scholarly journals ADAMTSL3/punctin-2, a gene frequently mutated in colorectal tumors, is widely expressed in normal and malignant epithelial cells, vascular endothelial cells and other cell types, and its mRNA is reduced in colon cancer

2007 ◽  
Vol 121 (8) ◽  
pp. 1710-1716 ◽  
Author(s):  
Bon-Hun Koo ◽  
Tiina Hurskainen ◽  
Katrina Mielke ◽  
Phyu Phyu Aung ◽  
Graham Casey ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Endothelial Cells ◽  
Epithelial Cells ◽  
Vascular Endothelial Cells ◽  
Cell Types ◽  
Vascular Endothelial ◽  
Colorectal Tumors

scholarly journals The Effect of Sodium Bicarbonate, a Beneficial Adjuvant Molecule in Cystic Fibrosis, on Bronchial Epithelial Cells Expressing a Wild-Type or Mutant CFTR Channel

2020 ◽  
Vol 21 (11) ◽  
pp. 4024 ◽  
Author(s):  
Ilona Gróf ◽  
Alexandra Bocsik ◽  
András Harazin ◽  
Ana Raquel Santa-Maria ◽  
Gaszton Vizsnyiczai ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Endothelial Cells ◽  
Epithelial Cells ◽  
Sodium Bicarbonate ◽  
Vascular Endothelial Cells ◽  
Bronchial Epithelium ◽  
Barrier Properties ◽  
Vascular Endothelial ◽  
Wild Type ◽  
Bronchial Epithelial

Clinical and experimental results with inhaled sodium bicarbonate as an adjuvant therapy in cystic fibrosis (CF) are promising due to its mucolytic and bacteriostatic properties, but its direct effect has not been studied on respiratory epithelial cells. Our aim was to establish and characterize co-culture models of human CF bronchial epithelial (CFBE) cell lines expressing a wild-type (WT) or mutant (deltaF508) CF transmembrane conductance regulator (CFTR) channel with human vascular endothelial cells and investigate the effects of bicarbonate. Vascular endothelial cells induced better barrier properties in CFBE cells as reflected by the higher resistance and lower permeability values. Activation of CFTR by cAMP decreased the electrical resistance in WT but not in mutant CFBE cell layers confirming the presence and absence of functional channels, respectively. Sodium bicarbonate (100 mM) was well-tolerated by CFBE cells: it slightly reduced the impedance of WT but not that of the mutant CFBE cells. Sodium bicarbonate significantly decreased the more-alkaline intracellular pH of the mutant CFBE cells, while the barrier properties of the models were only minimally changed. These observations indicate that sodium bicarbonate is beneficial to deltaF508-CFTR expressing CFBE cells. Thus, sodium bicarbonate may have a direct therapeutic effect on the bronchial epithelium.

scholarly journals Studies on microperoxisomes. VII. Pigment epithelial cells and other cell types in the retina of rodents.

1975 ◽  
Vol 65 (2) ◽  
pp. 324-334 ◽  
Author(s):  
P M Leuenberger ◽  
A B Novikoff
Keyword(s):  
Epithelial Cells ◽  
Vascular Endothelial Cells ◽  
Smooth Endoplasmic Reticulum ◽  
Photoreceptor Cells ◽  
Cell Types ◽  
Vascular Endothelial ◽  
Pigment Epithelial ◽  
Large Numbers ◽  
And Storage ◽  
Pigment Epithelial Cells

The pigment epithelial cell of the retina actively participates in two aspects of lipid metabolism: (a) the fatty acid esterification of vitamin A and its storage and transport to the photoreceptors, and (b) the phagocytosis and degradation of the lipoprotein membrane disks shed from the photoreceptor cells. Study of the pigment epithelial cells of adult albino and pigmented rodents has revealed the abundance of an organelle, microperoxisomes, not previously known to exist in this cell type. The metabolism, transport, and storage of lipids are major functions of other cell types which possess large numbers of microperoxisomes associated with a highly developed smooth endoplasmic reticulum. Microperoxisomes were encountered, but relatively rarely, in Müller cells and vascular endothelial cells. A tubular system in photoreceptor terminals is reactive in the cytochemical procedure used to visualize microperoxisomes.

scholarly journals Axl Is Essential for in-vitro Angiogenesis Induced by Vitreous From Patients With Proliferative Diabetic Retinopathy

2021 ◽  
Vol 8 ◽  
Author(s):  
Wenyi Wu ◽  
Huizuo Xu ◽  
Zhishang Meng ◽  
Jianxi Zhu ◽  
Siqi Xiong ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Diabetic Retinopathy ◽  
Proliferative Diabetic Retinopathy ◽  
Tyrosine Kinases ◽  
Vascular Endothelial Cells ◽  
Specific Inhibitor ◽  
Cell Types ◽  
Specific Protein ◽  
Vascular Endothelial

Proliferative diabetic retinopathy (PDR), characterized mainly with abnormal epiretinal angiogenesis forming fibrovascular membranes (FVMs), threatens vision of people with diabetes; FVMs consist of extracellular matrix and a variety of cell types including vascular endothelial cells. Axl, one of receptor tyrosine kinases, can be activated indirectly by vascular endothelial growth factor-A (VEGF-A) via an intracellular route for promoting angiogenesis. In this study, we revealed that growth arrest-specific protein 6 (Gas6), a specific ligand of Axl, was elevated in vitreous from patients with PDR and that Axl was activated in FVMs from patients with PDR. In addition, we demonstrated that in cultured human retinal microvascular endothelial cells (HRECs), Axl inhibition via suppression of Axl expression with Clustered Regularly Interspaced Short Palindromic Repeats/ CRISPR-associated protein 9 or through inactivation with its specific inhibitor R428 blocked PDR vitreous-induced Akt activation and proliferation of HRECs. Furthermore, PDR vitreous-heightened migration and tube formation of HRECs were also blunted by restraining Axl. These results indicate that in the pathogenesis of PDR, Axl can be activated by Gas6 binding directly and by VEGF-A via an intracellular route indirectly, suggesting that Axl plays a pivotal role in the development of PDR and that Axl inhibition shows a bright promise for PDR therapy.

Origin and diversity of embryonic endothelium/endocardium

2018 ◽  
Author(s):  
LeShana SaintJean ◽  
H.S. Baldwin
Keyword(s):  
Endothelial Cells ◽  
Heart Development ◽  
Vascular Endothelial Cells ◽  
Coronary Vessels ◽  
Cell Types ◽  
Genetic Profile ◽  
Vascular Endothelial ◽  
Tremendous Progress

The endocardium represents a distinct population of endothelial cells that arises during the initiation of heart development. Endocardial cells can easily be distinguished from most of the other cardiac cell types. However, endocardial and vascular endothelial cells contain a similar genetic profile that limits the ability to study each group independently. Despite these limitations, tremendous progress has been made in identifying the different roles of endocardial cells throughout heart development. Initial studies focused on the origin of endocardial cells and their role in valvulogenesis, trabeculation, and formation of the ventricular and atrial septum. With the advancement of microscopy and the availability of endocardial specific reporter models (in vitro and in vivo) we have obtained more insight into the molecular, structural, and functional complexity of the endocardium. Additional studies have demonstrated how the endocardium is also involved in the development of coronary vessels within the compact myocardium and in heart regeneration.

Thrombomodulin-mediated catabolism of protein C by pleural mesothelial and vascular endothelial cells

2007 ◽  
Vol 98 (09) ◽  
pp. 627-634 ◽  
Author(s):  
Alireza Rezaie ◽  
Steven Idell ◽  
Alexei Iakhiaev
Keyword(s):  
Endothelial Cells ◽  
Protein C ◽  
Vascular Endothelial Cells ◽  
Degradation Products ◽  
Cell Types ◽  
Model Systems ◽  
Vascular Endothelial ◽  
Wild Type ◽  
Endothelial Protein C Receptor ◽  
Gla Domain

SummaryPleural mesothelial and vascular endothelial cells express protein C (PC) pathway components including thrombomodulin (TM) and endothelial protein C receptor (EPCR) and activate PC by the thrombin-TM dependent mechanism.We used these cells as model systems to identify molecules involved in endocytosis and degradation of PC. We find that mesothelial and endothelial cells can bind, internalize and degrade PC.Addition of thrombin markedly induced degradation of PC by these cells in a TM-dependent fashion, implicating the involvement of the thrombin-TM complex in internalization and degradation of PC. This observation defines a novel function for the thrombin-TM complex as a degradation receptor for PC and suggests that PC is degraded concurrent with its activation.A PC Gla-domain mutant, which is unable to bind to the EPCR, was degraded by the cells to a lesser extent than wild-type PC, implicating the PC degradation concurrent with its activation. Consistent with the role of thrombin-TM complex as a degradation receptor, the catalytically inactive thrombin-S195A also induced PC degradation though to a lesser extent than wild-type thrombin.This suggests that generation of activated PC (APC) can contribute to accumulation of degradation products, but is not essential for the thrombin-induced degradation of PC. The thrombin-TMmediated degradation of PC by both cell types suggest a previously unrecognized mechanism, which can contribute to PC consumption.This mechanism may be pathophysiologically relevant and can contribute to an acquired PC deficiency in conditions characterized by sustained thrombin generation.

A monokine regulates colony-stimulating activity production by vascular endothelial cells

Blood ◽  
1983 ◽  
Vol 62 (3) ◽  
pp. 663-668 ◽  
Author(s):  
GC Jr Bagby ◽  
E McCall ◽  
KA Bergstrom ◽  
D Burger
Keyword(s):  
Endothelial Cells ◽  
Bone Marrow Cells ◽  
Vascular Endothelial Cells ◽  
Umbilical Vein ◽  
Cell Types ◽  
Colony Growth ◽  
Mononuclear Phagocytes ◽  
Vascular Endothelial ◽  
Blood Monocytes ◽  
Colony Stimulating Activity

Abstract Human umbilical vein endothelial cells were cultured in supernatants of peripheral blood monocytes that had been cultured for 3 days with and without lactoferrin. Colony-stimulating activity (CSA) was measured in supernatants of the endothelial cell cultures and appropriate control cultures using normal, T-lymphocyte-depleted, phagocyte-depleted, low- density bone marrow cells in colony growth (CFU-GM) assays. Monocyte- conditioned medium contained a nondialyzable, heat labile factor that enhanced 4–15--fold the production of CSA by endothelial cells. The addition of lactoferrin to monocyte cultures reduced the activity of this monokine by 69%. Lactoferrin did not inhibit CSA production by monokine-stimulated endothelial cells. Therefore, vascular endothelial cells are potent sources of CSA, the production of CSA by these cells is regulated by a stimulatory monokine, and the production and/or release of the monokine is inhibited by lactoferrin, a neutrophil- derived putative feedback inhibitor of granulopoiesis. Inasmuch as a similar monokine is known to stimulate CSA production by fibroblasts and T lymphocytes, we suggest that mononuclear phagocytes play a pivotal role in the regulation of granulopoiesis by recruiting a variety of cell types to produce CSA.

scholarly journals Extracellular 2′,3′-cAMP and 3′,5′-cAMP stimulate proliferation of preglomerular vascular endothelial cells and renal epithelial cells

2012 ◽  
Vol 303 (7) ◽  
pp. F954-F962 ◽  
Author(s):  
Edwin K. Jackson ◽  
Delbert G. Gillespie
Keyword(s):  
Endothelial Cells ◽  
Epithelial Cells ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Tubular Epithelial Cells ◽  
Proximal Tubular Cells ◽  
Extracellular Adenosine ◽  
Tubular Cells ◽  
Proximal Tubular Epithelial Cells ◽  
Proximal Tubular

Kidneys release into the extracellular compartment 3′,5′-cAMP and its positional isomer 2′,3′-cAMP. The purpose of the present study was to investigate the metabolism of extracellular 2′,3′-cAMP and 3′,5′-cAMP in preglomular vascular endothelial and proximal tubular epithelial cells and to determine whether these cAMPs and their downstream metabolites affect cellular proliferation. In preglomerular vascular endothelial and proximal tubular epithelial cells, 1) extracellular 2′,3′-cAMP increased extracellular levels of 3′-AMP and 2′-AMP, whereas extracellular 3′,5′-cAMP increased extracellular levels of 5′-AMP; 2) extracellular 5′-AMP, 3′-AMP, and 2′-AMP increased extracellular adenosine; 3) α,β-methylene-adenosine-5′-diphosphate (CD73 inhibitor) prevented the 5′-AMP-induced increase in extracellular adenosine in preglomerular vascular endothelial cells, but did not affect the 5′-AMP-induced increase in extracellular adenosine in proximal tubular cells or the 3′-AMP-induced or 2′-AMP-induced increase in extracellular adenosine in either cell type; 4) extracellular 2′,3′-cAMP, 3′-AMP, 2′-AMP, 3′,5′-cAMP, 5′-AMP, and adenosine stimulated proliferation of both preglomerular vascular endothelial and proximal tubular cells; and 5) MRS-1754 (selective A2B receptor antagonist) abolished the progrowth effects of extracellular 2′,3′-cAMP, 3′-AMP, 2′-AMP, 3′,5′-cAMP, 5′-AMP, and adenosine in both cell types. Extracellular 2′,3′-cAMP and 3′,5′-cAMP stimulate proliferation of preglomerular vascular endothelial cells and proximal tubular cells. The mechanism by which the cAMPs increase cell proliferation entails 1) metabolism to their respective AMPs, 2) metabolism of their respective AMPs to adenosine (which for 5′-AMP in preglomerular vascular endothelial cells is mediated by CD73), and 3) activation of A2B receptors. Both extracellular 2′,3′-cAMP and 3′,5′-cAMP may help restore architecture of the preglomerular microcirculation and tubular system following kidney injury.

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