scholarly journals Etanercept Protected Against Cigarette Smoke Extract-Induced Inflammation and Apoptosis of Human Pulmonary Artery Endothelial Cells via Regulating TNFR1

2021 ◽  
Vol Volume 16 ◽  
pp. 1329-1345
Author(s):  
Hong Xue ◽  
Baosong Xie ◽  
Nengluan Xu ◽  
Hongru Li ◽  
Qianshun Chen ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Pulmonary Artery ◽  
Cigarette Smoke ◽  
Cigarette Smoke Extract ◽  
Human Pulmonary Artery

Cigarette smoke extract induces endothelin-1 via protein kinase C in pulmonary artery endothelial cells

2001 ◽  
Vol 281 (2) ◽  
pp. L403-L411 ◽  
Author(s):  
Sang-Do Lee ◽  
Dong-Soon Lee ◽  
Yong-Gam Chun ◽  
Tae-Sun Shim ◽  
Chae-Man Lim ◽  
...  
Keyword(s):  
Gene Expression ◽  
Endothelial Cells ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Pulmonary Artery ◽  
Cigarette Smoke ◽  
De Novo ◽  
Ex Vivo ◽  
Cigarette Smoke Extract ◽  
Kinase C

We examined the mechanism of endothelin (ET)-1 regulation by cigarette smoke extract (CSE) and the effect of platelets on CSE-induced stimulation of ET-1 gene expression in human and bovine pulmonary artery endothelial cells (PAECs). Our data show that CSE (1%) induces ET-1 gene expression (after 1 h) and ET-1 peptide synthesis (after 4 h) in bovine PAECs. The induction of preproET-1 mRNA level was due to de novo transcription, and new protein synthesis was not required for this induction. The protein kinase C inhibitors staurosporine (10−8mol/l) and calphostin C (10−7mol/l) abolished the induction of ET-1 gene expression by CSE in bovine and human PAECs. Although a lower concentration of platelets (106cells/ml in bovine PAECs; 107cells/ml in human PAECs) did not significantly alter ET-1 gene expression in PAECs, incubation of platelets with CSE (1%) and PAECs produced a significant increase in preproET-1 mRNA and ET-1 peptide compared with the values in the presence of CSE (1%) alone. CSE (1%) induced platelet aggregation and increased the expression of platelet membrane glycoproteins ex vivo. Thus our data suggest that CSE stimulates ET-1 gene expression via PKC in PAECs. CSE and platelets showed a synergistic effect on ET-1 gene expression, possibly through the activation of platelets by CSE.

scholarly journals Extracellular vesicles from human airway basal cells respond to cigarette smoke extract and affect vascular endothelial cells

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ashish Saxena ◽  
Matthew S. Walters ◽  
Jae-Hung Shieh ◽  
Ling-Bo Shen ◽  
Kazunori Gomi ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cigarette Smoke ◽  
Extracellular Vesicles ◽  
Basal Cell ◽  
Mapk Signaling ◽  
Cigarette Smoke Extract ◽  
Vegf Receptor ◽  
Vascular Endothelial ◽  
Basal Cells ◽  
Human Airway

AbstractThe human airway epithelium lining the bronchial tree contains basal cells that proliferate, differentiate, and communicate with other components of their microenvironment. One method that cells use for intercellular communication involves the secretion of exosomes and other extracellular vesicles (EVs). We isolated exosome-enriched EVs that were produced from an immortalized human airway basal cell line (BCi-NS1.1) and found that their secretion is increased by exposure to cigarette smoke extract, suggesting that this stress stimulates release of EVs which could affect signaling to other cells. We have previously shown that primary human airway basal cells secrete vascular endothelial growth factor A (VEGFA) which can activate MAPK signaling cascades in endothelial cells via VEGF receptor–2 (VEGFR2). Here, we show that exposure of endothelial cells to exosome-enriched airway basal cell EVs promotes the survival of these cells and that this effect also involves VEGFR2 activation and is, at least in part, mediated by VEGFA present in the EVs. These observations demonstrate that EVs are involved in the intercellular signaling between airway basal cells and the endothelium which we previously reported. The downstream signaling pathways involved may be distinct and specific to the EVs, however, as increased phosphorylation of Akt, STAT3, p44/42 MAPK, and p38 MAPK was not seen following exposure of endothelial cells to airway basal cell EVs.

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.

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