Electron-immunocytochemistry of peptides in endothelial cells of rabbit cerebral vessels following perfusion with a perfluorocarbon emulsion

1993 ◽  
Vol 611 (2) ◽  
pp. 333-337 ◽  
Author(s):  
Andrzej Loesch ◽  
Floyd R. Domer ◽  
Barry Alexander ◽  
Geoffrey Burnstock
Keyword(s):  
Endothelial Cells ◽  
Cerebral Vessels ◽  
Perfluorocarbon Emulsion ◽  
Electron Immunocytochemistry

scholarly journals Evidence that Functional Glutamate Receptors are not Expressed on Rat or Human Cerebromicrovascular Endothelial Cells

1998 ◽  
Vol 18 (4) ◽  
pp. 396-406 ◽  
Author(s):  
Paul Morley ◽  
Daniel L. Small ◽  
Christine L. Murray ◽  
Geoffrey A. Mealing ◽  
Michael O. Poulter ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Nmda Receptor ◽  
Glutamate Receptors ◽  
Glutamate Receptor ◽  
Ampa Receptor ◽  
Cortical Neurons ◽  
Cerebral Vessels ◽  
Rt Pcr ◽  
Metabotropic Glutamate ◽  
Rat Cortical Neurons

Excitatory amino acids can modify the tone of cerebral vessels and permeability of the blood-brain barrier (BBB) by acting directly on endothelial cells of cerebral vessels or indirectly by activating receptors expressed on other brain cells. In this study we examined whether rat or human cerebromicrovascular endothelial cells (CEC) express ionotropic and metabotropic glutamate receptors. Glutamate and the glutamate receptor agonists N-methyl-d-aspartate (NMDA), α-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid (AMPA), and kainate failed to increase [Ca2+]i in either rat or human microvascular and capillary CEC but elicited robust responses in primary rat cortical neurons, as measured by fura-2 fluorescence. The absence of NMDA and AMPA receptors in rat and human CEC was further confirmed by the lack of immunocytochemical staining of cells by antibodies specific for the AMPA receptor subunits GluR1, GluR2/3, and GluR4 and the NMDA receptor subunits NR1, NR2A, and NR2B. We failed to detect mRNA expression of the AMPA receptor subunits GluR1 to GluR4 or the NMDA receptor subunits NR11XX, NR10XX, and NR2A to NR2C in both freshly isolated rat and human microvessels and cultured CEC using reverse transcriptase polymerase chain reaction (RT-PCR). Cultured rat CEC expressed mRNA for KA1 or KA2 and GluR5 subunits. Primary rat cortical neurons were found to express GluR1 to GluR3 and NR1, NR2A, and NR2B by both immunocytochemistry and RT-PCR and KA1, KA2, GluR5, GluR6, and GluR7 by RT-PCR. Moreover, the metabotropic glutamate receptor agonist 1-amino-cyclopentyl-1 S, 3 R-dicorboxylate (1 S,3 R-trans-ACPD), while eliciting both inositol trisphosphate and [Ca2+]i increases and inhibiting forskolin-stimulated cyclic AMP in cortical neurons, was unable to induce either of these responses in rat or human CEC. These results strongly suggest that both rat and human CEC do not express functional glutamate receptors. Therefore, excitatory amino acid-induced changes in the cerebral microvascular tone and BBB permeability must be affected indirectly, most likely by mediators released from the adjacent glutamate-responsive cells.

scholarly journals Lyophilized Powder of Catalpol and Puerarin Protected Cerebral Vessels from Ischemia by Its Anti-apoptosis on Endothelial Cells

2017 ◽  
Vol 13 (3) ◽  
pp. 327-338 ◽  
Author(s):  
Yang Liu ◽  
Qing Tang ◽  
Siying Shao ◽  
Yi Chen ◽  
Weihai Chen ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cerebral Vessels

scholarly journals Endothelial cells form transient Notch-dependent NO-containing cystic structures during zebrafish cerebrovascular development

2018 ◽  
Author(s):  
E. Kugler ◽  
K. Chhabria ◽  
S. Daetwyler ◽  
J. Huisken ◽  
K. Plant ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cerebral Vessels ◽  
Transgenic Zebrafish ◽  
Filamentous Actin ◽  
Parent Vessel ◽  
Cell Behaviour ◽  
Spherical Structures ◽  
Endothelial Growth Factor

AbstractEndothelial cell behaviour during blood vessel formation is highly complex and dynamic. Transgenic zebrafish have provided many new insights into these processes, due to their ability to provide detailed in vivo imaging.We here report a previously undescribed endothelial cell behaviour during zebrafish embryonic development. Endothelial cells of the cerebral vessels of 3-5d post fertilisation embryos extruded large membranous spherical structures. These were only found on the cerebral vessels, and did not detach from the parent vessel, instead regressing back into the endothelial cell. These structures did not communicate with the vessel lumen, exhibited periodic oscillations in size and shape, and were enriched with filamentous actin at their neck. Due to their unknown nature and spherical appearance we termed these structures kugeln (German for sphere).Pharmacological inhibition of vascular endothelial growth factor (VEGF) signalling significantly increased kugel number while Notch inhibition significantly reduced both kugel number and diameter. Kugeln contain little cytoplasm, but are highly positive for nitric oxide (NO) reactivity, suggesting they represent a novel NO containing organelle specific to the cerebral vessels.

scholarly journals Epileptic seizures increase circulating endothelial cells in peripheral blood as early indicators of cerebral vascular damage

2010 ◽  
Vol 298 (6) ◽  
pp. H1687-H1698 ◽  
Author(s):  
Helena Parfenova ◽  
Charles W. Leffler ◽  
Dilyara Tcheranova ◽  
Shyamali Basuroy ◽  
Aliz Zimmermann
Keyword(s):  
Endothelial Cells ◽  
Peripheral Blood ◽  
Glucose Transporter ◽  
Mononuclear Cells ◽  
Epileptic Seizures ◽  
Vascular Damage ◽  
Cerebral Vessels ◽  
Circulating Endothelial Cells ◽  
Cerebral Vascular ◽  
Early Indicators

Circulating endothelial cells (CECs) are nonhematopoetic mononuclear cells in peripheral blood that are dislodged from injured vessels during cardiovascular disease, systemic vascular disease, and inflammation. Their occurrence during cerebrovascular insults has not been previously described. Epileptic seizures cause the long-term loss of cerebrovascular endothelial dilator function. We hypothesized that seizures cause endothelial sloughing from cerebral vessels and the appearance of brain-derived CECs (BCECs), possible early indicators of cerebral vascular damage. Epileptic seizures were induced by bicuculline in newborn pigs; venous blood was then sampled during a 4-h period. CECs were identified in the fraction of peripheral blood mononuclear cells by the expression of endothelial antigens (CD146, CD31, and endothelial nitric oxide synthase) and by Ulex europeaus lectin binding. In control animals, few CECs were detected. Seizures caused a time-dependent increase in CECs 2–4 h after seizure onset. Seizure-induced CECs coexpress glucose transporter-1, a blood-brain barrier-specific glucose transporter, indicating that these cells originate in the brain vasculature and are thus BCECs. Seizure-induced BCECs cultured in EC media exhibited low proliferative potential and abnormal cell contacts. BCEC appearance during seizures was blocked by a CO-releasing molecule (CORM-A1) or cobalt protoporphyrin (heme oxygenase-1 inducer), which prevented apoptosis in cerebral arterioles and the loss of cerebral vascular endothelial function during the late postictal period. These findings suggest that seizure-induced BCECs are injured ECs dislodged from cerebral microvessels during seizures. The correlation between the appearance of BCECs in peripheral blood, apoptosis in cerebral vessels, and the loss of postictal cerebral vascular function suggests that BCECs are early indicators of late cerebral vascular damage.

scholarly journals Immunoreactivity and a new staining method of monocarboxylate transporter 1 located in endothelial cells of cerebral vessels of human brain in distinguishing cerebral venules from arterioles

2021 ◽  
Vol 65 (s1) ◽  
Author(s):  
Yuan Cao ◽  
Dong-Hui Ao ◽  
Chao Ma ◽  
Wen-Ying Qiu ◽  
Yi-Cheng Zhu
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Human Brain ◽  
Smooth Muscle Actin ◽  
Cerebral Vessels ◽  
Monocarboxylate Transporter ◽  
Specific Marker ◽  
Cerebral Veins ◽  
Internal Elastic Lamina ◽  
Monocarboxylate Transporter 1

Distinguishing brain venules from arterioles with arteriolosclerosis is less reliable using traditional staining methods. We aimed to immunohistochemically assess the monocarboxylate transporter 1 (MCT1), a specific marker of venous endothelium found in rodent studies, in different caliber vessels in human brains. Both largeand small-caliber cerebral vessels were dissected from four autopsy donors. Immunoreactivity for MCT1 was examined in all autopsied human brain tissues, and then each vessel was identified by neuropathologists using hematoxylin and eosin stain, the Verhoeff’s Van Gieson stain, immunohistochemical stain with antibodies for α-smooth muscle actin and MCT1 in sequence. A total of 61 cerebral vessels, including 29 arteries and 32 veins were assessed. Immunoreactivity for MCT1 was observed in the endothelial cells of various caliber veins as well as the capillaries, whereas that was immunenegative in the endothelium of arteries. The different labeling patterns for MCT1 could aid in distinguishing various caliber veins from arteries, whereas assessment using the vessel shape, the internal elastic lamina, and the pattern of smooth muscle fibers failed to make the distinction between small-caliber veins and sclerotic arterioles. In conclusion, MCT1 immunohistochemical staining is a sensitive and reliable method to distinguish cerebral veins from arteries.

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.

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