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At least 145 records · Page 8Linked to original sources
PubMed2003

Phagocytosis of Escherichia coli by amoeboid microglial cells in the developing brain.

Amoeboid microglial cells (AMC) in the corpus callosum of 1-day-old rats receiving a single intracerebral injection of Escherichia coli ( E. Coli) were examined at various time intervals following the injection. A large number of E. coli were internalized by the AMC at 1-3 h after the injection. However, no E. coli were identifiable at 1 day after the injection, but large phagosomes were observed in the cytoplasm of AMC. With time, the phagosomes in the AMC were reduced so that by 7 days the cells appeared comparable to the controls. Apoptotic or necrotic AMC were not encountered during the study period. This is consistent with the results of cell counts, which showed no significant change in the AMC population following E. coli injection compared with controls. The present results suggest that AMC are capable of removing live bacteria from their vicinity. Up-regulation of complement type 3 receptors and induction of major histocompatibility complex class II antigens were observed in the AMC at days 1-3 and 7 following E. coli administration. This may be related to their involvement in mediating endocytosis and their possible role in antigen presentation.

Animals↗
PubMed2001

CD8+ phagocytes in focal ischemia of the rat brain: predominant origin from hematogenous macrophages and targeting to areas of pannecrosis.

We have recently described a novel population of CD8+ phagocytes that are strongly recruited to focal ischemic lesions of the rat brain but absent from axotomized central fiber tracts. To assess the relative contribution of infiltrating macrophages and resident microglia to the CD8+ phagocyte response, we selectively depleted peripheral macrophages by systemic administration of dichloromethylene diphosphonate-filled liposomes prior to the induction of permanent ischemia by photothrombosis of cortical microvessels. Macrophage depletion led to a dramatic reduction but not complete abolishment of CD8+ cells in the ensuing infarcts. Systemic administration of monoclonal antibody Ox-8 eliminated CD8+ cells from peripheral lymphoid organs but had no effect on CD8+ phagocytes in the ischemic brain lesions. To further characterize the lesion conditions inducing the recruitment of CD8+ phagocytes, we induced mild focal ischemia by transient occlusion of the middle cerebral artery that leads to a core infarction with ischemic pannecrosis surrounded by areas with selective neuronal cell death. Recruitment of CD8+ phagocytes was restricted to areas of ischemic pannecrosis. In areas undergoing selective neuronal loss microglia up-regulated complement receptor-3, exhibited ED1 immunoreactivity (indicating phagocytic activity), and to some extent expressed CD4, but not CD8 antigens. In conclusion our present study shows that CD8+ phagocytes in focal brain ischemia are predominantly derived from hematogenous macrophages and selectively target to areas of ischemic pannecrosis.

Animals↗
PubMed2005

Stromal cells as the major source for matrix metalloproteinase-2 in cutaneous melanoma.

Matrix metalloproteinases (MMPs) are essential for tumor progression, invasion and metastases formation. Expression of these proteinases is not only restricted to the tumor cells themselves, but also is found in normal stromal cells. Moreover, immunohistochemistry suggests stromal cells as the major source. To scrutinize this hypothesis we established a slowly growing, syngeneic tumor model using the B16-melanoma cell line B78D14. In vitro analysis demonstrated that B78D14 cells secreted MMP-2, MT1-MMP, and to a lesser degree MMP-9; in addition they expressed both MT1-MMP and EMMPRIN on their surface. In subcutaneous (s.c.) tumors of these cells MMP-2 expression was predominantly present at the tumor-stroma border indicating stromal cells as primary source for this protease in vivo. Indeed, double staining experiments and in situ zymography confirmed that tumor adjacent stromal cells at the invasive front expressed MMP-2 and only at this site activated MMP-2 was detectable. Notably, in an experimental pulmonary metastases model neither tumor nor stromal cells expressed MMP-2, suggesting that the capacity of stromal cells is largely dependent on the surrounding microenvironment.

Animals↗
PubMed2006

Lack of evidence for caveolin-1 and CD147 interaction before and after bleomycin-induced lung injury.

Immunohistochemical and in vitro studies indicate that caveolin-1, which occurs abundantly in alveolar epithelial type I cells and microvascular endothelial cells of the lung, is selectively downregulated in the alveolar epithelium following exposure to bleomycin. Bleomycin is also known to enhance the expression levels of metalloproteinases and of the metalloproteinase inducer CD147/EMMPRIN in lung cells. Experimental in vitro data has showed that MMP-inducing activity of CD147 is under the control of caveolin-1. We studied the effects of bleomycin on the expression of caveolin-1, CD147 and metalloproteinases using an alveolar epithelial rat cell line R3/1 with properties of both alveolar type I and type II cells and explanted rat lung slices. In parallel, retrospective samples of bleomycin-induced fibrosis in rats and mice as well as samples of wild type and caveolin-1 knockout animals were included for immunohistochemical comparison with in vitro data. Here we report that treatment with bleomycin downregulates caveolin-1 and increases CD147 and MMP-2 and -9 expression/activity in R3/1 cells using RT-PCR, Western blot analysis, MMP-2 activity assay and immunocytochemistry. Immunofluorescence double labeling revealed that caveolin-1 and CD147 were not colocalized in vitro. The in vitro findings were confirmed through immunohistochemical studies of the proteins in paraffin embedded precision-cut rat lung slices and in fibrotic rat lung tissues. The caveolin-1-negative hyperplastic ATII cells exhibited enhanced immunoreactivity for CD147 and MMP-2. Caveolin-1-negative ATI cells of fibrotic samples were mostly CD147 negative. There were no differences in the pulmonary expression of CD147 between the normal and caveolin-1 deficient animals. The results demonstrate that bleomycin-induced lung injury is associated with an increase in CD147 expression and MMP activity, particularly in alveolar epithelial cells. In addition, our data exclude any functional interaction between CD147 and alveolar epithelial caveolin-1.

Animals↗
PubMed2000

Induction of the blood-brain barrier marker neurothelin/HT7 in endothelial cells by a variety of tumors in chick embryos.

Neurothelin/HT7, a transmembrane glycoprotein of the immunoglobulin superfamily, is a marker of blood-brain barrier (BBB)-forming endothelial cells. We have studied the expression of neurothelin in tumors grown on the chorioallantoic membrane (CAM) of chick embryos. We inoculated each 3-5 x 10(6) rat C6 glioma, rat 10AS pancreatic carcinoma, human A375 melanoma, and human mammary duct adenoma cells on the CAM of 10-day-old chick embryos. The tumors were harvested on day 17. All four tumor cell lines formed solid tumors which were supplied by vessels of CAM origin. Foci of bleeding were regularly observed within the tumors. All four tumors induced the expression of neurothelin/HT7 (but not of glucose transporter-1) in tumor endothelial cells, whereas expression in adjacent endothelial cells of normal CAM did not occur. Confocal laser scanning microscopy revealed that the pattern of neurothelin expression in tumor endothelial cells was different from that in normal central nervous system (CNS) endothelium, but the relative molecular weight of neurothelin, studied by western blot analysis, was the same in brain and in tumors. It has been shown that, with increasing malignancy, vessels of CNS tumors lose their morphological characteristics, and BBB markers such as the glucose transporter-1 are downregulated. Our results show that, in contrast, the BBB marker, neurothelin, is expressed de novo in tumor endothelial cells. Potential common functions of neurothelin in endothelial cells of the CNS and tumors are discussed.

Allantois↗
PubMed2003

Correlation of emmprin expression in vascular endothelial cells with blood-brain-barrier function: a study using magnetic resonance imaging enhanced by Gd-DTPA and immunohistochemistry in brain tumors.

In a previous study, we demonstrated that the expression levels in tumor cells of emmprin (CD147) correlated with the grade of astrocytic tumors. Also, we found that emmprin was expressed in vascular endothelial cells of the non-neoplastic brain and hypothesized that emmprin expression could be associated with normal blood-brain-barrier (BBB) function of vascular endothelial cells. In this study, this possibility was examined in non-neoplastic brain, glioma and metastatic carcinoma tissues by comparing emmprin immunohistochemistry with gadolinium diethylenetriaminepentaacetic acid (Gd-DTPA) enhancement of magnetic resonance imaging (MRI), which is a clinical indicator of the BBB function. This study included 10 cases of non-neoplastic brain tissues, 7 of metastatic carcinoma, 7 of diffuse astrocytoma, 4 of anaplastic astrocytoma and 13 of glioblastoma multiforme. In all the cases, MRI with administration of Gd-DTPA was performed. The lesions were resected using the microdissection method with the help of ultrasonography and a neuronavigator. The tissues from Gd-DTPA-enhanced or non-enhanced areas were processed into frozen sections and subjected to immunohistochemistry with anti-emmprin antibody. The expression of emmprin in brain vascular endothelial cells inversely correlated with Gd-DTPA-enhancement of MRI: emmprin was positive in tissues not enhanced by Gd-DTPA and was negative in DTPA-enhanced tissues. Since BBB function presumably remains unimpaired in regions in which MR images are not Gd-DTPA-enhanced, emmprin expression appears to be associated with unimpaired BBB function. This is the first report to demonstrate a possible correlation between emmprin expression and BBB function in humans.

Adult↗
PubMed2002

Developmental changes of HT7 expression in the microvessels of the chick embryo brain.

The neurothelin/HT7 antigen is a chick-specific, cell-surface glycoprotein expressed by the brain endothelial cells and widely utilized in experimental studies as a marker of barrier-provided vessels. Previous immunohistochemical studies have demonstrated that HT7 is already expressed in the embryonic brain vessels and that it is first detectable on embryonic day 10 and developmentally regulated. In the present study, the vascular expression of HT7 was investigated in different regions of the central nervous system from the 5th day right up to the latest stage of the chick embryo development. The study was carried out utilizing a monoclonal antibody anti-HT7, which was detected by both enzymatic and fluorescent immunohistochemical methods. The observations demonstrated the presence of HT7-stained vessels as early as embryonic day 6 in the rhombencephalon and mesencephalon, and at embryonic day 9 in the prosencephalon. Regional differences were also evidenced within the rhombencephalon and mesencephalon, since the endothelial antigen HT7 was expressed earlier in the brain stem (tegmentum of the medulla oblongata, pons and mesencephalon) than in the cerebellum and optic tectum. The caudo-cranial and ventro-dorsal gradients of HT7 expression were temporally and spatially related to the development of the brain vessels. The early detection of HT7 staining in the choroid plexus epithelium and perineural vessel endothelium, sites of the blood-cerebrospinal fluid barrier and pial barrier, respectively, has confirmed this antigen to be a precocious marker for all the barrier systems in the brain.

Animals↗
PubMed2003

Effects of 6-aminonicotinamide gliotoxin on blood-brain barrier differentiation in the chick embryo cerebellum.

The hypothesis of astroglial cell involvement in prenatal setting up of the blood-brain barrier (BBB) has been examined by producing glial degeneration in cerebellum of chicken embryos submitted to the action of gliotoxin 6-aminonicotinamide (6-AN), which was applied onto the embryo chorioallantoic membrane during both early and late embryonic development. The effects of 6-AN on the cerebellum astroglial cells and microvessels were analysed under the light microscope by immunostaining for 3CB2 (chick-specific glial marker) and HT7 (chick-specific marker of BBB-provided brain endothelia), under the electron microscope, as well as by the vascular permeability tracer horseradish peroxidase. The results, showing good suitability of the 6-AN model also when applied in early embryonic development, demonstrated a correlation between perivascular glia depletion and endothelial barrier impairment and suggested that astroglia play a role in the BBB prenatal differentiation.

6-Aminonicotinamide↗
PubMed1999

A comparison of blood-brain barrier and blood-nerve barrier endothelial cell markers.

A number of major properties of endothelial cells (EC) at the blood-brain barrier (BBB) have been shown to be astrocyte-dependent. Whether analogous properties at the blood-nerve barrier (BNB) are induced and maintained by Schwann cells has not been investigated. As a preliminary investigation we have undertaken a comparative study of six EC membrane markers at the BBB and BNB and perineurium. Employing immunoblotting and immunocytochemistry the relative distribution between rat brain cortex and sciatic nerve was determined for the glucose transporter (GLUT-1), the transferin receptor (OX-26), the endothelial barrier antigen (EBA) and the OX-47 antigen. Using enzyme cytochemistry the same comparison was made for gamma-glutamyl transpeptidase (GGTP) and alkaline phosphatase. By immunocytochemistry GLUT-1 was uniformly strongly represented in brain EC, nerve EC and perineurium. OX-26 was strongly positive in brain EC but present only in trace quantities in nerve EC and perineurium. EBA similarly showed strong positivity in brain EC and trace amounts in nerve EC but was absent from perineurium. OX-47 was present moderately in brain EC and perineurium but absent from nerve EC. Quantitative immunoblotting of brain and sciatic nerve homogenates showed statistically significant differences in the level of expression of EBA and OX-26 between the two tissues. Enzyme cytochemistry showed that GGTP was strongly positive in brain EC but absent from nerve EC and perineurium. Alkaline phosphatase stained strongly in brain and nerve EC and was absent from perineurium. In summary the six membrane markers were heterogeneously represented in nerve compared with brain. This pattern of distribution in the nerve cannot simply be accounted for by the absence of astrocytes and their inductive influences. Any inductive influences of Schwann cells require investigation.

Alkaline Phosphatase↗
PubMed2003

The functional interaction between CD98 and CD147 in regulation of virus-induced cell fusion and osteoclast formation.

Membrane fusion is an important event in the functioning of a living organism. Life starts as a sperm fuses with the membrane of an egg, leading to its fertilization. Membrane fusion is also required for myogenesis, osteogenesis and placenta formation. Multinucleated giant cells originating from monocytes-macrophages are associated with granulomatous lesions formed in response to foreign bodies, viruses, and bacteria. The CD4 molecule acts as a receptor for HIV. The major virus envelope glycoprotein, gp120, attaches to CD4 molecules expressed on the host cell surface. After binding to CD4 on the target cells, HIV is internalized via direct, pH-independent fusion of the viral and cell membranes. However, attachment of HIV to CD4 on the target cells is not sufficient for fusion. Interaction of gp160-expressing cells with neighboring cells bearing surface CD4 molecules is also required for syncytium formation. Syncytium formation and subsequent generalized cell fusion have been reported as potentially important mechanisms of virus-induced cytotoxic effects. Some antibodies against CD98/FRP-1 suppressed virus-induced cell fusion and CD98-mediated cell fusion of monocytes, indicating that CD98/FRP-1 molecules are able to regulate cell fusion. In this study, the functional interaction between CD98 and CD147 was investigated. Three kinds (Ab1, 2, and 3) of anti-CD147 and three kinds of anti-CD98 antibodies were used. Ab1 suppressed CD98-mediated cell fusion, but showed no effect on cell aggregation of Cd(+)U2ME-7 cells, U937-2 cells expressing HIV gp160. On the other hand, Ab2 enhanced the CD98-mediated cell fusion. Ab1 showed suppressive effect at early stage and Ab2 showed enhancing effect at later stage. Ab2 and 3 suppressed the spontaneous cell agglutination and cell fusion of Cd(+)JME-2 cells, Jurkat cells expressing HIV gp160. Ab2 suppressed CD98-mediated cell fusion, but showed no effect on cell aggregation of Cd(+)JME-2 cells. Ab2 cancelled suppression of cell fusion induced by suppressive antibody against CD98. Ab2 and 3 also suppressed CD98-mediated cell fusion of monocytes. This study indicates the functional interaction between CD98 and CD147 in the regulation of cell fusion.

Antibodies, Monoclonal↗
PubMed2003

The blood-brain barrier of the chick glycogen body (corpus gelatinosum) and its functional implications.

Among recent vertebrates only birds possess a glycogen body (corpus gelatinosum), located in the rhomboidal sinus of the lumbosacral region of the spinal cord and separated from the neural tissue proper. Because of the specific topographical situation of this circumventricular organ, the structure of its vascular system is of special interest with respect to the still unsolved functional problems. The existence of a blood-brain barrier is demonstrated by the exclusion of intravascularly injected tracer (horseradish peroxidase), and immunocytochemical demonstration of glucose transporter-1 as a functional marker and of neurothelin, occludin and ZO-1 as structural markers. Alkaline phosphatase and gamma-glutamyltransferase activities, two enzyme reactions frequently used for demonstration of an established blood-brain barrier in vitro, were localized histochemically on the plasmalemma of glycogen body cells and were absent from the endothelium. In addition, local enlargements of the intercellular space were observed by transmission and scanning electron microscopy. In accordance with the concept of a third circulation the cerebrospinal fluid may be the vehicle for distributing substances originating in the glycogen body to the CNS, while the vascular endothelium maintains the internal milieu by virtue of its dynamic barrier functions.

Alkaline Phosphatase↗
PubMed2006

Modifying the soil to affect the seed: role of stromal-derived matrix metalloproteinases in cancer progression.

In the 1980's, as the importance of matrix metalloproteinases (MMPs) in cancer progression was discovered, it was recognized that in most tumors these proteases were abundantly and sometimes exclusively expressed not by tumor cells, but by normal host-derived cells like fibroblasts, vascular endothelial cells, myofibroblasts, pericytes or inflammatory cells that contribute to the tumor microenvironment. Later experiments in mice deficient in specific MMPs revealed that host-derived MMPs play a critical role not only in tumor cell invasion, but also in carcinogenesis, angiogenesis, vasculogenesis and metastasis. Tumor cells secrete many factors, cytokines and chemokines that directly or indirectly increase the expression of these MMPs in the tumor microenvironment where they exert extracellular matrix (ECM) degrading and sheddase activities. The knowledge of the complex role that stromal-derived MMPs play in the interaction between tumor cells and stromal cells should allow us to consider specific windows in cancer treatment when MMP inhibition could have a valuable therapeutic effect.

Animals↗
PubMed1990

Correlation of blood-brain barrier function and HT7 protein distribution in chick brain circumventricular organs.

The HT7 protein defined by a monoclonal antibody is a specific marker for chick brain endothelial cells (EMBO J., 5 (1986) 3179-3183). In this study, we have investigated the expression of this protein in the brain circumventricular organs which lack a blood-brain barrier. Using immunohistochemical techniques we found that the protein was absent from the vascular system of the pituitary, median eminence, subfornical organ, pineal gland, the organum vasculosum lamina terminalis and the layer of sinusoid blood vessels of the area postrema. In some regions of the median eminence and, more strikingly, in the pineal gland, parenchymal cells expressed the HT7 antigen. Immunoblots of proteins from brain, pituitary, pineal gland and retina showed that the antigen is very abundant in the retina. Lower amounts were present in brain and pineal gland. The glucose transporter was found to be an independent reliable marker for blood-brain barrier endothelium. In the chick brain the distribution of the biochemically distinct proteins was very similar. Using a postembedding technique we have ultrastructurally localized the HT7 protein specifically in blood-brain barrier endothelial cells. Thus, the expression of the HT7 protein and glucose transporter correlated with blood-brain barrier function.

Animals↗
PubMed1992

Induction of the blood-brain barrier specific HT7 and neurothelin epitopes in endothelial cells of the chick chorioallantoic vessels by a soluble factor derived from astrocytes.

Some blood-brain barrier properties of microvascular endothelial cells have been shown to be inducible by astrocytes. We tested the hypothesis that this cellular interaction is mediated by a soluble factor(s). Chick chorioallantoic vessels in ovo were constantly exposed to astrocyte-conditioned medium. We found that endothelial cells exposed to astrocyte-derived factors, but not to glioma- or endothelial cell-derived factors, expressed the HT7 antigen and neurothelin, two specific markers of the blood-brain barrier phenotype. These results indicate that a soluble factor(s) secreted by astrocytes is capable to induce specific blood-brain barrier properties in endothelial cells of non-neural origin.

Animals↗
PubMed1994

Organization of the mouse GP42/Basigin gene: a member of the Ig superfamily.

We have mapped and sequenced the GP42/Basigin gene isolated from a Balb/C mouse genomic library. The genomic organization and upstream, putative regulatory, regions of this gene have not been previously reported. Our data show that exon 5 of the GP42/Basigin gene encodes the carboxy proximal half of the second Ig-like domain, the highly conserved transmembrane region and a portion of the cytoplasmic tail. This inclusion of Ig-like and other functional domains in a single exon is unusual. Splice junction analysis indicates that two reported alternate GP42/Basigin cDNA isoforms are likely due to cloning artifacts. In addition, we find that GP42/Basigin is polymorphic in mice. Our data also support the proposal that the transmembrane domain and portions of the cytoplasmic region of GP42/Basigin have been evolutionarily conserved.

Amino Acid Sequence↗
PubMed1996

Developing brain cells produce factors capable of inducing the HT7 antigen, a blood-brain barrier-specific molecule, in chick endothelial cells.

Homeostasis of the neural microenvironment is maintained by the blood-brain barrier (BBB). To analyze the molecular mechanisms by which the BBB is induced during embryonic development, we have taken advantage of an in vivo model of BBB induction based on the expression of the HT7 cell surface protein. This protein is a transmembrane glycoprotein of the immunoglobulin superfamily. It is expressed in the chick BBB-forming endothelial cells, but not in peripheral endothelial cells. Here we show that the HT7 protein is induced in vessels which had vascularized a quail embryonic brain graft transplanted in the coelomic cavity of chick embryo. The quail brain graft was vascularized by both chick and quail-derived vessels. All chick host-derived vessels in the brain transplant were found to express HT7 while the neighboring chick vessels were negative. We conclude that the invading host endothelial cells differentiated into BBB-forming vessels under the influence of developing quail brain cells. This model reproduces the BBB induction during development. It may be useful for further approaches to study the molecular mechanisms involved in BBB induction.

Animals↗
PubMed1989

Cloning of cDNA for a novel mouse membrane glycoprotein (gp42): shared identity to histocompatibility antigens, immunoglobulins and neural-cell adhesion molecules.

A full-length clone encoding a murine membrane glycoprotein, gp42, was selected from a mouse fibroblast cDNA expression library by screening with a polyclonal antiserum. The deduced amino acid (aa) sequence indicates that gp42 is a transmembrane protein of 273 aa with a large N-terminal portion exposed outside the cell and a short cytoplasmic domain. Computer assisted analysis shows that gp42 is distinct from previously characterized proteins, but shares a number of structural features with the class II histocompatibility antigens. The sizes of the extracellular domains of gp42 and of class II histocompatibility antigens are similar, the position of four cysteines and the location of several aa residues are conserved. Some of these conserved residues are also present in immunoglobulins (Ig) and in the neural-cell adhesion molecule, thus indicating that gp42 is a new member of the Ig superfamily.

Amino Acid Sequence↗
PubMed2004

Downregulation of vascular matrix metalloproteinase inducer and activator proteins in hypertensive patients.

BACKGROUND: Peripheral vasculature undergoes extensive vascular remodeling in the hypertensive state. Regulation of extracellular matrix turnover by the matrix metalloproteinase (MMP) system is an important step in the vascular remodeling process. However, the expression pattern of the vascular MMP system in human hypertension remained unknown. METHODS AND RESULTS: Internal mammary artery specimens were obtained from normotensive (n = 13) and hypertensive (n = 19) patients undergoing coronary artery bypass grafting surgery. Zymographic analysis indicated a threefold decrease in total gelatinolytic activity of MMP-2 and MMP-9 in hypertension. MMP-1 activity was also decreased by fourfold without a significant change in protein levels. Tissue levels of extracellular matrix inducer protein (EMMPRIN), MMP activator protein (MT1-MMP), MMP-1, MMP-2, and MMP-9, as well as tissue inhibitors of MMPs (TIMP-1 and TIMP-2) were assessed by immunoblotting and yielded a significant decrease in MMP-9, EMMPRIN, and MT1-MMP levels in hypertension. In addition, measurement of plasma markers of collagen synthesis (procollagen type I amino-terminal propeptide [PINP]) and collagen degradation (carboxy-terminal telopeptide of collagen type I [ICTP]) indicated no difference in PINP levels but suppressed degradation of collagen in hypertension. Evaluation of profibrotic growth factors demonstrated higher levels of fibroblast growth factor (FGF)-2 in tissue preparations from hypertensive patients but no difference in transforming growth factor-beta1 levels. CONCLUSIONS: These findings demonstrate that not only MMP-1 and MMP-9, but MMP inducer and activator proteins are also downregulated in the hypertensive state. Augmented FGF-2 levels may contribute to parallel decreases in MMP activity and MMP induction system resulting in enhanced collagen deposition in hypertension.

Antigens, CD↗