Pulmonary vascular endothelial cells modulate stretch-induced DNA and connective tissue synthesis in rat pulmonary artery segments

CHEST Journal ◽  
1988 ◽  
Vol 93 (3) ◽  
pp. 169S-170 ◽  
Author(s):  
C. A. Tozzi ◽  
G. J. Poiani ◽  
A. M. Harangozo ◽  
C. J. Boyd ◽  
D. J. Riley
Keyword(s):  
Endothelial Cells ◽  
Connective Tissue ◽  
Pulmonary Artery ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial

Pulmonary Vascular Endothelial Cells Modulate Stretch-induced DNA and Connective Tissue Synthesis in Rat Pulmonary Artery Segments

CHEST Journal ◽  
1988 ◽  
Vol 93 (3) ◽  
pp. 169S-170S ◽  
Author(s):  
Carol A. Tozzi ◽  
George J. Poiani ◽  
Andrea M. Harangozo ◽  
Charles J. Boyd ◽  
David J. Riley
Keyword(s):  
Endothelial Cells ◽  
Connective Tissue ◽  
Pulmonary Artery ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial

scholarly journals Reconciling VEGF With VPF: The Importance of Increased Vascular Permeability for Stroma Formation in Tumors, Healing Wounds, and Chronic Inflammation

2021 ◽  
Vol 9 ◽  
Author(s):  
Harold F. Dvorak
Keyword(s):  
Endothelial Cells ◽  
Connective Tissue ◽  
Vascular Permeability ◽  
Vascular Endothelial Cells ◽  
Inflammatory Diseases ◽  
Expression Patterns ◽  
Vascular Endothelial ◽  
Vascular Permeability Factor ◽  
Healing Wounds

It is widely believed that vascular endothelial growth factor (VEGF) induces angiogenesis by its direct mitogenic and motogenic actions on vascular endothelial cells. However, these activities are only detected when endothelial cells are cultured at very low (0.1%) serum concentrations and would not be expected to take place at the much higher serum levels found in angiogenic sites in vivo. This conundrum can be resolved by recalling VEGF’s original function, that of an extremely potent vascular permeability factor (VPF). In vivo VPF/VEGF increases microvascular permeability such that whole plasma leaks into the tissues where it undergoes clotting by tissue factor that is expressed on tumor and host connective tissue cells to deposit fibrin and generate serum. By providing tissue support and by reprogramming the gene expression patterns of cells locally, fibrin and serum can together account for the formation of vascular connective tissue stroma. In sum, by increasing vascular permeability, VPF/VEGF triggers the “wound healing response,” setting in motion a fundamental pathophysiological process that induces the mature stroma that is found not only in healing wounds but also in solid tumors and chronic inflammatory diseases. Once initiated by increased vascular permeability, this response may be difficult to impede, perhaps contributing to the limited success of anti-VEGF therapies in treating cancer.

scholarly journals Human pulmonary artery endothelial cells upregulate ACE2 expression in response to iron-regulatory elements: potential implications for SARS-CoV-2 infection of vascular endothelial cells.

2021 ◽  
Author(s):  
Quezia K Toe ◽  
Theo Issitt ◽  
Abdul Mahomed ◽  
Ioannis Panselinas ◽  
Fatma Almaghlouth ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Pulmonary Artery ◽  
Vascular Endothelial Cells ◽  
Vascular Dysfunction ◽  
Severe Disease ◽  
The Elderly ◽  
Regulatory Elements ◽  
Adverse Outcomes ◽  
Vascular Endothelial ◽  
Human Pulmonary Artery

Emerging studies from the ongoing covid-19 pandemic have implicated vascular dysfunction and endotheliitis in many patients presenting with severe disease. However, there is limited evidence for the expression of ACE2 (the principal co-receptor for Sars-Cov-2 cellular attachment) in vascular endothelial cells which has prompted the suggestion that the virus does not infect these cell types. However, the studies presented here demonstrate enhanced expression of ACE2 at the level of both mRNA and protein, in human pulmonary artery endothelial cells (PAECs) challenged with either IL-6 or hepcidin. Notably elevated levels both these iron-regulatory elements have been described in Covid-19 patients with severe disease and are further associated with morbidity and mortality. Additionally, levels of both IL-6 and hepcidin are often elevated in the elderly and in chronic disease settings, these populations being at greater risk of adverse outcomes from Sars-Cov-2 infection. A role for IL-6 and hepcidin as modulators of ACE2 expression seems plausible, additional, studies are required to determine if viral infection can be demonstrated in PAECs challenged with either of these iron-regulatory elements.

Pollutant particles enhanced H2O2 production from NAD(P)H oxidase and mitochondria in human pulmonary artery endothelial cells

2006 ◽  
Vol 291 (2) ◽  
pp. C357-C365 ◽  
Author(s):  
Zhuowei Li ◽  
Xhevahire Hyseni ◽  
Jacqueline D. Carter ◽  
Joleen M. Soukup ◽  
Lisa A. Dailey ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Pulmonary Artery ◽  
Health Effects ◽  
Vascular Endothelial Cells ◽  
Water Soluble ◽  
H2o2 Production ◽  
Vascular Endothelial ◽  
Human Pulmonary Artery ◽  
P38 Mapks

Particulate matter (PM) induces oxidative stress and cardiovascular adverse health effects, but the mechanistic link between the two is unclear. We hypothesized that PM enhanced oxidative stress in vascular endothelial cells and investigated the enzymatic sources of reactive oxygen species and their effects on mitogen-activated protein kinase (MAPK) activation and vasoconstriction. We measured the production of extracellular H2O2, activation of extracellular signal-regulated kinases1/2 (ERK1/2) and p38 MAPKs in human pulmonary artery endothelial cells (HPAEC) treated with urban particles (UP; SRM1648), and assessed the effects of H2O2 on vasoconstriction in pulmonary artery ring and isolated perfused lung. Within minutes after UP treatment, HPAEC increased H2O2 production that could be inhibited by diphenyleneiodonium (DPI), apocynin (APO), and sodium azide (NaN3). The water-soluble fraction of UP as well as its two transition metal components, Cu and V, also stimulated H2O2 production. NaN3 inhibited H2O2 production stimulated by Cu and V, whereas DPI and APO inhibited only Cu-stimulated H2O2 production. Inhibitors of other H2O2-producing enzymes, including Nω-methyl-l-argnine, indomethacin, allopurinol, cimetidine, rotenone, and antimycin, had no effects. DPI but not NaN3 attenuated UP-induced pulmonary vasoconstriction and phosphorylation of ERK1/2 and p38 MAPKs. Knockdown of p47phox gene expression by small interfering RNA attenuated UP-induced H2O2 production and phosphorylation of ERK1/2 and p38 MAPKs. Intravascular administration of H2O2 generated by glucose oxidase increased pulmonary artery pressure. We conclude that UP induce oxidative stress in vascular endothelial cells by activating NAD(P)H oxidase and the mitochondria. The endothelial oxidative stress may be an important mechanism for PM-induced acute cardiovascular health effects.

scholarly journals Connective tissue growth factor: a cysteine-rich mitogen secreted by human vascular endothelial cells is related to the SRC-induced immediate early gene product CEF-10.

1991 ◽  
Vol 114 (6) ◽  
pp. 1285-1294 ◽  
Author(s):  
D M Bradham ◽  
A Igarashi ◽  
R L Potter ◽  
G R Grotendorst
Keyword(s):  
Endothelial Cells ◽  
Growth Factor ◽  
Connective Tissue ◽  
Connective Tissue Growth Factor ◽  
Culture Media ◽  
Vascular Endothelial Cells ◽  
Tissue Growth ◽  
Biologically Active ◽  
Early Gene ◽  
Vascular Endothelial

Human umbilical vein endothelial (HUVE) cells have been previously reported to express the genes for the A and B chains of PDGF and to secrete PDGF-related factors into culture media. Antihuman PDGF IgG affinity chromatography was used to purify PDGF-related activity from HUVE cell-conditioned media. Immunoblot analysis of the affinity-purified proteins with anti-PDGF IgG and antibodies specific for the A or B chain peptides of PDGF combined with chemotactic and mitogenic assays revealed that the major PDGF immunorelated molecule secreted by HUVE cells is a monomer of approximately 36-38 kD and that less than 10% of the purified biologically active molecules are PDGF A or B chain peptides. Screening of an HUVE cell cDNA library in the expression vector lambda gtl 1 with the anti-PDGF antibody resulted in the cloning and sequencing of a cDNA with an open reading frame encoding a 38-kD cysteine-rich secreted protein which we show to be the major PDGF-related mitogen secreted by human vascular endothelial cells. The protein has a 45% overall homology to the translation product of the v-src-induced CEF-10 mRNA from chick embryo fibroblasts. We have termed this new mitogen connective tissue growth factor.

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