Vascular ultrastructure in human meningiomas and schwannomas

1973 ◽  
Vol 38 (4) ◽  
pp. 409-419 ◽  
Author(s):  
Don M. Long
Keyword(s):  
Electron Microscopy ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Fluorescence Microscopy ◽  
Cell Junctions ◽  
Content Type ◽  
Cerebrovascular Permeability ◽  
Human Meningiomas ◽  
Fine Print

✓ Nineteen meningiomas and schwannomas have been studied by fluorescence microscopy and electron microscopy. Increased cerebrovascular permeability to protein was demonstrated in each tumor. The anatomical explanation for this increased permeability to protein was found in open endothelial cell junctions, gaps between endothelial cells, and fenestrations in capillary endothelial membranes.

Evidence for telomerase involvement in the angiogenesis of astrocytic tumors: expression of human telomerase reverse transcriptase messenger RNA by vascular endothelial cells

2001 ◽  
Vol 94 (6) ◽  
pp. 961-971 ◽  
Author(s):  
Roberto Pallini ◽  
Francesco Pierconti ◽  
Maria Laura Falchetti ◽  
Daniela D'Arcangelo ◽  
Eduardo Fernandez ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Endothelial Cell Proliferation ◽  
Vascular Endothelial ◽  
Astrocytic Tumors ◽  
Htert Mrna ◽  
Content Type ◽  
Human Telomerase ◽  
Fine Print

Object. Evidence from recent in vitro studies indicates that reactivation of telomerase, the enzyme that synthesizes the telomere ends of chromosomes, is a crucial event in the unlimited clonal expansion of endothelial cells that precedes the neoplastic conversion of these cells. It is known that high-grade gliomas express telomerase and that, in these neoplasms, proliferating endothelial cells may undergo transformational changes with development of sarcomatous components within the primitive tumor. To assess whether telomerase is involved in the endothelial cell proliferation that characterizes brain tumor angiogenesis, the authors investigated at the single-cell level the expression of messenger (m)RNA for the human telomerase catalytic subunit human telomerase reverse transcriptase (hTERT) by vascular cells of astrocytic tumors. Methods. The in situ hybridization (ISH) method was performed by processing histological sections with specific riboprobes for hTERT and for c-myc, an oncogene that is known to upregulate hTERT. Results of the ISH studies were compared with proliferative activity, as estimated by Ki-67 immunostaining. The expression of hTERT mRNA by vascular endothelial cells was related to the histological grade of the tumor because it was detected in five (29%) of 17 low-grade astrocytomas, nine (56%) of 16 anaplastic astrocytomas, and 19 (100%) of 19 glioblastomas multiforme (GBMs). Expression of c-myc mRNA was strictly correlated with that of hTERT mRNA. In low-grade astrocytomas and anaplastic astrocytomas, a dissociation was noted between hTERT mRNA expression and the proliferation rate of endothelial cells. Conversely, GBMs displayed a significant correlation between the level of hTERT mRNA expression and endothelial cell proliferation. Data from an in vitro assay in which human umbilical vein endothelial cells were stimulated to proliferate by adding vascular endothelial growth factor and an ISH study of newly formed vessels surrounding brain infarcts confirmed that expression of hTERT mRNA does not merely reflect the proliferative status of endothelial cells but represents a specific feature of brain tumor neovascularization. Conclusions. The results of this study are consistent with a role of telomerase in the angiogenesis of astrocytic tumors. Expression of hTERT mRNA by tumor vascular cells is an early event during the progression of astrocytic tumors, which precedes endothelial cell proliferation and may represent a first sign of dedifferentiation. Other than elucidating the mechanisms of tumor angiogenesis, these results encourage research on antitelomerase drugs for the treatment of malignant gliomas.

Oxyhemoglobin-induced apoptosis in cultured endothelial cells

1999 ◽  
Vol 91 (3) ◽  
pp. 459-465 ◽  
Author(s):  
Kotaro Ogihara ◽  
Alexander Y. Zubkov ◽  
David H. Bernanke ◽  
Adam I. Lewis ◽  
Andrew D. Parent ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Transmission Electron Microscopy ◽  
Endothelial Cells ◽  
Time Dependent ◽  
Dependent Manner ◽  
Content Type ◽  
Aortic Endothelial Cells ◽  
Bovine Aortic Endothelial Cells ◽  
Transmission Electron ◽  
Fine Print

Object. Oxyhemoglobin (OxyHb) is one of the most important spasmogens for cerebral vasospasm that follows aneurysmal subarachnoid hemorrhage. The cytotoxic effect of OxyHb has been documented in endothelial and smooth-muscle cells; however, the pattern of cell death—necrosis or apoptosis—as the final stage of cell damage has not been demonstrated. This study was undertaken to determine if OxyHb induces apoptotic changes in cultured bovine aortic endothelial cells.Methods. Confluent bovine aortic endothelial cells were treated with OxyHb in a concentration- and time-dependent manner. Cell density was assayed by counting the number of cells that attached to culture dishes after exposure to OxyHb. To identify apoptotic changes, the investigators used three specific methods: DNA fragmentation (electrophoreses), the apoptotic body (transmission electron microscopy), and cleavage of poly (adenosine diphosphate ribose) polymerase (PARP [Western blotting]).Conclusions. Oxyhemoglobin decreased cell density in a concentration- and time-dependent manner. Analysis of DNA showed a pattern of internucleosomal cleavage characteristic of apoptosis (DNA ladder). Transmission electron microscopy demonstrated condensation of nuclei and apoptotic bodies in OxyHb-treated endothelial cells. Western blotting with the PARP antibody revealed that the 116-kD PARP was cleaved to the 85-kD apoptosis-related fragment. These results for the first time demonstrated that the OxyHb induces apoptosis in cultured endothelial cells.

Scanning electron microscope study of human arachnoid villi

1983 ◽  
Vol 59 (4) ◽  
pp. 620-626 ◽  
Author(s):  
Domenico D'Avella ◽  
Rocco Cicciarello ◽  
Francesca Albiero ◽  
Giancarlo Andrioli
Keyword(s):  
Electron Microscopy ◽  
Endothelial Cells ◽  
Cell Contact ◽  
Surgical Biopsy ◽  
Scanning Electron Microscope Study ◽  
Content Type ◽  
Arachnoid Villi ◽  
Biopsy Specimens ◽  
Fine Print ◽  
Scanning Electron

✓ The functional morphology of human arachnoid villi obtained from surgical biopsy specimens has been studied by scanning electron microscopy (SEM). On SEM examination, the villi appeared to be distended, as if functioning normally. The endothelial cells constituting the cerebrospinal fluid (CSF)-blood interface were covered by numerous microvilli, uniformly oriented along the major axis of the villus. Examination for cell-to-cell contact revealed only occasional areas of tight adherence between adjacent endothelial cells, while widened intercellular spaces were frequently observed. Generally corresponding to the apex of the villus, points of emergence of endothelium-lined hollow structures were identified; these may represent apical openings of open pathways from the subarachnoid space to the venous system. Ultrastructural arrangements consistent with a closed system of CSF reabsorption were also observed. Large cells maximally distended and protruding into the sinus lumen were commonly seen; these were interpreted as the result of the formation of giant vacuoles within the endothelium covering the villus. This study has provided ultrastructural evidence for both closed and open systems of CSF reabsorption. Ultrastructural findings, such as gaps between endothelial cells and tubule-like endothelium-lined structures as previously identified in animals and observed in man by transmission electron microscopy, were demonstrated in human biopsy specimens by SEM.

Vascular corrosion casts mirroring early morphological changes that lead to the formation of saccular cerebral aneurysm: an experimental study in rats

2005 ◽  
Vol 102 (3) ◽  
pp. 532-535 ◽  
Author(s):  
Mohammad A. Jamous ◽  
Shinji Nagahiro ◽  
Keiko T. Kitazato ◽  
Koichi Satoh ◽  
Junichiro Satomi
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Endothelial Cell ◽  
Cerebral Aneurysm ◽  
Morphological Changes ◽  
Cerebral Aneurysms ◽  
Content Type ◽  
Aneurysmal Dilation ◽  
Hemodynamic Shear Stress ◽  
Fine Print

Object. The formation of cerebral aneurysms involves complex processes and little is known about the mechanisms by which they originate, grow, and rupture. The purpose of this study was to identify early ultrastructural morphological changes that lead to the formation of experimental cerebral aneurysms. Methods. Twenty male Sprague—Dawley rats were subjected to cerebral aneurysm induction (renal hypertension and right common carotid artery ligation); 10 intact rats served as the control group. The animals were killed after 2 months, and a vascular corrosion cast of their cerebral arteries was prepared and screened for aneurysm development by using a scanning electron microscope. Sequential morphological changes observed at the cerebral artery bifurcation in response to hemodynamic shear stress included endothelial changes, intimal pad elevation, and saccular dilation. Endothelial cell changes were the first observed morphological changes; they were followed by various degrees of artery wall dilation. No aneurysmal changes developed in any of the control rats. Of the 20 surgically treated rats, 11 displayed aneurysmal changes. In five of these animals only changes in the endothelial cell imprints could be identified. In the other six rats morphological changes in endothelial cells were associated with different stages of aneurysmal dilation. Conclusions. This is the first study to demonstrate in vivo early morphological changes that lead to the formation of cerebral aneurysms. The morphological findings indicate the principal role of endothelial cells in the pathogenesis of cerebral aneurysms and suggest that hemodynamic shear stress and blood flow patterns may precipitate these early changes.

Induction of transformational changes in normal endothelial cells by cultured human astrocytoma cells

1991 ◽  
Vol 75 (4) ◽  
pp. 604-612 ◽  
Author(s):  
Daniel L. Silbergeld ◽  
Francis Ali-Osman ◽  
H. Richard Winn
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Dna Synthesis ◽  
Cell Line ◽  
Glioblastoma Cell Line ◽  
Glioblastoma Cell ◽  
Content Type ◽  
Human Glioblastoma Cell ◽  
Malignant Astrocytomas ◽  
Fine Print

✓ Endothelial cell proliferation is a significant biological feature of malignant astrocytomas. The ability of the cells of these tumors to elaborate mitogenic angiogenesis factors has been well documented. However, less is known about the transformational effects that neoplastic astrocytes may have on the endothelial cells within malignant astrocytomas. In this study, the hypothesis that humoral factors elaborated by cells derived from malignant astrocytomas induce transformational changes in normal endothelial cells in vitro is investigated. Conditioned medium (CM) was prepared from exponentially growing cultures of a human glioblastoma cell line (UW18) and from two rat brain-tumor cell lines: an anaplastic astrocytoma (R175A) and a glioblastoma with sarcomatous elements (9L). Subconfluent target bovine aortic arch endothelial cells (BAEC's) were exposed for 48 hours to varying concentrations of CM prepared from each of these tumors, and then evaluated for transformational changes. Different molecular weight (MW) fractions of UW18 CM were prepared by molecular ultrafiltration, and each fraction was tested for transforming activity. Transformation endpoints included changes in cellular deoxyribonucleic acid (DNA) and ribonucleic acid (RNA) content and distribution (measured by differential flow cytometry) and changes in de novo DNA synthesis determined by 3H-thymidine incorporation. Significant changes in the amount and distribution of DNA and RNA were observed in the BAEC's treated with UW18 CM compared to untreated BAEC's. At 10% concentrations of UW18 CM, changes in the RNA profile of target BAEC's were evident, and at 30% concentrations of UW18 CM, an irregular bimodal distribution was well established. Patterns of DNA were also altered in a concentration-dependent manner, with significant aneuploidy developing at UW18 CM concentrations of 20%. The DNA synthesis in BAEC's increased with increasing CM concentrations, up to a maximum of about 250% of control values at 30% concentrations of UW18 CM. The transformational changes induced after exposure of BAEC's to CM prepared from R175A and 9L were significantly less than those observed with UW18 CM. Molecular ultrafiltration was used to prepare UW18 CM fractions with MW cutoffs of less than 10 kD, 10 to 30 kD, and greater than 30 kD. Transformational activity was significant only in CM's with an MW of 10 to 30 kD. It is concluded that the UW18 human glioblastoma cell line elaborates a soluble factor, or group of factors, with an MW in the 10- to 30-kD range, capable of inducing transformational alterations in target normal endothelial cells, and that such transformation may account for some of the abnormal endothelial cell changes associated with malignant astrocytomas.

scholarly journals Two Strikingly Different Signaling Pathways Are Induced by Meningococcal Type IV Pili on Endothelial and Epithelial Cells

2011 ◽  
Vol 80 (1) ◽  
pp. 175-186 ◽  
Author(s):  
Hervé Lécuyer ◽  
Xavier Nassif ◽  
Mathieu Coureuil
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Epithelial Cells ◽  
Signaling Pathways ◽  
Cell Response ◽  
Adrenergic Receptor ◽  
Type Iv Pili ◽  
Cell Junctions ◽  
Content Type ◽  
Type Iv

ABSTRACTFollowing adhesion on brain microvasculature,Neisseria meningitidisis able to cross the blood-brain barrier (BBB) by recruiting the polarity complex and the cell junction proteins, thus allowing the opening of the paracellular route. This feature is the consequence of the activation by the type IV pili of the β2-adrenergic receptor/β-arrestin signaling pathway. Here, we have extended this observation to primary peripheral endothelial cells, and we report that the interaction ofN. meningitidiswith the epithelium is strikingly different. The recruitment of the junctional components byN. meningitidisis indeed restricted to endothelial cell lines, and no alteration of the cell-cell junctions can be seen in epithelial monolayers following meningococcal type IV pilus-mediated colonization. Consistently, the β2-adrenergic receptor/β-arrestin pathway was not hijacked by bacteria adhering on epithelial cells. In addition, we showed that the consequences of the bacterial signaling on epithelial cells is different from that of endothelial cells, sinceN. meningitidis-induced signaling which protects the microcolonies from shear stress on endothelial cells is unable to do so on epithelial cells. Finally, we report that the minor pilin PilV, which has been shown to be essential for endothelial cell response, is not a required bacterial determinant to induce an epithelial cell response. These data demonstrate that even though pilus-mediated signaling induces an apparently similar cortical plaque, in epithelial and endothelial cell lineages, the signaling pathways are strikingly different in both models.

A new rat model of chronic cerebral hypoperfusion associated with arteriovenous malformations

2002 ◽  
Vol 97 (5) ◽  
pp. 1198-1202 ◽  
Author(s):  
Jian Hai ◽  
Meixiu Ding ◽  
Zhilin Guo ◽  
Bingyu Wang
Keyword(s):  
Electron Microscopy ◽  
Animal Model ◽  
Arteriovenous Malformations ◽  
Perfusion Pressure ◽  
Chronic Cerebral Hypoperfusion ◽  
Cerebral Hypoperfusion ◽  
Model Group ◽  
Content Type ◽  
The Right ◽  
Fine Print

Object. A new experimental model of chronic cerebral hypoperfusion was developed to study the effects of systemic arterial shunting and obstruction of the primary vessel that drains intracranial venous blood on cerebral perfusion pressure (CPP), as well as cerebral pathological changes during restoration of normal perfusion pressure. Methods. Twenty-four Sprague—Dawley rats were randomly assigned to either a sham-operated group, an arteriovenous fistula (AVF) group, or a model group (eight rats each). The animal model was readied by creating a fistula through an end-to-side anastomosis between the right distal external jugular vein (EJV) and the ispilateral common carotid artery (CCA), followed by ligation of the left vein draining the transverse sinus and bilateral external carotid arteries. Systemic mean arterial pressure (MAP), draining vein pressure (DVP), and CPP were monitored and compared among the three groups preoperatively, immediately postoperatively, and again 90 days later. Following occlusion of the fistula after a 90-day interval, blood—brain barrier (BBB) disruption and water content in the right cortical tissues of the middle cerebral artery territory were confirmed and also quantified with transmission electron microscopy. Formation of a fistula resulted in significant decreases in MAP and CPP, and a significant increase in DVP in the AVF and model groups. Ninety days later, there were still significant increases in DVP and decreases in CPP in the model group compared with the other groups (p < 0.05). Damage to the BBB and brain edema were noted in animals in the model group during restoration of normal perfusion pressure by occlusion of the fistula. Electron microscopy studies revealed cerebral vasogenic edema and/or hemorrhage in various amounts, which correlated with absent astrocytic foot processes surrounding some cerebral capillaries. Conclusions. The results demonstrated that an end-to-side anastomosis between the distal EJV and CCA can induce a decrease in CPP, whereas a further chronic state of cerebral hypoperfusion may be caused by venous outflow restriction, which is associated with perfusion pressure breakthrough. This animal model conforms to the basic hemodynamic characteristics of human cerebral arteriovenous malformations.

Hemangiopericytoma of the spinal canal

1978 ◽  
Vol 49 (6) ◽  
pp. 914-920 ◽  
Author(s):  
Darrell J. Harris ◽  
Victor L. Fornasier ◽  
Kenneth E. Livingston
Keyword(s):  
Endothelial Cells ◽  
Differential Diagnosis ◽  
High Risk ◽  
Spinal Canal ◽  
Vertebral Column ◽  
Soft Tissues ◽  
Surgical Removal ◽  
Vascular Neoplasm ◽  
Content Type ◽  
Fine Print

✓ Hemangiopericytoma is a vascular neoplasm consisting of capillaries outlined by an intact basement membrane that separates the endothelial cells of the capillaries from the spindle-shaped tumor cells in the extravascular area. These neoplasms are found in soft tissues but have rarely been shown to involve the spinal canal. This is a report of three such cases. Surgical removal of the tumor from the spinal canal was technically difficult. A high risk of recurrence has been reported but in these three cases adjunctive radiotherapy appeared to be of benefit in controlling the progression of the disease. These cases, added to the six cases in the literature, confirm the existence of hemangiopericytoma involving the vertebral column with extension into the spinal canal. This entity should be included in the differential diagnosis of lesions of the spinal canal. The risk of intraoperative hemorrhage should be anticipated.

Neoplastic and pharmacological influence on the permeability of an in vitro blood-brain barrier

1995 ◽  
Vol 82 (6) ◽  
pp. 1053-1058 ◽  
Author(s):  
Paul A. Grabb ◽  
Mark R. Gilbert
Keyword(s):  
Endothelial Cell ◽  
Rat Brain ◽  
Phospholipase A ◽  
Cell Permeability ◽  
Capillary Endothelium ◽  
Brain Capillary ◽  
Content Type ◽  
Endothelial Cell Permeability ◽  
Fine Print

✓ The authors investigated the effects of glioma cells and pharmacological agents on the permeability of an in vitro blood-brain barrier (BBB) to determine the following: 1) whether malignant glia increase endothelial cell permeability; 2) how glucocorticoids affect endothelial cell permeability in the presence and absence of malignant glia; and 3) whether inhibiting phospholipase A2, the enzyme that releases arachidonic acid from membrane phospholipids, would reduce any malignant glioma—induced increase in endothelial cell permeability. Primary cultures of rat brain capillary endothelium were grown on porous membranes; below the membrane, C6, 9L rat glioma, T98G human glioblastoma, or no cells (control) were cocultured. Dexamethasone (0.1 µM), bromophenacyl bromide (1.0 µM), a phospholipase A2 inhibitor, or nothing was added to culture media 72 hours prior to assaying the rat brain capillary endothelium permeability. Permeability was measured as the flux of radiolabeled sucrose across the rat brain capillary endothelium monolayer and then calculated as an effective permeability coefficient (Pe). When neither dexamethasone nor bromophenacyl bromide was present, C6 cells reduced the Pe significantly (p < 0.05), whereas 9L and T98G cells increased Pe significantly (p < 0.05) relative to rat brain capillary endothelium only (control). Dexamethasone reduced Pe significantly for all cell preparations (p < 0.05). The 9L and T98G cell preparations coincubated with dexamethasone had the lowest Pe of all cell preparations. The Pe was not affected in any cell preparation by coincubation with bromophenacyl bromide (p > 0.45). These in vitro BBB experiments showed that: 1) malignant glia, such as 9L and T98G cells, increase Pe whereas C6 cells probably provide an astrocytic influence by reducing Pe; 2) dexamethasone provided significant BBB “tightening” effects both in the presence and absence of glioma cells; 3) the in vivo BBB is actively made more permeable by malignant glia and not simply because of a lack of astrocytic induction; 4) tumor or endothelial phospholipase A2 activity is probably not responsible for glioma-induced increased in BBB permeability; and 5) this model is useful for testing potential agents for BBB protection and for studying the pathophysiology of tumor-induced BBB disruption.

Estrogen and progestin binding by cytosolic and nuclear fractions of human meningiomas

1985 ◽  
Vol 62 (5) ◽  
pp. 750-756 ◽  
Author(s):  
Robert L. Martuza ◽  
Douglas C. Miller ◽  
David T. MacLaughlin
Keyword(s):  
Control Mechanism ◽  
Hormonal Control ◽  
Binding Assays ◽  
Tissue Samples ◽  
Content Type ◽  
Cellular Density ◽  
Equilibrium Binding ◽  
Frozen Tissue ◽  
Human Meningiomas ◽  
Fine Print

✓ Frozen tissue samples were obtained from meningiomas in 42 patients. Both cytosolic and nuclear fractions were tested for estradiol and progestin binding using equilibrium binding assays. The results were correlated with the age of the patient and the histological type and cellular density of the tumor. Cytosolic estradiol binding was noted in 25 (60%) of 42 tumors, with eight (19%) of the 42 having levels over 10 femtomoles (fM)/mg protein. Nuclear estradiol binding was detected in 16 (57%) of 28 tumors, with six (21%) of the 28 having levels over 10 fM/mg protein. Cytosolic progestin binding was noted in 16 (73%) of 22 samples, with levels in nine (41%) of 22 being greater than 10 fM/mg protein. There was no correlation between the level of cytoplasmic progestin binding and either the level of cytoplasmic estradiol binding or the level of nuclear estradiol binding. In several specimens, levels of cytoplasmic progestin binding in excess of 100 fM/mg protein were found in tissues demonstrating little or no estradiol binding by either the nucleus or the cytosol. This discrepancy differs from the situation found in other hormonally responsive tissues such as breast or uterus, and suggests either a possible derangement of the normal cellular hormonal control mechanism or that the measured hormone binder is a molecule other than a classical hormone receptor.

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