Tmem100 ‐BAC‐EGFP mice to selectively mark and purify embryonic endothelial cells of large caliber arteries in mid‐gestational vascular formation

genesis ◽  
2021 ◽  
Author(s):  
Yumi Kinugasa‐Katayama ◽  
Yusuke Watanabe ◽  
Takashi Hisamitsu ◽  
Yuichiro Arima ◽  
Norika M. Liu ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Vascular Formation

Controlling shape and position of vascular formation in engineered tissues by arbitrary assembly of endothelial cells

2015 ◽  
Vol 7 (4) ◽  
pp. 045006 ◽  
Author(s):  
Hiroaki Takehara ◽  
Katsuhisa Sakaguchi ◽  
Masatoshi Kuroda ◽  
Megumi Muraoka ◽  
Kazuyoshi Itoga ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Engineered Tissues ◽  
Vascular Formation

scholarly journals Importance of endothelial Hey1 expression for thoracic great vessel development and its distal enhancer for Notch-dependent endothelial transcription

2020 ◽  
Vol 295 (51) ◽  
pp. 17632-17645
Author(s):  
Yusuke Watanabe ◽  
Daiki Seya ◽  
Dai Ihara ◽  
Shuhei Ishii ◽  
Taiki Uemoto ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Regulatory Region ◽  
Mouse Embryos ◽  
Great Vessel ◽  
Distal Enhancer ◽  
Enhancer Activity ◽  
Cell Specificity ◽  
Vascular Formation

Thoracic great vessels such as the aorta and subclavian arteries are formed through dynamic remodeling of embryonic pharyngeal arch arteries (PAAs). Previous work has shown that loss of a basic helix-loop-helix transcription factor Hey1 in mice causes abnormal fourth PAA development and lethal great vessel anomalies resembling congenital malformations in humans. However, how Hey1 mediates vascular formation remains unclear. In this study, we revealed that Hey1 in vascular endothelial cells, but not in smooth muscle cells, played essential roles for PAA development and great vessel morphogenesis in mouse embryos. Tek-Cre–mediated Hey1 deletion in endothelial cells affected endothelial tube formation and smooth muscle differentiation in embryonic fourth PAAs and resulted in interruption of the aortic arch and other great vessel malformations. Cell specificity and signal responsiveness of Hey1 expression were controlled through multiple cis-regulatory regions. We found two distal genomic regions that had enhancer activity in endothelial cells and in the pharyngeal epithelium and somites, respectively. The novel endothelial enhancer was conserved across species and was specific to large-caliber arteries. Its transcriptional activity was regulated by Notch signaling in vitro and in vivo, but not by ALK1 signaling and other transcription factors implicated in endothelial cell specificity. The distal endothelial enhancer was not essential for basal Hey1 expression in mouse embryos but may likely serve for Notch-dependent transcriptional control in endothelial cells together with the proximal regulatory region. These findings help in understanding the significance and regulation of endothelial Hey1 as a mediator of multiple signaling pathways in embryonic vascular formation.

Three-Dimensional Culture of Vascular Endothelial Cells Using Vascular Endothelial Growth Factor-Loaded Apatite-Fiber Scaffolds with Enhanced Mechanical Property

2012 ◽  
Vol 529-530 ◽  
pp. 402-406
Author(s):  
K. Kayashima ◽  
R. Oyama ◽  
M. Emoto ◽  
H. Maehashi ◽  
Tomokazu Matsuura ◽  
...  
Keyword(s):  
Mechanical Property ◽  
Vascular Endothelial Growth Factor ◽  
Endothelial Cells ◽  
Growth Factor ◽  
Vascular Endothelial Cells ◽  
Three Dimensional ◽  
Vascular Endothelial ◽  
Fiber Scaffolds ◽  
Endothelial Growth Factor ◽  
Vascular Formation

We have successfully developed the apatite-fiber scaffold (AFS) with enhanced mechanical porosity for tissue engineering of bone and liver via two routes: i) use of two type of carbon beads with diameter of ~150 μm and ~20 μm and following ii) uniaxial pressing of the green compacts. Our Aim is to add vascular formation ability into the above AFS in order to maintain the regenerated tissues for a long time. In the present study, the AFSs with various porosities (68±2.4, 85±1.5, 89±0.6, 92±1.0%) were fabricated, and then loaded with vascular endothelial growth factor (VEGF). Drug release from VEGF-loaded AFSs with various porosities was examined by immersing them into phosphate buffer. The AFSs with the highest porosity (92%) could be released with the most VEGF among examined AFSs. In addition, we carried out preliminary study for the compatibility of vascular endothelial cells, M1 cells established by Matsuura et al. to the VEGF-loaded AFS (porosity: 92%), in order to account for the vascular formation into the pore of the AFS. The numbers of M1 cells cultured in/on the VEGF-loaded AFS were about 1.5 times that of VEGF-free AFS over a period of cell culture. These results demonstrate that the VEGF-loaded AFS with enhanced mechanical property have a good compatibility to the M1 cells as a model of vascular endothelial cells.

Endotoxin Alteration of the Mucopolysaccharide Blood Vessel Coating in Rats

1974 ◽  
Vol 32 ◽  
pp. 148-149
Author(s):  
D. E. Philpott ◽  
A. Takahashi
Keyword(s):  
Skeletal Muscle ◽  
Endothelial Cells ◽  
Salivary Gland ◽  
Carotid Artery ◽  
Basement Membrane ◽  
Coronary Vessels ◽  
Ruthenium Red ◽  
E Coli ◽  
Old Rats ◽  
The Brain

Two month, eight month and two year old rats were treated with 10 or 20 mg/kg of E. Coli endotoxin I. P. The eight month old rats proved most resistant to the endotoxin. During fixation the aorta, carotid artery, basil arartery of the brain, coronary vessels of the heart, inner surfaces of the heart chambers, heart and skeletal muscle, lung, liver, kidney, spleen, brain, retina, trachae, intestine, salivary gland, adrenal gland and gingiva were treated with ruthenium red or alcian blue to preserve the mucopolysaccharide (MPS) coating. Five, 8 and 24 hrs of endotoxin treatment produced increasingly marked capillary damage, disappearance of the MPS coating, edema, destruction of endothelial cells and damage to the basement membrane in the liver, kidney and lung.

Complex Vesicles, Microtubules, and Cytoplasmic Filaments in the Endothelial Cells of Normal Dog Aorta

1968 ◽  
Vol 26 ◽  
pp. 172-173
Author(s):  
C. N. Sun ◽  
J. J. Ghidoni
Keyword(s):  
Electron Microscopy ◽  
Endothelial Cells ◽  
Cross Sections ◽  
Functional Significance ◽  
Tubular Structures ◽  
Aldehyde Fixation ◽  
Cytoplasmic Filaments

Endothelial cells in longitudinal and cross sections of aortas from 3 randomly selected “normal” mongrel dogs were studied by electron microscopy. Segments of aorta were distended with cold cacodylate buffered 5% glutaraldehyde for 10 minutes prior to being cut into small, well oriented tissue blocks. After an additional 1-1/2 hour period in glutaraldehyde, the tissue blocks were well rinsed in buffer and post-fixed in OsO4. After dehydration they were embedded in a mixture of Maraglas, D.E.R. 732, and DDSA.Aldehyde fixation preserves the filamentous and tubular structures (300 Å and less) for adequate demonstration and study. The functional significance of filaments and microtubules has been recently discussed by Buckley and Porter; the precise roles of these cytoplasmic components remains problematic. Endothelial cells in canine aortas contained an abundance of both types of structures.

Ultrastructural Alterations in Sinusoidal Endothelial Fenestrae as a Result of Hypoxia

1976 ◽  
Vol 34 ◽  
pp. 168-169
Author(s):  
Waykin Nopanitaya ◽  
Raeford E. Brown ◽  
Joe W. Grisham ◽  
Johnny L. Carson
Keyword(s):  
Endothelial Cells ◽  
Experimental Model ◽  
Hepatic Lobule ◽  
Ultrastructural Alterations ◽  
Large Type ◽  
Sinusoidal Endothelial Fenestrae ◽  
General Size ◽  
Sem Studies

Mammalian endothelial cells lining hepatic sinusoids have been found to be widely fenestrated. Previous SEM studies (1,2) have noted two general size catagories of fenestrations; large fenestrae were distributed randomly while the small type occurred in groups. These investigations also reported that large fenestrae were more numerous and larger in the endothelial cells at the afferent ends of sinusoids or around the portal areas, whereas small fenestrae were more numerous around the centrilobular portion of the hepatic lobule. It has been further suggested that under some physiologic conditions small fenestrae could fuse and subsequently become the large type, but this is, as yet, unproven.We have used a reproducible experimental model of hypoxia to study the ultrastructural alterations in sinusoidal endothelial fenestrations in order to investigate the origin of occurrence of large fenestrae.

Ultrastructural studies on the interaction of haemophilus influenzae with human endothelial cells in vitro

1990 ◽  
Vol 48 (3) ◽  
pp. 636-637
Author(s):  
D.J.P. Ferguson ◽  
M. Virji ◽  
H. Kayhty ◽  
E.R. Moxon
Keyword(s):  
Endothelial Cells ◽  
Haemophilus Influenzae ◽  
Intercellular Junctions ◽  
Blood Stream ◽  
Ultrastructural Studies ◽  
Endothelial Barriers ◽  
Serotype B ◽  
Meningitis In Children ◽  
Respiratory Epithelial

Haemophilus influenzae is a human pathogen which causes meningitis in children. Systemic H. influenzae infection is largely confined to encapsulated serotype b organisms and is a major cause of meningitis in the U.K. and elsewhere. However, the pathogenesis of the disease is still poorly understood. Studies in the infant rat model, in which intranasal challenge results in bacteraemia, have shown that H. influenzae enters submucosal tissues and disseminates to the blood stream within minutes. The rapidity of these events suggests that H. influenzae penetrates both respiratory epithelial and endothelial barriers with great efficiency. It is not known whether the bacteria penetrate via the intercellular junctions, are translocated within the cells or carried across the cellular barrier in 'trojan horse' fashion within phagocytes. In the present studies, we have challenged cultured human umbilical cord_vein endothelial cells (HUVECs) with both capsulated (b+) and capsule-deficient (b-) isogenic variants of one strain of H. influenzae in order to investigate the interaction between the bacteria and HUVEC and the effect of the capsule.

Antiflammin-1 inhibits the adhesion of neutrophils to endothelial cells induced by LPS

2010 ◽  
Vol 34 (8) ◽  
pp. S66-S66
Author(s):  
Jinfeng Li ◽  
Wenli Liu ◽  
Xiaojuan Shi ◽  
Wei Liu ◽  
Chen Li ◽  
...  
Keyword(s):  
Endothelial Cells

Intrapericardial lymphangioma with podoplanin immunohistochemical characterization of lymphatic endothelial cells

2000 ◽  
Vol 37 (1) ◽  
pp. 85-95 ◽  
Author(s):  
E Sinzelle ◽  
J P Duong Van Huyen ◽  
S Breiteneder-Geleff ◽  
E Braunberger ◽  
A Deloche ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Lymphatic Endothelial Cells
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