Vasculature ◽  
Pulmonary Vascular Disease ◽  
Antigen Uptake ◽  
Human Pulmonary Artery

Even though endothelial cells from different locations have similarities, there are potential morphological and functional differences between cells from different vascular regions, as well as between species. Our laboratory is interested in studying the molecular regulation of vasoactive substances in pulmonary vasculature. Therefore, we have developed reproducible methodology to isolate and maintain cultures of human pulmonary artery endothelial cells. The major innovation has been the employment of sections of pulmonary artery from heart transplant donors, from which endothelial cells are isolated. Cell monolayers were identified as endothelial cells by phase-contrast microscopy. Representative dishes of cells were further characterized by indirect immunofluorescent staining for factor VIII antigen, uptake of acetylated low-density lipoprotein, and electron microscopy. These cells were also evaluated for the expression of endothelin-1 (ET-1), a vasoactive 21-amino acid peptide derived from endothelial cells. The cells expressed ET-1 peptide and mRNA as determined by radioimmunoassay and Northern analysis, respectively. We also demonstrated that these cells are useful in transient transfection experiments for potential evaluation of promoter elements. The availability and relevance of these cells provide an important investigative tool for studies on human pulmonary vascular disease.

Monocrotaline pyrrole protein targets in pulmonary artery endothelial cells.

2009 ◽  
pp. 394-401
Author(s):  
M. W. Lamé ◽  
A. D. Jones ◽  
D. W. Wilson ◽  
S. K. Dunston ◽  
H. J. Segall
Keyword(s):  
Endothelial Cells ◽  
Pulmonary Artery ◽  
Protein Targets ◽  
Monocrotaline Pyrrole

Response of cultured human pulmonary artery endothelial cells to endotoxin

1995 ◽  
Vol 268 (2) ◽  
pp. L239-L244 ◽  
Author(s):  
B. Meyrick ◽  
L. C. Berry ◽  
B. W. Christman
Keyword(s):  
Endothelial Cells ◽  
Lactate Dehydrogenase ◽  
Pulmonary Artery ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Prostaglandin E2 ◽  
Adult Respiratory Distress Syndrome ◽  
Distress Syndrome ◽  
Human Pulmonary Artery

Endotoxemia is the leading cause of the adult respiratory distress syndrome. The effects of endotoxin on pulmonary endothelium, both in vivo and in culture, are diverse and complicated, and vary between species and cellular origin. Species such as sheep and cows are particularly sensitive to endotoxin, whereas rats and mice are more resistant. Studies using cultured pulmonary endothelial cells confirm these findings. Such species variations lead us to question whether human pulmonary artery endothelial cells (HPAEC) are directly affected by endotoxin. The present study examined the effects of endotoxin on HPAEC. Cells were exposed to endotoxin (0.001-10 micrograms/ml) for 24 h and were examined by phase-contrast microscopy, and measurements were made of lactate dehydrogenase, prostacyclin, and prostaglandin E2 release in the cell-free supernatant. In the presence of serum, endotoxin doses as small as 0.01 microgram/ml resulted in endothelial retraction and pyknosis compared with controls (P < 0.05). Exposure to 10 micrograms/ml of endotoxin resulted in a significant increase in the number of pyknotic cells (P < 0.05), and lactate dehydrogenase release paralleled this finding. Endotoxin also resulted in a gradual increase in prostaglandin E2 release, reaching significance at 1 and 10 micrograms/ml of endotoxin (P < 0.05). A similar trend was noted for prostacyclin release. We conclude that the direct cytotoxic effects elicited by endotoxin on HPAEC may contribute to the onset of pulmonary edema in patients with adult respiratory distress syndrome.

Ghrelin protects human pulmonary artery endothelial cells against hypoxia-induced injury via PI3-kinase/Akt

Peptides ◽  
2013 ◽  
Vol 42 ◽  
pp. 112-117 ◽  
Author(s):  
Dan Yang ◽  
Zhihong Liu ◽  
Hongliang Zhang ◽  
Qin Luo
Keyword(s):  
Endothelial Cells ◽  
Pulmonary Artery ◽  
Pi3 Kinase ◽  
Human Pulmonary Artery
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