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At least 703 records · Page 39Linked to original sources

PubMed2004

Angiotensin II AT1 receptor antagonism downregulates stress-related gene expression in brain microvessels from spontaneously hypertensive and normotensive rats.

We studied the effect of treatment with the Angiotensin II AT(1) receptor antagonist candesartan (0.3 mg/kg/day via osmotic minipumps for 4 weeks compared with administration of vehicle) in brain microvessels in adult spontaneously hypertensive rats (SHR) that were vulnerable to stroke and normotensive control rats (WKY). At the dose administered, candesartan normalized blood pressure in SHR without significantly affecting blood pressure in WKY rats. We performed the gene expression analysis in rat brain microvessels using the Affymetrix Gene Chip Expression Analysis Technique. From a total of 8,799 probe array sets analyzed, we found abundant abnormalities in gene expression in SHR. Because stress has been suggested as a precipitant factor in brain ischemia and treatment with AT(1) receptor antagonist candesartan prevents the hormonal and sympathoadrenal reaction to isolation stress and protects from stress-induced gastric ulcers, we focused on the expression of stress-related genes. We found a higher number of probe array sets modified by candesartan treatment in normotensive WKY rats than in hypertensive SHR. AT(1) receptor blockade decreased the transcription levels of the stress-related tyrosine kinase receptor, stathmin, and fibroblast growth receptor genes in WKY and SHR rats. Our results indicate that Angiotensin II and its AT(1) receptors can influence gene expression independently of the effects on blood pressure. In addition, AT(1) receptor regulation of stress-related genes in brain microvessels may explain the proposed association between stress and ischemic disorders of the brain.

Angiotensin II↗

PubMed1984

Identification and characterization of the insulin receptor of bovine retinal microvessels.

The presence of specific, high affinity receptors for insulin has been demonstrated in purified preparations of bovine retinal microvessels. The binding of [125I]insulin to isolated retinal microvessels was inhibited by unlabeled insulin, but not by other peptide hormones. Scatchard analysis of the [125I]insulin binding data gave a curvilinear plot similar to that exhibited by insulin receptors in known insulin-sensitive tissues such as adipocytes and hepatocytes. Binding of [125I]insulin to retinal microvessels, followed by covalent cross-linking of the bound ligand to the alpha-subunit of the insulin receptor with the bifunctional reagent disuccinimidyl suberate, yielded a prominent specific [125I]insulin-labeled band when analyzed by sodium dodecyl sulfate-gel electrophoresis followed by autoradiography, and this band had a mobility identical to that of the corresponding complex obtained with rat liver plasma membranes (mol wt, 125,000). These results demonstrate for the first time that the retinal microvasculature, a major site of pathological injury in diabetes mellitus, contains insulin receptors that are similar to those present in known insulin-sensitive tissues, such as liver, fat, and muscle.

Animals↗

PubMed1987

Abnormalities of endoneurial microvessels and sural nerve pathology in diabetic neuropathy.

We measured the cellular components of 290 endoneurial microvessels in sural nerve of 34 diabetics and of 185 microvessels from 23 healthy subjects. Numbers of endothelial nuclei, area of endothelium, and thickness of basement membrane were significantly greater in diabetics with neuropathy than in controls and were statistically associated with severity of neuropathologic abnormality of myelinated fibers. The range of lumen areas was greater in diabetics than in controls, suggesting capillary dilatation of some vessels. Microvessels had pericytic debris in 8.5% of vessels from diabetics and none in controls.

Adult↗

PubMed2000

Heterogeneous distribution of thrombomodulin and von Willebrand factor in endothelial cells in the human pulmonary microvessels.

Laser scanning confocal fluorescence microscopy techniques were used to study the localization of von Willebrand factor (vWf; Factor VIII-related antigen) and thrombomodulin (transmembrane receptor for thrombin) in the microvascular endothelial cells in the normal human lung. Tissues were obtained from lobectomy specimens resected for solitary nodules (7 adenocarcinomas and 4 hamartomas) from 11 patients. The plasma membranes of the capillary endothelial cells in the alveolar zones (A-zones) showed red linear fluorescence for thrombomodulin. However, their cytoplasm was mostly unreactive for vWf. The microvessels which were located in the connective tissue (C-zones), including peribronchial, and subpleural areas and large vascular walls, consistently demonstrated band-like green fluorescence for vWf in their cytoplasm, and their plasma membranes usually lacked reactivity for thrombomodulin. Only a limited number of peribronchial capillaries measuring <10 microm in diameter showed a mosaic-like appearance, in which red fluorescence along the plasma membranes was found together with green fluorescence in the subjacent cytoplasm. In the juxtaalveolar (J-zones) microvessels located along the borders between A- and C-zones, and measuring up to 40 microm in diameter, the endothelial cells showed a mosaic-like pattern of distribution of the two antigens. However, the localization of thrombomodulin in the J-zone microvessels was separate and independent from that of vWf. The thrombomodulin-reactive cells were directly connected to the alveolar capillary endothelial cells. Heterogeneous patterns of distribution of thrombomodulin and vWf suggest that topographic differences of endothelial function occur to maintain a balance of coagulation and anticoagulation in the normal human lung.

Adult↗

PubMed2005

Demonstration of microvessel networks and endothelial cell phenotypes in the normal murine lung.

The vascular endothelial cells (ECs) express various antigens related to coagulation factors, including factor VIII-related antigen or von Willebrand factor (vWF) in the cytoplasm and thrombomodulin (TM; a thrombin receptor)along the plasma membrane. CD34 (a hematogenic stem cell marker) is also expressed along the surface membrane of the ECs. Using these EC markers and fluorescein-isothiocyanate-labeled dextran (FITC-dextran)(Sigma Co., St. Louis, MO), we attempted to demonstrate the complex network of microvessels and their EC phenotypes in tracheo-bronchial trees and lung parenchyma of the normal adult ICR male mice. Under anesthesia, saline with heparin was infused slowly through left ventricle to drain off the blood. Following brief fixation with 4% buffered paraformaldehyde solution (PFA) through the same route, one group of animals received, 1) FITC-dextran injection via left ventricle, and the large airways and lungs were further fixed in PFA, or 2) The airways and lungs of the other group were rapidly frozen, and the thin sections were stained with two antibodies of vWF and Alexa Fluor 594-labeled CD34. The vWF antibody was later labeled by FITC. The microvessels of airways and lungs were observed by a laser scanning confocal microscope (TC-SP, Leica, Heidelberg, Germany). The phenotypic characteristics of microvessel ECs appeared mostly identical with those described previously in the human lung, although CD34 was applied instead of TM in the present study. The topographical heterogeneity of immunohistochemical properties of ECs would suggest functional differences at different sites of the lung, that would provide a novel insight for understanding the pathogenesis of human lung diseases.

Animals↗

PubMed2006

Study of microvessel density and the expression of the angiogenic factors VEGF, bFGF and the receptors Flt-1 and FLK-1 in benign, premalignant and malignant prostate tissues.

PURPOSE: Vascular endothelial growth factor (VEGF) is an angiogenic factor that stimulates endothelial cell growth and enhances vascular permeability. VEGF exerts its action by binding to the specific cell surface receptors, fms-like tyrosine kinase 1 (Flt-1) and fetal liver kinase 1 (FLK/KDR). In tumor angiogenesis, Vascular endothelial growth factor stimulates endothelial cells to produce Basic fibroblastic growth factor (bFGF), which further enhances angiogenic activity. Very little information on the expression of VEGF, bFGF, and the receptors Flt-1 and FLK/KDR is available. Herein, we evaluate the expression of these angiogenic factors and receptors in normal prostate, high grade prostate intraepithelial neoplasia (HGPIN) and prostatic cancer (CaP). MATERIALS AND METHODS: 58 selected surgical specimens exhibiting areas of normal prostate, HGPIN, and CaP were evaluated for microvessel density, and for VEGF, bFGF, Flt-1 and FLK/KDR protein expression by immunohistochemistry. Results were correlated with pathological data. RESULTS: There was a statistically significant increase in the microvessel density and in the expression of the angiogenic factors VEGF, bFGF and the receptors FLK/KDR and Flt-1, in the premalignant and malignant tissues in comparison with normal prostatic glands. Microvessel density also correlated with higher Gleason grade, pathological stage and the expression of the receptors FLK/KDR and Flt-1. CONCLUSIONS: The "initiation switch" of angiogenesis was observed to be an early event consistent with the recruitment of new vasculature into high grade PIN lesions and it increased in the progression of prostatic cancer.

Adenocarcinoma↗

PubMed1983

Effect of pantethine on fatty acid oxidation in microvessels of rat brain.

Fatty acid oxidation in brain microvessels decreased greatly when persistent hypertension developed in spontaneously hypertensive rats (SHR). Treatment of SHR with pantethine [D-bis-(N-pantothenyl-beta-aminoethyl) disulfide] in vivo for 4 weeks restored their fatty acid oxidation activity to the control level. The mechanism of the activating effect of pantethine on fatty acid oxidation was investigated in brain microvessels. Pantethine and its metabolites (pantetheine and 4'-phosphopantetheine) activated three steps of fatty acid oxidation, i.e., acyl-CoA synthetase, carnitine acyltransferase and intramitochondrial oxidation. The relation between changes in fatty acid oxidation activities and injuries of brain microvessels and the protective effect of pantethine against such injuries is discussed.

Animals↗

PubMed1993

Microscopic laser Doppler velocimeter measuring blood velocity in single microvessel.

A microscopic laser Doppler velocimeter to measure blood velocity in single microvessels was developed. In order to measure the blood velocity in microvessels correctly, the influence of stray scattered light from vessel wall should be removed. Because it provokes low-frequency spurious components. The spectra of the spurious components overlap with that of Doppler signal and induces considerable error in the result of the blood velocity when the velocity is reduced. The optical configuration of the velocimeter was optimized to eliminate the influence of the stray scattered light. The blood velocity in microvessels in rat mesentery was measured with the microscopic laser Doppler velocimeter and the periodical fluctuation of the velocity was analyzed. Pulsatile velocity fluctuation could be observed even in capillary.

Animals↗

PubMed1996

Human brain microvessel endothelial cell culture as a model system to study vascular factors of ischemic brain.

Cerebral ischemia is caused by reduced blood supply at the microcirculatory level. In the microvessels, the main elements of the reperfusion injury following brain ischemia are the transformation of endothelial cell-surface from anticoagulant to procoagulant property, leukocyte adhesion, sludge or clot formation. There is a paucity of information on how hemostatic factors, cytokines, lipoprotein(a) (Lp(a)) and endothelin-1 (ET-1), being responsible for ischemic/reperfusion injury, interact with human brain microvessel endothelium (HBEC). There are no data furthermore about the expression of complement proteins of HBEC influenced by cytokines or fibrinolytic factors. Previously we established optimal conditions for culturing HBEC. Cell contraction induced by thrombin, plasmin, miniplasmin was recorded. The reassembly of F-actin was observed after thrombin treatment. ICAM-1 upregulation was measured following TNF-alpha, IL-1-alpha and thrombin incubation. Plasmin and miniplasmin downregulated the ICAM-1 in our cell culture system. Lp(a) modulated the thromboresistant cell-surface by reduction of t-PA and u-PA, but PAI-1 remained unchanged. Lp(a) modulated the ET-1 production by early increasing and late decreasing, in a bimodal manner. The increased secretion of ET-1 by cytokines (TNF-alpha, IL-1-alpha) was reduced in the presence of Lp(a). Gradual increase of complement proteins (factor H, factor B, C4) was induced by cytokines. Plasmin and miniplasmin augmented a rapid increase of C4. Some factors of complex relationship between regulators and modulators of endothelial adhesion molecules have been demonstrated in a human cell culture system prepared from brain microvessel endothelium. A unified concept of sequential events of ischemia/reperfusion in the brain has not yet developed.

Biological Factors↗

PubMed1985

Insulin stimulates DNA synthesis in cerebral microvessel endothelium and smooth muscle.

Experiments were performed to test the hypothesis that insulin stimulates DNA synthesis in cerebral microvessel endothelium and smooth muscle. Cultured endothelium and smooth muscle derived from isolated mouse cerebral microvessels were exposed to insulin in serum-free medium, and [3H]-thymidine incorporation in the cells was measured. Up to 40-fold stimulation of DNA synthesis in endothelium and fourfold stimulation in smooth muscle were observed. Stimulation became maximal in both cell types at an insulin concentration of approximately 10(4) ng/ml, although an effect was observed at much lower concentrations. Similar concentrations of insulin produced a less-dramatic (approximately twofold) increase in both endothelial and smooth muscle cell numbers. This effect of insulin, observed in microvessel endothelium and smooth muscle, but not in bovine aortic endothelium, emphasizes another way in which large- and small-vessel endothelia appear to differ.

Animals↗

PubMed1995

Status of antioxidants in brain microvessels of monkey and rat.

Levels of certain antioxidants namely reduced glutathione (GSH), ascorbic acid (Vit C), alpha-tocopherol (Vit E) and antioxidant enzymes, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GR) were compared in monkey and rat brain microvessels which constitute the blood-brain barrier (BBB). The BBB of both the species contains appreciable amounts of the antioxidants to protect against oxidative damage. The level of protection in rat seems to be more efficient than monkey since rat microvessels contain higher concentrations of some of the bio-antioxidants. The comparative status of enzymatic and non-enzymatic protective system against oxidation in the brain microvessels has been discussed.

Animals↗

PubMed1997

A semiautomatic procedure for edge detection of in vivo pulmonary microvessels and interstitial space.

OBJECTIVE: To develop an algorithm to detect the edges between lung tissue, perivascular interstitium, and microvessel using digital processing of in vivo microscopic images of lung surface. METHODS: A numerical technique was developed to identify three different regions (namely, pulmonary microvessel, perivascular interstitium, and lung tissue) based on their corresponding gray level distributions. We present a theoretical demonstration of the method and a semiautomatic procedure that, once the edges are detected, determines microvascular diameters and perivascular interstitium thickness. RESULTS: Microvessel diameters and perivascular interstitium thickness were calculated for precapillary arteriolar branching (40 to 140 microns) and saved in an ASCII file. CONCLUSIONS: We proved that the maximum value of the moving variance is useful to detect the edge between two adjacent regions whose gray level distributions satisfy the condition: magnitude of sigma Y2 - sigma X2 < or = (mu X - mu Y)2, where mu X, mu Y, sigma X2, sigma Y2 are the statistical moments of the two regions X and Y. Moreover, when the regions have similar means, the above conditions is not met, but the edge between them can be detected by the maximum of the moving variance error.

Algorithms↗

PubMed1997

Estimated functional diameter of alveolar septal microvessels at the zone I-II border.

OBJECTIVE: To measure the functional diameter of alveolar septal microvessels under conditions in which the pulmonary arterial pressure and the lung inflation pressure are equal, at 25 cm H2O (zone I-II border), and to compare these results with those obtained when inflation pressure exceeded arterial pressure by 5 or 10 cm H2O (zone l). METHODS: We perfused isolated rat lungs (PA 25, PPA 25, PLA 0 cm H2O) with fluorescent latex particles of specific diameters (0.49, 1.05, 2.0, 4.0, or 10 microns) and then prepared samples for histology. Using a confocal, laser-scanning fluorescence microscope, we measured latex particle densities within the septal plane of individual alveoli. We compared these particle densities with those in arterioles supplying the septa and calculated the density ratio. We fit curves produced by the Verniory equation to these ratios to estimate the septal microvessel functional diameter. RESULTS: Particle densities in septa ranged from 0.06 +/- 0.02 particles per microns2 for 0.49-micron-diameter particles to 0.007 +/- 0.004 particles per microns2 for 4.0-microns-diameter particles. The 10-microns particles did not enter septa. Calculations based on these data suggest a septal microvessel functional diameter of 6-8 microns. CONCLUSIONS: In a previous study, conducted at the same value of Pinflat, but with PPA set at 15 or 20 (5 or 10 cm H2O into zone I). We estimated the capillary diameter to be 1.7 microns. Thus, the septal capillary diameter seems to increase by three- to fourfold as PPA is raised to equal Pinflat.

Animals↗

PubMed2006

Thrombin and inflammatory proteins are elevated in Alzheimer's disease microvessels: implications for disease pathogenesis.

The notion that microvascular abnormalities contribute to deleterious changes in the Alzheimer's disease (AD) brain is supported by work from our laboratory and others demonstrating biochemical and functional alterations of the microcirculation in AD. The objective of this study is to determine whether levels of neurotoxic (thrombin) and inflammatory (interleukin 8 (IL-8), integrins alphaVbeta3 and alphaVbeta5) proteins are altered in microvessels isolated from AD patients compared to levels in vessels obtained from non-demented age-matched controls. We also evaluate in AD and control microvessels expression of the transcription factor hypoxia-inducible factor 1-alpha(HIF1-alpha), which regulates pro-inflammatory gene expression, and the regulation of HIF1-alpha expression by thrombin in cultured brain endothelial cells. Our results indicate that in AD there are high levels of expression of the neurotoxic protease thrombin and the inflammation-associated proteins IL-8 and alphaVbeta3 and alphaVbeta5 integrins. HIF1-alpha is higher in AD microvessels compared to control and thrombin treatment of cultured brain endothelial cells results in increased expression of HIF1-alpha. These data suggest that in AD the cerebral microcirculation is a source of neurotoxic and inflammatory mediators and as such contributory to pathologic processes ongoing in the AD brain.

Aged↗

PubMed2002

Clinical prognostic values of vascular endothelial growth factor, microvessel density,and p53 expression in esophageal carcinomas.

Vascular endothelial growth factor (VEGF) is known to play a key role in tumor angiogenesis. The tumor-suppressor gene p53 has been thought to regulate VEGF. We investigated the effect of VEGF on esophageal carcinoma and the correlation between VEGF and p53. Tissue samples were taken from 81 patients with esophageal carcinoma after surgery. VEGF and p53 expressions were examined by immunohistochemical staining. Microvessels in the tumor stained for CD34 antigen were also counted. VEGF and p53 expressions were observed in 51.3% (41/80) and 51.9% (41/79), respectively. The microvessel density was 70.9+/-6.7 (mean+/-SE) in VEGF-positive group and 68.7+/-5.1 in VEGF-negative group. However, no correlation was noted between VEGF and p53 expression. Whereas the tumor size, nodal status, depth of invasions, and tumor stage were associated with poor overall survival, VEGF expression or p53 expression was not. These results indicate that VEGF and p53 are highly expressed in esophageal carcinomas. Since the VEGF expression is not correlated with the p53 expression, microvessel density or clinicopathological findings, further studies with other angiogenic molecules are needed to determine the role in esophageal carcinomas.

Adult↗

PubMed1998

Prognostic value of tumor cell proliferation and intratumor microvessel density in advanced gastric cancer treated with curative surgery.

To clarify the prognostic value of tumor cell proliferation [proliferating cell nuclear antigen (PCNA)-positive rate assessed by anti-PCNA immunostaining] and intratumor microvessel density (/0.74 mm2, assessed by anti-CD34 immunostaining) in gastric cancer, 192 advanced gastric cancer patients who underwent curative surgery were investigated. Multivariate analysis showed that the following variables were significantly related to prognosis: age (P=0.029), depth of invasion (P=0.005), lymph node metastasis (P=0.006), lymphatic invasion (P=0.038), venous invasion (P=0.0005), PCNA-positive rate (P=0.049) and intratumor microvessel density (P=0. 011). In conclusion, tumor cell proliferation and intratumor microvessel density were independent prognostic factors in patients with advanced gastric cancer undergoing curative surgery.

Adult↗

PubMed1996

[Microvessel count and vascular endothelial growth factor in renal cell carcinoma].

BACKGROUND: Angiogenesis plays an important role in the growth of solid tumors. The objective of this study is to investigate the relationship between microvessel density and mRNA measurement for vascular endothelial growth factor (VEGF) as well as the kinase domain receptor (KDR) in renal cell carcinoma (RCC). METHODS: From 1992 to 1994, expression of mRNAs of VEFG, KDR and microvessel count by Factor VIII immunohistochemical staining were examined in 22 cases of RCC. RESULTS: Northern blot hybridization demonstrated that 18 tumors (82%) expressed a higher level of VEGF gene than corresponding normal renal tissues (T/N > 1) and that the expression of VEGF gene in the tumors correlated well with that of KDR gene (r = 0.780, p = 0.001). Most of the tumor cells positively reacted to immunohistochemical staining for VEGF, but all of the normal renal tissue elements did not. RT-PCR analysis revealed that mRNAs of VEGF expressed in the tumors were of soluble subclasses. The mean number of microvessels (< 50 micrometers in diameter) in the tumors was 62.7 +/- 39.1/mm2 (range 13.7-133.1) and significantly correlated with the expression of VEGF gene (r = 0.636, p = 0.001). CONCLUSIONS: The results indicate that RCC cells actively produce soluble VEGF and strongly suggest that VEGF and its receptor KDR cooperate to enhance the angiogenesis of this tumor.

Adult↗

PubMed1999

Investigation of microvessel density after irradiation.

It is believed that malignant cell populations need the development of microvessels to grow and metastasize. The aim of our investigation was to find out whether gamma irradiation can affect proliferation of endothelial cells and thus can affect microvessel density in vivo. We used fertilized chicken eggs. The vascularized part of the yolk sac membrane (area vasculosa) of the eggs received single doses of 2 to 10 Gy. Forty-eight hours after irradiation, the area vasculosa was photographed in vivo, and prints of known magnification were evaluated to determine the density of the blood vessels. Microvessel count is the well-established marker used to determine vascular density. In addition, the proliferative activity of endothelial cells in the yolk sac membrane was determined by estimating the expression of proliferating cell nuclear antigen (PCNA). PCNA immunostaining was assessed immunohistochemically. After a single dose of 10 Gy, a statistically significant increase in vascular density was found compared to values determined at 0, 2, 4 and 8 Gy (P < 0.05). Twenty-four hours after 10 Gy irradiation, 44.8% (mean) of the endothelial cells were PCNA-positive. This was significantly higher (P < 0.05) compared to the results 24 h after 4.0 Gy (22.7%) and compared to control (19.4%). Twenty-four hours later, i.e. 48 h after irradiation with 10 Gy, the endothelial cells also showed a significantly (P < 0.05) higher PCNA positivity with a mean of 34.1% compared to the nonirradiated area vasculosa (18.1%) and compared to the results after 4.0 Gy irradiation (12.0%). The prerequisite for blood vessel formation is the proliferation of endothelial cells. Thus a single-dose irradiation with 10 Gy induces endothelial cell proliferation and subsequent neovascularization in the area vasculosa of the fertilized egg.

Animals↗