Paraquat-Induced Oxidative Stress and Dysfunction of the Glutathione Redox Cycle in Pulmonary Microvascular Endothelial Cells

2002 ◽  
Vol 178 (2) ◽  
pp. 82-92 ◽  
Author(s):  
Maki Tsukamoto ◽  
Yoshiko Tampo ◽  
Minoru Sawada ◽  
Masanori Yonaha
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Microvascular Endothelial Cells ◽  
Redox Cycle ◽  
Pulmonary Microvascular Endothelial Cells ◽  
Glutathione Redox Cycle ◽  
Microvascular Endothelial ◽  
Glutathione Redox

scholarly journals Iloprost Attenuates Oxidative Stress-Dependent Activation of Collagen Synthesis Induced by Sera from Scleroderma Patients in Human Pulmonary Microvascular Endothelial Cells

Molecules ◽  
2021 ◽  
Vol 26 (16) ◽  
pp. 4729
Author(s):  
Roberta Giordo ◽  
Duong Thi Bich Thuan ◽  
Anna Maria Posadino ◽  
Annalisa Cossu ◽  
Angelo Zinellu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Collagen Synthesis ◽  
Cell Injury ◽  
Microvascular Endothelial Cells ◽  
Early Event ◽  
Pulmonary Microvascular Endothelial Cells ◽  
Antioxidant Mechanism ◽  
Microvascular Endothelial ◽  
Stress Dependent

Endothelial cell injury is an early event in systemic sclerosis (SSc) pathogenesis and several studies indicate oxidative stress as the trigger of SSc-associated vasculopathy. Here, we show that circulating factors present in sera of SSc patients increased reactive oxygen species (ROS) production and collagen synthesis in human pulmonary microvascular endothelial cells (HPMECs). In addition, the possibility that iloprost, a drug commonly used in SSc therapy, might modulate the above-mentioned biological phenomena has been also investigated. In this regard, as compared to sera of SSc patients, sera of iloprost-treated SSc patients failed to increased ROS levels and collagen synthesis in HPMEC, suggesting a potential antioxidant mechanism of this drug.

Proproliferative phenotype of pulmonary microvascular endothelial cells

2007 ◽  
Vol 292 (3) ◽  
pp. L671-L677 ◽  
Author(s):  
Victor Solodushko ◽  
Brian Fouty
Keyword(s):  
Endothelial Cells ◽  
Barrier Function ◽  
Pulmonary Arteries ◽  
D1 Protein ◽  
Coagulation Cascade ◽  
Microvascular Endothelial Cells ◽  
Significant Heterogeneity ◽  
Pulmonary Microvascular Endothelial Cells ◽  
Microvascular Endothelial ◽  
Pulmonary Microcirculation

Endothelial cells perform a number of important functions including release of vasodilators, control of the coagulation cascade, and restriction of solutes and fluid from the extravascular space. Regulation of fluid balance is of particular importance in the microcirculation of the lung where the loss of endothelial barrier function can lead to alveolar flooding and life-threatening hypoxemia. Significant heterogeneity exists between endothelial cells lining the microcirculation and cells from larger pulmonary arteries, however, and these differences may be relevant in restoring barrier function following vascular injury. Using well-defined populations of rat endothelial cells harvested from the pulmonary microcirculation [pulmonary microvascular endothelial cells (PMVEC)] and from larger pulmonary arteries [pulmonary artery endothelial cells (PAEC)], we compared their growth characteristics in low serum conditions. Withdrawal of serum inhibited proliferation and induced G0/G1 arrest in PAEC, whereas PMVEC failed to undergo G0/G1 arrest and continued to proliferate. Consistent with this observation, PMVEC had an increased cdk4 and cdk2 kinase activity with hyperphosphorylated (inactive) retinoblastoma (Rb) relative to PAEC as well as a threefold increase in cyclin D1 protein levels; overexpression of the cdk inhibitors p21Cip1/Waf1 and p27Kip1 induced G0/G1 arrest. While serum withdrawal failed to induce G0/G1 arrest in nonconfluent PMVEC, confluence was associated with hypophosphorylated Rb and growth arrest; loss of confluence led to resumption of growth. These data suggest that nonconfluent PMVEC continue to proliferate independently of growth factors. This proliferative characteristic may be important in restoring confluence (and barrier function) in the pulmonary microcirculation following endothelial injury.

Expression of simple epithelial cytokeratins in bovine pulmonary microvascular endothelial cells

1990 ◽  
Vol 143 (1) ◽  
pp. 140-149 ◽  
Author(s):  
Wayne F. Patton ◽  
Min Ung Yoon ◽  
J. Steven Alexander ◽  
Nancy Chung-Welch ◽  
Herbert B. Hechtman ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Microvascular Endothelial Cells ◽  
Pulmonary Microvascular Endothelial Cells ◽  
Microvascular Endothelial
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