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Results for “Microvessels”

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PubMed1998

Relationship among cystectomy, microvessel density and prognosis in stage T1 transitional cell carcinoma of the bladder.

PURPOSE: The selection of therapy for stage T1 bladder cancer is controversial, and reliable biomarkers that identify patients likely to require cystectomy for local disease control have not been established. We evaluated our experience with T1 bladder cancer to determine whether early cystectomy improves prognosis, and whether microvessel density has prognostic value for T1 lesions and could be used for patient selection. MATERIALS AND METHODS: We retrospectively reviewed the records of 88 patients with T1 transitional cell carcinoma of the bladder. Patient outcome was correlated with therapeutic intervention. Paraffin embedded tissue from 54 patients was available for factor VIII immunohistochemical staining for microvessel density quantification. RESULTS: Median followup was 48 months (range 12 to 239). Of the patients 34% had no tumor recurrence. The rates of recurrence only and progression to higher stage disease were 41 and 25%, respectively. The survival of patients in whom disease progressed was diminished (p = 0.0002). Grade did not predict recurrence or progression nor did cystectomy provide a survival advantage. Microvessel density did not correlate with recurrence or progression. CONCLUSIONS: Patients with T1 bladder cancer have a high risk of recurrence and progression. Tumor progression has a significant negative impact on survival. Neither grade nor early tumor recurrence predicted disease progression. Because early cystectomy did not improve patient outcome, we suggest reserving cystectomy for patients with progression or disease refractory to local therapy. Microvessel density is not a prognostic marker for T1 bladder cancer and has no value in selecting patients with T1 disease for cystectomy.

Capillaries↗

PubMed1997

[Influence of reperfusion following ischemia on microvessels and microcirculation of skeletal muscle].

In order to study the influence of reperfusion following ischemia on microvesseles and microcirculation of skeletal muscle, unilateral hindlimbs of 16 rabbits were subjected to normothermic ischemia for 2 and 5 hours by tourniquet. After release of the tourniquet, microcirculation of the peritenon on dorsum of the foot was observed for 1 hours by intravital microscope. At 1 hour and 72 hours following reperfusion, the anterior tibia muscle biopsiy were taken and the specimens were subjected to light and electron microscopic examinations. It was found that after release of the tourniquet, in the limbs undergone 2 hours ischemia, there was immediate and well distributed reflow in the microvesseles of peritenon though a few aggregates of red cells and increase in the number of adherent leukocytes occured in some venules, and the microvesseles of the skeletal muscle only showed signs of minimal injury, the muscle fibers could survive in the limbs undergone 5 hours of ischemia, however, there was serious disturbance of microcirculation in the peritenon, which was characterized by "no reflow" in most area and there was significant increase in the number of leukocytes adherent to venular endothelium, and the microvesseles of the skeletal muscle showed signs of severe injury, including remarkable swelling of the endothelial cell, disruption of the basement membrane and interstitial edema, and finally, most of the muscle fibers had necrosis occured. The results demonstrated that reperfusion following ischimia might result in microvascular injury and microcirculation disorder in the ischemic area. The degree of the injury and disorder depended on the duration of ischemic period, and was an important factor which determined the fate of the parenchymal cell.

Animals↗

PubMed1999

VEGF, VEGFR-1, VEGFR-2, microvessel density and endothelial cell proliferation in tumours of the ovary.

VEGF is an angiogenic factor with potent endothelial cell (EC) proliferative actions. Our aim was to investigate whether expression of VEGF and its receptors and EC proliferation differ between ovarian tumour types and regions of the vasculature. VEGF, VEGFR-1, VEGFR-2 and EC proliferation were examined immuno-histochemically, and in situ hybridisation (ISH) studies of VEGF mRNA expression were performed and assessed in regions of high (HVD) and average (AVD) vessel density. VEGF immunostaining was significantly stronger in HVD regions of malignant compared with borderline serous tumours. VEGF immunostaining did not differ between tumour types; however, the percentage of VEGFR-1- and VEGFR-2-positive vessels was significantly lower in mucinous tumours. No differences were observed between HVD and AVD regions. VEGF ISH signal was observed in 2/7 borderline mucinous tumours, 8/14 malignant serous tumours and 5/13 benign tumours. The EC proliferation index was significantly lower in the HVD regions of serous relative to benign tumours. A negative correlation between VEGFR-1 immunostaining and microvessel density was observed in benign and serous tumours. However, EC proliferation index and VEGFR-1 positivity were positively correlated in benign tumours. Our results suggest that VEGF may play a role in the control of angiogenesis in serous and benign tumours but it does not appear to contribute to the previously reported higher microvessel density in mucinous tumours or to influence heterogeneity of microvessel density in ovarian tumours.

Adenocarcinoma, Mucinous↗

PubMed2002

Encephalitogenic T cells use LFA-1 for transendothelial migration but not during capture and initial adhesion strengthening in healthy spinal cord microvessels in vivo.

LFA-1 on the surface of encephalitogenic T cells has been suggested to be involved in the pathogenesis of experimental autoimmune encephalomyelitis. By applying a novel technique of intravital fluorescence microscopy that enables us to visualize the interaction of circulating encephalitogenic T lymphoblasts within the healthy spinal cord white matter microvasculature in vivo, we investigated the possible involvement of LFA-1 on circulating encephalitogenic T cells in their multi-step interaction with the blood-brain barrier endothelium in vivo. LFA-1 was found to mediate neither the G-protein-independent capture nor the G-protein-dependent initial adhesion strengthening of encephalitogenic T cell blasts within spinal cord microvessels. In contrast, blocking of LFA-1 on encephalitogenic T lymphoblasts resulted in a significantly reduced number of T cells firmly adhering within spinal cord microvessels 2 h after injection and in a significantly reduced number of T cells subsequently migrating across the vascular wall into the spinal cord parenchyme. Our study provides the first direct evidence that encephalitogenic T cells use LFA-1 for transendothelial migration but not for capture and initial adhesion in spinal cord microvessels in vivo.

Animals↗

PubMed2006

Prognostic value of bone marrow angiogenesis in multiple myeloma: use of light microscopy as well as computerized image analyzer in the assessment of microvessel density and total vascular area in multiple myeloma and its correlation with various clinical, histological, and laboratory parameters.

We studied the prognostic value of parameters of angiogenesis on bone marrow biopsies in newly diagnosed multiple myeloma (MM) patients. Angiogenesis parameters studied were the microvessel count done manually on light microscopy (MVD-A), microvessel count done by using computerized image analyzer (MVD-B), and total vascular area (TVA) measured by computerized image analyzer. One hundred ten newly diagnosed cases of MM treated at Institute Rotary Cancer Hospital, All India Institute of Medical Sciences, were analyzed with respect to clinical features, laboratory findings, histological features, angiogenesis parameters, and responses to the treatment on follow-up. Twenty age- and sex-matched controls were studied for comparing with angiogenesis of the test cases. Bone marrow microvessels were examined using immunohistochemical staining for CD34. MVD-A (range 4.9-85.2; mean 28.2; SD 19.4), MVD-B (range 2.0-26.9; mean 11.7; SD 5.9), and TVA measured in percentage (range 0.1-17.1; mean 2.4; SD 2.5) were measured for test cases (n = 110). Grading of angiogenesis parameters of the test cases were done; such that angiogenesis parameters of controls (taken as baseline) were grade I. There was a statistically highly significant correlation between (MVD-A vs MVD-B, pcc = 0.92; MVD-A vs TVA, pcc = 0.78; MVD-B vs TVA, pcc = 0.76). The myeloma cases had significantly higher angiogenesis parameters when compared with controls (Kruskall-Wallis test, P < 0.001). "Complete responders" (n = 38/110) had significant lower angiogenesis (Mann-Whitney U test, P < 0.001) than "nonresponders" (n = 72/110). On treatment follow-up "rapid disease progressors" had the highest levels of angiogenesis (mean rank for MVD-A = 84.7, MVD-B = 82.1, and TVA = 81.1). On multivariate (logistic regression) analysis, factors found to have independent prognostic significance in complete responders (adjusted odd ratio (95% CI, P value)] were: (a) MVD-B grade I [0.134 (0.10-0.16, P < 0.001)], (b) clinical substage A [0.163 (0.12-0.19, P = 0.008)], (c) Bartl's histological stage II & I [0.262 (0.2-0.32, P = 0.021)], (d) MVD-A grade I [0.28 (0.22-0.36, P = 0.03)], (e) beta2 microglobulin levels less than 3,400 ng/dl [0.31 (0.23-0.42, P = 0.04)]. Kaplan-Meier survival analysis for myeloma-related death (n = 16) shows a mean survival time (in months) of 24.75; SE = 3; 95% CI = 21-28. We conclude that MVD (particularly MVD-B) is a very good predictor for the complete response in patients of MM and should be done routinely on bone marrow biopsies.

Adult↗

PubMed1980

Cerebral microvessel 2-deoxy-D-glucose uptake during ischemia-induced seizures.

Microvessels were isolated by albumin flotation and glass bead filtration from cerebral cortices of gerbils decapitated during pentylenetetrazol (PTZ)-induced seizures and ischemia-induced seizures. The uptake of 2-deoxy-D-glucose (2-DG) into these microvessels was studied in vitro. This uptake was increased during PTZ-induced seizures, in keeping with mechanisms whereby glucose transport into brain is increased to keep pace with the augmented tissue glycolysis provoked by enhanced neuronal activity. Uptake of 2-DG was decreased in microvessels isolated from animals that were decapitated while undergoing a seizure during ischemia and 90 to 120 minutes after ischemia. In contrast to results obtained when seizures are due to other causes, these results suggest that brain glucose transport is decreased during a seizure if the microvasculature has been previously subjected to ischemia. The results are discussed in relation to clinical stroke and Todd's postepileptic paralysis.

Animals↗

PubMed2003

Morphological features in human cortical brain microvessels after head injury: a three-dimensional and immunocytochemical study.

We studied the morphology of cortical microvessels in the brains of 10 patients who had died after receiving a traumatic head injury (THI). Scanning electron microscopy (SEM) of vascular corrosion casts, confocal microscopy of histological sections after immunocytochemistry, and detection of apoptosis by terminal dUTP nick end labeling (TUNEL) were used. Microvascular casts showed an angioarchitectonic distribution that was defined as normal according to results obtained in a previous, nontraumatic series of subjects. However, when we compared them with previous works, the cast surface of some of the microvessels showed three types of morphological alterations: longitudinal folds, sunken surfaces with craters, and a significant flattening with reduction of lumen. The vessels that were primarily affected were the arterioles and capillaries of the middle and deep cortical vascular zones. Immunostaining with the monoclonal antibody MAS-336 against endothelial cells also showed the presence of longitudinal folds with a thinning of the vascular lumen, cytoplasmic round bodies, and a thickening of the endothelial cell membrane. The TUNEL technique revealed a positive staining of some endothelial cells. The structural alterations we observed indicate that microvessels undergo endothelial cell damage after THI. We suggest that this kind of lesion and the secondary functional injury to the blood-brain barrier (BBB) could play an important role in the development of the secondary lesions that these patients show in the subacute phase.

Adolescent↗

PubMed1993

Nitric oxide and endothelin secretion by brain microvessel endothelial cells: regulation by cyclic nucleotides.

Endothelin (ET)-1 was originally characterized as a potent vasoconstrictor peptide secreted by vascular endothelial cells. It possesses a wide range of biological activities within the cardiovascular system and in other organs, including the brain. Also secreted by endothelial cells, nitric oxide (NO), has recently been identified as a relaxing factor, as well as a pleiotropic mediator, second messenger, immune defence molecule, and neurotransmitter. Most of the data concerning the secretion of these two agents in vitro has been collected from studies on macrovascular endothelial cells. Given the remarkable heterogeneity of endothelia in terms of morphology and function, we have analyzed the ability of brain microvessel endothelial cells in vitro to release ET-1 and NO, which, at the level of the blood-brain barrier, have perivascular astrocytes as potential targets. The present study was performed with immortalized rat brain microvessel endothelial cells, which display in culture a non transformed phenotype. Our data demonstrate that: (1) these cells release NO when induced by IFN gamma and TNF alpha, (2) they constitutively secrete ET-1, and (3) cAMP potentiates the cytokine-induced NO release and exerts a biphasic regulation on ET-1 secretion: micromolar concentrations of 8-Br-cAMP inhibit and higher doses stimulate ET-1 secretion. This stimulation is blocked by EGTA and the calmodulin antagonist W7, but not by protein kinase C inhibitors, suggesting the involvement of the calmodulin branch of the calcium messenger system. These results suggest that cerebral microvessel endothelial cells may participate in vivo to the regulation of glial activity in the brain through the release of NO and ET-1.

Amino Acid Oxidoreductases↗

PubMed2006

Microvessel density estimation in the human brain by means of dynamic contrast-enhanced echo-planar imaging.

Animal studies have shown that in vivo estimates of microvessel density in the brain may be obtained from an MRI-measurable index (Q) provided that a sufficiently high dose of an intravascular paramagnetic contrast agent is employed. Q is determined from the shifts in the transverse relaxation rates induced by the contrast agent, and a high dose is required for the validity of analytic expressions relating Q to the microvessel density. However, the steady-state imaging techniques used in these prior investigations are not appropriate for humans, as the required contrast agent dose is too large. Here results of a pilot study with three subjects are reported. The results suggest that reliable Q measurements can be performed in the human brain at 1.5 T by using an interleaved spin-echo (SE)/gradient-echo (GE) echo-planar imaging (EPI) sequence and a bolus injection of a triple dose of Gd-DTPA. Lower- and upper-bound estimates for the microvessel density were derived from the Q-values, and were found to be in reasonable accord with previously cited values determined by histology.

Adult↗

PubMed2002

VHL mutations and their correlation with tumour cell proliferation, microvessel density, and patient prognosis in clear cell renal cell carcinoma.

Mutations of the von Hippel-Lindau (VHL) gene are considered critical for the initiation of clear cell renal cell carcinoma. The VHL protein is involved in regulation of the cell cycle and neo-vascularization. In this study, the association of VHL mutations with tumour cell proliferation, angiogenesis, and clinical outcome was analysed in 113 clear cell renal cell carcinomas. The degree of angiogenesis and tumour cell proliferation was immunohistochemically determined by counting microvessels (microvessel density, anti-CD34 antibody) and cells with proliferating activity (Ki-67 labelling index, MIB-1 antibody). Forty-eight different VHL sequence alterations were found in 38 of 113 patients (34%) by direct sequencing. Nineteen VHL mutations were frameshifts and nonsense mutations, predicted to change the open reading frame of VHL. These 'loss-of-function' mutations correlated with worse prognosis in univariate analysis (p=0.02). Tumour grade, stage, microvessel density, and tumour cell proliferation were not associated with VHL alterations. These findings may indicate that 'loss-of-function' VHL mutations are involved in the progression of a clear cell renal cell carcinoma subset, whereas regulation of angiogenesis and proliferation of renal carcinoma in vivo is apparently not directly influenced by VHL alterations.

Analysis of Variance↗

PubMed2000

Endostatin inhibits microvessel formation in the ex vivo rat aortic ring angiogenesis assay.

Endostatin has demonstrated potent antiangiogenic and antitumor activity in mouse models. We have investigated the ex vivo rat aortic ring assay and a human vein model to assess the biological activity of murine and human endostatin. Rat aortic rings were exposed to recombinant murine endostatin (Spodoptera frugipera; Calbiochem, San Diego, CA) or recombinant human endostatin (Pichia pastoris; EntreMed, Rockville, MD). After 5 days, murine endostatin (500 microgram/ml) demonstrated inhibition of microvessel outgrowth with dose-dependent effects (down to 16 microgram/ml). No significant inhibition was observed with human endostatin in the rat assay. Human endostatin at 250 and 500 microgram/ml inhibited outgrowths from human saphenous vein rings after a 14-day incubation. Electron microscopy assessed the formation of basal lamina, confirming that the microvessels were progenitors of patent vessels. Immunostaining for Factor VIII or CD34 demonstrated that the microvessel cells were endothelial. BrdU incorporation assays supported the presence of proliferating endothelial cells, correlating with neovascularization from the aortic wall. We conclude that the rat aortic ring assay confirms the antiangiogenic activity of murine but not human endostatin, suggesting that the model may have species specificity. However, the human form shows biological activity against human vascular tissue.

Angiogenesis Inhibitors↗

PubMed1996

Differential effects of endotoxin and cytokines on prostaglandin E2 formation in cerebral microvessels and brain parenchyma: implications for the pathogenesis of fever.

Prostaglandin(PG) E2 is regarded as an essential mediator in the central action of pyrogens and fever. However, it is not clear how the appearance of cytokines in the circulation leads to the rise of PGE2 in brain (fever to an external noxa), nor is it clear whether bacterial toxins originating within the brain activate PGE2 directly or via the cytokines (fever to a central noxa). We have previously reported that human interleukin 1 (hIL-1) has no effect on PGE2 synthesis in isolated, feline cerebral microvessels. Since cytokine action may be species-specific and interleukin 6 (IL-6) is considered as important as IL-1 for fever, we have now examined the response of isolated, murine cerebral microvessels to homologous and heterologous IL-1 beta (rIL-1 beta and hIL-1 beta), heterologous IL-6 (hIL-6), and endotoxin. The same pyrogens were tested on rat cerebrocortical minces. We have found that PGE2 formation in the microvessels is not changed by either IL-1 beta (both forms) or hIL-6. Conversely, in brain minces rIL-1 beta (but not hIL-1 beta or hIL-6) is a PGE2 activator. Endotoxin stimulated PGE2 synthesis in both preparations and its action in brain was fully reversed by the hIL-1 receptor antagonist (hIL-1ra). Our data indicate that the cerebral microvasculature does not lend itself to a transducing function in the fever to an external noxa. In addition, they point to a mediator role of IL-1 in the fever to a central noxa.

Animals↗

PubMed1997

Uterine leiomyosarcoma has deregulated cell proliferation, but not increased microvessel density compared with uterine leiomyoma.

OBJECTIVE: To investigate the differences of biological aggressiveness in terms of proliferating cell nuclear antigen (PCNA) expression, cell proliferation, and microvessel density between uterine leiomyosarcoma and leiomyoma. STUDY DESIGN: All patients with uterine leiomyosarcoma undergoing surgery at National Cheng Kung University Hospital were eligible. Forty-four patients with uterine myoma were also studied as the benign counterpart. The paraffin-embedded slides were stained with hematoxylin and eosin to confirm the presence of tumor and to quantitate mitoses, PC 10 for measurement of PCNA expression, MIB 1 for measurement of cell proliferation, and factor VIII for quantitation of microvessel density. The immunohistochemical findings of the slides were correlated with clinocopathologic findings of the patients, and the data were analyzed by either chi2 or unpaired t test. RESULTS: Six patients with uterine leiomyosarcoma and 44 patients with uterine leiomyoma were studied. Statistically significant higher mean levels of PCNA and MIB 1 were observed in uterine leiomyosarcoma compared with those of uterine myoma (for PCNA expression, P = 0.0001; for MIB 1, 11.61 +/- 11.42% vs 0.45 +/- 0.21%, P < 0.0001). No significant difference of microvessel density was observed between these two groups (65.73 +/- 48.62 vs 41.97 +/- 28.20, P = 0.084). Among the six patients with leiomyosarcoma, two patients with a higher percentage of MIB 1-positive tumor cells died of recurrent disease. In contrast, two patients with lower MIB 1 counts were disease-free for 3 years or more. CONCLUSION: Deregulated cell growth in uterine leiomyosarcoma may account for the biological aggressiveness of this tumor. Furthermore, the percentage of MIB 1-positive tumor cells seems to be associated with the prognosis or extent of uterine leiomyosarcoma.

Adult↗

PubMed2000

Notch4 and Jagged-1 induce microvessel differentiation of rat brain endothelial cells.

The mouse Notch4 gene is expressed specifically in endothelial cells. Notch4/int-3, a truncated form of Notch4, acts as a constitutive activated Notch receptor. We used rat brain microvessel endothelial cells (RBE4) to study the role of Notch4 and Jagged-1 in endothelial cell differentiation. Both Notch4/int-3 and Jagged-1 were able to induce microvessel-like structures with morphological and biochemical properties similar to brain endothelial microvessels. Ectopic expression of full-length Notch4 did not effect RBE4 cells. Activation of the Notch signal transduction pathway was measured by the induction of endogenous Notch4 and Jagged-1 genes and of Jagged-1 proteins. The observed morphological changes to RBE4 cells correlated with endogenous Notch4 and Jagged-1 gene activation. Our observations demonstrate that Notch signaling can promote endothelial cell differentiation and morphogenesis.

Animals↗

PubMed1993

Selection for enhanced adhesion to microvessel endothelial cells or resistance to interferon-gamma modulates the metastatic potential of murine RAW117 large-cell lymphoma cells.

Poorly liver metastatic large-cell lymphoma RAW117-P cells were sequentially selected in vitro for increased adhesion to murine hepatic sinusoidal endothelial cells. After three or four sequential selections, the selected sublines showed increased rates of adhesion to target hepatic microvessel endothelial cells and increased formation of experimental metastases in the liver. However, the endothelial cell adhesion-selected RAW117 sublines were generally unstable and gradually lost their enhanced adhesive and metastatic properties during passage in culture. Highly metastatic, liver-selected RAW117-H10 large-cell lymphoma cells were more resistant to the cytostatic effects of interferon-gamma (IFN-gamma) than poorly metastatic unselected parental RAW117-P cells. When tested for their sensitivity to IFN-gamma, the endothelial cell adhesion variants were significantly more resistant than the unselected RAW117-P cells, but after a 72-h treatment with IFN-gamma, the in vitro-selected cells lost their enhanced endothelial cell adhesion characteristics, their potential to colonize the liver, and their ability to grow when injected at subcutaneous or intramuscular sites. In contrast, the metastatic potential of similarly treated RAW117-P cells was unaffected by IFN-gamma during a 72-h treatment. Sequential selection of RAW117-P cells for increased resistance to IFN-gamma in vitro resulted in variant lines that were refractory to the growth-inhibiting effects of IFN-gamma, and these IFN-gamma-selected variants were also less adhesive to liver microvessel endothelial cells. The IFN-gamma-selected variants also lost their experimental metastatic potentials completely and their tumorigenicities at sites of subcutaneous or intramuscular injection. Cytofluorographic analysis indicated reduced cell surface expression of H-2Kd antigen and fibronectin receptor on the selected variant cells but no change in cell surface mu heavy chain immunoglobulin. The unselected and selected RAW117 lines had similar sensitivities to natural killer (NK) cell-mediated cytolysis, indicating that the in vivo differences were probably not due to differences in NK cell-mediated cytolysis. The results suggest that selection for adhesion to organ microvessel endothelial cells or sequential exposure to certain cytokines can affect the adhesive, growth and metastatic properties of RAW117 cells without modifying their responses to NK cells.

Animals↗

PubMed1994

Immunolabelling of hippocampal microvessel glucose transporter protein is reduced in Alzheimer's disease.

Changes in cerebral microvessel ultrastructure have been reported to occur in Alzheimer's disease (AD). In order to investigate whether these changes are associated with compromised blood-brain transport mechanisms, hippocampal formation sections from AD and age-matched normal brains were immunolabelled with an antibody to the GLUT-1 glucose transporter protein. GLUT-1 immunolabelling of microvessel endothelium was significantly reduced in the AD compared to normal hippocampal formation. Thus, AD is associated with a reduction in cerebral microvessel endothelium glucose transporter content, which may result in decreased glucose availability to the brain.

Aged↗

PubMed1995

Current pathologic methods for measuring intratumoral microvessel density within breast carcinoma and other solid tumors.

Abundant evidence has shown that tumor growth and metastasis are dependent upon tumor angiogenesis (TA). TA refers to the growth of new vessels toward and within the tumor. Until TA occurs, tumors grow no larger than 2-4 mm in diameter. Also, TA is necessary at the beginning and at the end of the metastatic cascade of events. Thus, it seems reasonable that increasing intratumoral microvascular density (iMVD) might correlate with greater tumor aggressiveness, such as a higher frequency of metastases and/or decreased survival. Indeed, in 1991 my colleagues and I reported a statistically significant association between greater incidence of metastases in patients with breast carcinoma and increasing iMVD. Microvessel density was measured with a light microscope in a single area of invasive tumor (200x field or 0.74 mm2) representative of the highest microvessel density (neovascular "hot spot"). This was done after endothelial cells, lining the microvessels, had been highlighted with anti-factor VIII-related antigen/von Willebrand's factor (F8RA/vWF). Subsequent studies by other investigators, using either anti-F8RA/vWF or other relatively vessel-specific reagents such as anti-CD31, have shown that the association of greater tumor aggressiveness with increasing iMVD exists not only in breast carcinoma, but also in other solid tumors. This article reviews the methods of highlighting intratumoral vessels and describes the techniques for counting these vessels for assessing iMVD.

Breast Neoplasms↗

PubMed1985

Ca2+ depletion-induced disconnection of tight junctions in isolated rat brain microvessels.

Cerebral microvessels were isolated from rat brains. One part of the microvessel pellets was incubated for 25 or 90 min in Krebs-Henseleit bicarbonate buffer (KHB) at pH 7.5 (control group). The other part of the pellets was treated for the same periods of time with Ca2+-free KHB, containing 2.2 mM EGTA and 2 mM glucose (experimental group). Morphological changes of endothelial tight junctions were evaluated in 100 randomly selected interendothelial clefts from isolated cerebral microvessels of each groups by electron microscopy. Following 25 min of incubation time, either with Ca2+-containing or with Ca2+-free KHB, no significant changes of tight junctions were observed. After 90 min of incubation in Ca2+-free medium, 58% of tight junctions were altered (in 42% partial, and in 16% complete disconnection of tight junctions were found). This contrasted the control group, where only 14% of tight junctions were disconnected (12% partially and 2% completely). Our results are consistent with a role for intercellular Ca2+ in maintaining structural integrity of cerebral tight junctions.

Animals↗