The protective role of bioactive quinones in stress-induced senescence phenotype of endothelial cells exposed to cigarette smoke extract

2021 ◽  
Vol 177 ◽  
pp. S88
Author(s):  
Ilenia Cirilli ◽  
Patrick Orlando ◽  
Fabio Marcheggiani ◽  
Sonia Silvestri ◽  
Phiwayinkosi V. Dludla ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cigarette Smoke ◽  
Protective Role ◽  
Cigarette Smoke Extract ◽  
Senescence Phenotype

A Protective role of sulforaphane on alveolar epithelial cells exposed to cigarette smoke extract

2013 ◽  
Vol 39 (9) ◽  
pp. 379-386 ◽  
Author(s):  
Zongxian Jiao ◽  
Qiangnu Zhang ◽  
Jiachen Chang ◽  
Dengmei Nie ◽  
Min Li ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Cigarette Smoke ◽  
Protective Role ◽  
Cigarette Smoke Extract ◽  
Alveolar Epithelial Cells ◽  
Alveolar Epithelial

Cigarette smoke extract inhibits angiogenesis of pulmonary artery endothelial cells: the role of calpain

2004 ◽  
Vol 287 (4) ◽  
pp. L794-L800 ◽  
Author(s):  
Yunchao Su ◽  
Wengang Cao ◽  
Zhaosheng Han ◽  
Edward R. Block
Keyword(s):  
Endothelial Cells ◽  
Cigarette Smoke ◽  
Wound Repair ◽  
Cigarette Smoke Extract ◽  
Tube Formation ◽  
Calpain Inhibitor ◽  
Endothelial Monolayer ◽  
Calpain Activity ◽  
Dose Dependent

Angiogenesis is an integral part of both the pulmonary inflammatory response to chronic exposure to cigarette smoke and the lung tissue remodeling associated with cigarette smoke-induced chronic obstructive pulmonary disease (COPD). To investigate the role of angiogenesis in the pathogenesis of COPD, we evaluated the effect of cigarette smoke extract (CSE) on angiogenesis of pulmonary artery endothelial cells (PAEC). Incubation of PAEC with 2.5–10% CSE resulted in a dose-dependent inhibition of endothelial monolayer wound repair. CSE also caused inhibition of tube formation on Matrigel, migration in a Boyden chamber, and proliferation of PAEC. Because calpain, a family of calcium-dependent intracellular proteases, mediates cytoskeletal signaling in endothelial motility, we explored the role of calpain in the CSE-induced inhibition of endothelial angiogenesis. Incubation of CSE resulted in a dose-dependent decrease in calpain activity. Calpain inhibitor-1, a specific inhibitor of calpain, potentiates inhibitory effect of CSE on the endothelial monolayer wound repair, tube formation, cell migration, and cell proliferation. Transfection of PAEC with antisense oligodeoxyribonucleotides of calpastatin, the major endogenous calpain inhibitor, prevented CSE-induced increase in calpastatin protein content and CSE-induced decreases in calpain activity. It also prevented CSE-induced decreases in monolayer wound repair, tube formation, and migration. These results suggest that CSE attenuates angiogenesis of PAEC and the mechanism involves inhibition of calpain. Impaired angiogenesis may impede the repair process in the lungs of cigarette smokers and contribute to the altered structural remodeling observed in the lungs of patients with cigarette smoke-related COPD.

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 Dynamics of heat shock protein 60 in endothelial cells exposed to cigarette smoke extract

2011 ◽  
Vol 51 (5) ◽  
pp. 777-780 ◽  
Author(s):  
Simone Barbara Kreutmayer ◽  
Barbara Messner ◽  
Michael Knoflach ◽  
Blair Henderson ◽  
Harald Niederegger ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Cigarette Smoke ◽  
Cigarette Smoke Extract ◽  
Heat Shock Protein 60

Impairment of endothelium-dependent relaxation of rabbit aortas by cigarette smoke extract—role of free radicals and attenuation by captopril

1997 ◽  
Vol 131 (2) ◽  
pp. 195-202 ◽  
Author(s):  
Yasutaka Ota ◽  
Kiyotaka Kugiyama ◽  
Seigo Sugiyama ◽  
Masamichi Ohgushi ◽  
Toshiyuki Matsumura ◽  
...  
Keyword(s):  
Free Radicals ◽  
Cigarette Smoke ◽  
Cigarette Smoke Extract ◽  
Endothelium Dependent Relaxation

scholarly journals Mechanism of an indirect effect of aqueous cigarette smoke extract on the adhesion of monocytic cells to endothelial cells in an in vitro assay revealed by transcriptomics analysis

2014 ◽  
Vol 28 (5) ◽  
pp. 896-908 ◽  
Author(s):  
Carine Poussin ◽  
Inka Gallitz ◽  
Walter K. Schlage ◽  
Yvonne Steffen ◽  
Katrin Stolle ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cigarette Smoke ◽  
Indirect Effect ◽  
Cigarette Smoke Extract ◽  
In Vitro Assay ◽  
Monocytic Cells ◽  
Vitro Assay

scholarly journals Autophagic proteins regulate cigarette smoke induced apoptosis: Protective role of heme oxygenase-1

Autophagy ◽  
2008 ◽  
Vol 4 (7) ◽  
pp. 887-895 ◽  
Author(s):  
Hong Pyo Kim ◽  
Xue Wang ◽  
Seon-Jin Lee ◽  
Min-Hsin Huang ◽  
Yong Wan ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Heme Oxygenase ◽  
Protective Role ◽  
Heme Oxygenase 1 ◽  
Induced Apoptosis ◽  
Autophagic Proteins
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