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Osamu Hayaishi - One of the best experts on this subject based on the ideXlab platform.
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Cellular localization of lipocalin-type prostaglandin D synthase (?-trace) in the central nervous system of the adult rat
The Journal of comparative neurology, 2000Co-Authors: Carsten T. Beuckmann, Michael Lazarus, Dmitry Gerashchenko, Akira Mizoguchi, Sakashi Nomura, Ikuko Mohri, Akira Uesugi, Takeshi Kaneko, Noboru Mizuno, Osamu HayaishiAbstract:We applied high-resolution laser-scanning microscopy, electron microscopy, and non-radioactive in situ hybridization histochemistry to determine the cellular and intracellular localization of lipocalin-type prostaglandin D synthase, the major brain-derived protein component of cerebrospinal fluid, and its mRNA in leptomeninges, choroid plexus, and parenchyma of the adult rat brain. Both immunoreactivity and mRNA for prostaglandin D synthase were located in arachnoid Barrier Cells, arachnoid trabecular Cells, and arachnoid pia mater Cells. Furthermore, meningeal macrophages and perivascular microglial Cells, identified by use of ED2 antibody, were immunopositive for prostaglandin D synthase. In the arachnoid trabecular Cells, the immunoreactivity for prostaglandin D synthase was located in the nuclear envelope, Golgi apparatus, and secretory vesicles, indicating the active production and secretion of prostaglandin D synthase. In the meningeal macrophages, prostaglandin D synthase was not found around the nucleus but in lysosomes in the cytoplasm, pointing to an uptake of the protein from the cerebrospinal fluid. Furthermore, the existence of meningeal cyclooxygenase (COX) -1 and COX-2 was investigated by Western blot, Northern blot, and reverse transcriptase—polymerase chain reaction (RT-PCR), and the colocalization of COX-2 and prostaglandin D synthase was demonstrated in virtually all Cells of the leptomeninges, choroid plexus epithelial Cells, and perivascular microglial Cells, suggesting that these Cells synthesize prostaglandin D2 actively. Alternatively, oligodendrocytes showed prostaglandin D synthase immunoreactivity without detectable COX-2. The localization of lipocalin-type prostaglandin D synthase in meningeal Cells and its colocalization with COX-2 provide evidence for its function as a prostaglandin D2-producing enzyme. J. Comp. Neurol. 428:62–78, 2000. © 2000 Wiley-Liss, Inc.
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cellular localization of lipocalin type prostaglandin d synthase trace in the central nervous system of the adult rat
The Journal of Comparative Neurology, 2000Co-Authors: Carsten T. Beuckmann, Michael Lazarus, Dmitry Gerashchenko, Akira Mizoguchi, Sakashi Nomura, Ikuko Mohri, Akira Uesugi, Takeshi Kaneko, Noboru Mizuno, Osamu HayaishiAbstract:We applied high-resolution laser-scanning microscopy, electron microscopy, and non-radioactive in situ hybridization histochemistry to determine the cellular and intracellular localization of lipocalin-type prostaglandin D synthase, the major brain-derived protein component of cerebrospinal fluid, and its mRNA in leptomeninges, choroid plexus, and parenchyma of the adult rat brain. Both immunoreactivity and mRNA for prostaglandin D synthase were located in arachnoid Barrier Cells, arachnoid trabecular Cells, and arachnoid pia mater Cells. Furthermore, meningeal macrophages and perivascular microglial Cells, identified by use of ED2 antibody, were immunopositive for prostaglandin D synthase. In the arachnoid trabecular Cells, the immunoreactivity for prostaglandin D synthase was located in the nuclear envelope, Golgi apparatus, and secretory vesicles, indicating the active production and secretion of prostaglandin D synthase. In the meningeal macrophages, prostaglandin D synthase was not found around the nucleus but in lysosomes in the cytoplasm, pointing to an uptake of the protein from the cerebrospinal fluid. Furthermore, the existence of meningeal cyclooxygenase (COX) -1 and COX-2 was investigated by Western blot, Northern blot, and reverse transcriptase—polymerase chain reaction (RT-PCR), and the colocalization of COX-2 and prostaglandin D synthase was demonstrated in virtually all Cells of the leptomeninges, choroid plexus epithelial Cells, and perivascular microglial Cells, suggesting that these Cells synthesize prostaglandin D2 actively. Alternatively, oligodendrocytes showed prostaglandin D synthase immunoreactivity without detectable COX-2. The localization of lipocalin-type prostaglandin D synthase in meningeal Cells and its colocalization with COX-2 provide evidence for its function as a prostaglandin D2-producing enzyme. J. Comp. Neurol. 428:62–78, 2000. © 2000 Wiley-Liss, Inc.
Carsten T. Beuckmann - One of the best experts on this subject based on the ideXlab platform.
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Cellular localization of lipocalin-type prostaglandin D synthase (?-trace) in the central nervous system of the adult rat
The Journal of comparative neurology, 2000Co-Authors: Carsten T. Beuckmann, Michael Lazarus, Dmitry Gerashchenko, Akira Mizoguchi, Sakashi Nomura, Ikuko Mohri, Akira Uesugi, Takeshi Kaneko, Noboru Mizuno, Osamu HayaishiAbstract:We applied high-resolution laser-scanning microscopy, electron microscopy, and non-radioactive in situ hybridization histochemistry to determine the cellular and intracellular localization of lipocalin-type prostaglandin D synthase, the major brain-derived protein component of cerebrospinal fluid, and its mRNA in leptomeninges, choroid plexus, and parenchyma of the adult rat brain. Both immunoreactivity and mRNA for prostaglandin D synthase were located in arachnoid Barrier Cells, arachnoid trabecular Cells, and arachnoid pia mater Cells. Furthermore, meningeal macrophages and perivascular microglial Cells, identified by use of ED2 antibody, were immunopositive for prostaglandin D synthase. In the arachnoid trabecular Cells, the immunoreactivity for prostaglandin D synthase was located in the nuclear envelope, Golgi apparatus, and secretory vesicles, indicating the active production and secretion of prostaglandin D synthase. In the meningeal macrophages, prostaglandin D synthase was not found around the nucleus but in lysosomes in the cytoplasm, pointing to an uptake of the protein from the cerebrospinal fluid. Furthermore, the existence of meningeal cyclooxygenase (COX) -1 and COX-2 was investigated by Western blot, Northern blot, and reverse transcriptase—polymerase chain reaction (RT-PCR), and the colocalization of COX-2 and prostaglandin D synthase was demonstrated in virtually all Cells of the leptomeninges, choroid plexus epithelial Cells, and perivascular microglial Cells, suggesting that these Cells synthesize prostaglandin D2 actively. Alternatively, oligodendrocytes showed prostaglandin D synthase immunoreactivity without detectable COX-2. The localization of lipocalin-type prostaglandin D synthase in meningeal Cells and its colocalization with COX-2 provide evidence for its function as a prostaglandin D2-producing enzyme. J. Comp. Neurol. 428:62–78, 2000. © 2000 Wiley-Liss, Inc.
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cellular localization of lipocalin type prostaglandin d synthase trace in the central nervous system of the adult rat
The Journal of Comparative Neurology, 2000Co-Authors: Carsten T. Beuckmann, Michael Lazarus, Dmitry Gerashchenko, Akira Mizoguchi, Sakashi Nomura, Ikuko Mohri, Akira Uesugi, Takeshi Kaneko, Noboru Mizuno, Osamu HayaishiAbstract:We applied high-resolution laser-scanning microscopy, electron microscopy, and non-radioactive in situ hybridization histochemistry to determine the cellular and intracellular localization of lipocalin-type prostaglandin D synthase, the major brain-derived protein component of cerebrospinal fluid, and its mRNA in leptomeninges, choroid plexus, and parenchyma of the adult rat brain. Both immunoreactivity and mRNA for prostaglandin D synthase were located in arachnoid Barrier Cells, arachnoid trabecular Cells, and arachnoid pia mater Cells. Furthermore, meningeal macrophages and perivascular microglial Cells, identified by use of ED2 antibody, were immunopositive for prostaglandin D synthase. In the arachnoid trabecular Cells, the immunoreactivity for prostaglandin D synthase was located in the nuclear envelope, Golgi apparatus, and secretory vesicles, indicating the active production and secretion of prostaglandin D synthase. In the meningeal macrophages, prostaglandin D synthase was not found around the nucleus but in lysosomes in the cytoplasm, pointing to an uptake of the protein from the cerebrospinal fluid. Furthermore, the existence of meningeal cyclooxygenase (COX) -1 and COX-2 was investigated by Western blot, Northern blot, and reverse transcriptase—polymerase chain reaction (RT-PCR), and the colocalization of COX-2 and prostaglandin D synthase was demonstrated in virtually all Cells of the leptomeninges, choroid plexus epithelial Cells, and perivascular microglial Cells, suggesting that these Cells synthesize prostaglandin D2 actively. Alternatively, oligodendrocytes showed prostaglandin D synthase immunoreactivity without detectable COX-2. The localization of lipocalin-type prostaglandin D synthase in meningeal Cells and its colocalization with COX-2 provide evidence for its function as a prostaglandin D2-producing enzyme. J. Comp. Neurol. 428:62–78, 2000. © 2000 Wiley-Liss, Inc.
Carolyn B Coyne - One of the best experts on this subject based on the ideXlab platform.
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type iii interferons produced by human placental trophoblasts confer protection against zika virus infection
Cell Host & Microbe, 2016Co-Authors: Avraham Bayer, Nicholas J Lennemann, Yingshi Ouyang, John C Bramley, Stefanie Morosky, Ernesto Torres De Azeved Marques, Sara Cherry, Yoel Sadovsky, Carolyn B CoyneAbstract:During mammalian pregnancy, the placenta acts as a Barrier between the maternal and fetal compartments. The recently observed association between Zika virus (ZIKV) infection during human pregnancy and fetal microcephaly and other anomalies suggests that ZIKV may bypass the placenta to reach the fetus. This led us to investigate ZIKV infection of primary human trophoblasts (PHTs), which are the Barrier Cells of the placenta. We discovered that PHT Cells from full-term placentas are refractory to ZIKV infection. In addition, medium from uninfected PHT Cells protects non-placental Cells from ZIKV infection. PHT Cells constitutively release the type III interferon (IFN) IFNλ1, which functions in both a paracrine and autocrine manner to protect trophoblast and non-trophoblast Cells from ZIKV infection. Our data suggest that for ZIKV to access the fetal compartment, it must evade restriction by trophoblast-derived IFNλ1 and other trophoblast-specific antiviral factors and/or use alternative strategies to cross the placental Barrier.
Ernesto Torres De Azeved Marques - One of the best experts on this subject based on the ideXlab platform.
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type iii interferons produced by human placental trophoblasts confer protection against zika virus infection
Cell Host & Microbe, 2016Co-Authors: Avraham Bayer, Nicholas J Lennemann, Yingshi Ouyang, John C Bramley, Stefanie Morosky, Ernesto Torres De Azeved Marques, Sara Cherry, Yoel Sadovsky, Carolyn B CoyneAbstract:During mammalian pregnancy, the placenta acts as a Barrier between the maternal and fetal compartments. The recently observed association between Zika virus (ZIKV) infection during human pregnancy and fetal microcephaly and other anomalies suggests that ZIKV may bypass the placenta to reach the fetus. This led us to investigate ZIKV infection of primary human trophoblasts (PHTs), which are the Barrier Cells of the placenta. We discovered that PHT Cells from full-term placentas are refractory to ZIKV infection. In addition, medium from uninfected PHT Cells protects non-placental Cells from ZIKV infection. PHT Cells constitutively release the type III interferon (IFN) IFNλ1, which functions in both a paracrine and autocrine manner to protect trophoblast and non-trophoblast Cells from ZIKV infection. Our data suggest that for ZIKV to access the fetal compartment, it must evade restriction by trophoblast-derived IFNλ1 and other trophoblast-specific antiviral factors and/or use alternative strategies to cross the placental Barrier.
Duane E. Haines - One of the best experts on this subject based on the ideXlab platform.
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on the question of a subdural space
Anatomical Record-advances in Integrative Anatomy and Evolutionary Biology, 1991Co-Authors: Duane E. HainesAbstract:The structure of the meninges, with particular attention to the architecture of the inner portions of the dura mater and the arachnoid mater, has been reviewed in reference to the probable existence of a "subdural" space. The dura is composed of fibroblasts and large amounts of extracellular collagen. The innermost part of the dura is formed by the dural border cell layer. This layer is characterized by flattened Cells with sinuous processes, extracellular spaces containing an amorphous material, and the presence of junctions between its Cells. The dural border cell layer is continuous with the inner (meningeal) portions of the dura and may be attached to the underlying arachnoid by an occasional cell junction. The arachnoid consists of an outer part, the arachnoid Barrier cell layer, and an inner portion, the arachnoid trabeculae which bridge the subarachnoid space. Arachnoid Barrier Cells are electron-lucent, closely apposed to each other, and joined by many cell junctions; in this layer there is little extracellular space and essentially no intercellular material. Arachnoid trabecular Cells cross the subarachnoid space in a random manner, have extracellular collagen associated with their flattened processes, and form structures of variable shapes and sizes. There is no evidence of an intervening space between the arachnoid Barrier cell layer and the dural border cell layer that would correlate with what has been called the subdural space. When a tissue space is created in this general area of the meninges it is the result of tissue damage and represents, in most instances, a cleaving open of the dural border cell layer. In this situation, extracellular spaces in the dural border cell layer are enlarged, cell junctions are separated, and it is probable that cell membranes are damaged. A survey of reports describing the morphology of the inner and outer capsule of so-called subdural hematomas in humans reveals that dural border Cells are found in both parts of the capsule. Also, experimental infusion of blood into this portion of the meninges in animals frequently dissects open the dural border cell layer. These data support the view that what has been called a subdural hematoma is most frequently a lesion found within the layer formed by dural border Cells. It is suggested that the so-called subdural space is not a "potential" space since the creation of a cleft in this area of the meninges is the result of tissue damage. In this respect it shares no similarities with legitimate potential spaces (i.e., serous cavities) found at other locations in the body.(ABSTRACT TRUNCATED AT 400 WORDS)
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On the question of a subdural space.
The Anatomical Record, 1991Co-Authors: Duane E. HainesAbstract:The structure of the meninges, with particular attention to the architecture of the inner portions of the dura mater and the arachnoid mater, has been reviewed in reference to the probable existence of a “subdural” space. The dura is composed of fibroblasts and large amounts of extracellular collagen. The innermost part of the dura is formed by the dural border cell layer. This layer is characterized by flattened Cells with sinuous processes, extracellular spaces containing an amorphous material, and the presence of junctions between its Cells. The dural border cell layer is continuous with the inner (meningeal) portions of the dura and may be attached to the underlying arachnoid by an occasional cell junction. The arachnoid consists of an outer part, the arachnoid Barrier cell layer, and an inner portion, the arachnoid trabeculae which bridge the subarachnoid space. Arachnoid Barrier Cells are electron-lucent, closely apposed to each other, and joined by many cell junctions; in this layer there is little extracellular space and essentially no intercellular material. Arachnoid trabecular Cells cross the sub-arachnoid space in a random manner, have extracellular collagen associated with their flattened processes, and form structures of variable shapes and sizes. There is no evidence of an intervening space between the arachnoid Barrier cell layer and the dural border cell layer that would correlate with what has been called the subdural space. When a tissue space is created in this general area of the meninges it is the result of tissue damage and represents, in most instances, a cleaving open of the dural border cell layer. In this situation, extracellular spaces in the dural border cell layer are enlarged, cell junctions are separated, and it is probable that cell membranes are damaged. A survey of reports describing the morphology of the inner and outer capsule of so-called subdural hematomas in humans reveals that dural border Cells are found in both parts of the capsule. Also, experimental infusion of blood into this portion of the meninges in animals frequently dissects open the dural border cell layer. These data support the view that what has been called a subdural hematoma is most frequently a lesion found within the layer formed by dural border Cells. It is suggested that the so-called subdural space is not a “potential” space since the creation of a cleft in this area of the meninges is the result of tissue damage. In this respect it shares no similarities with legitimate potential spaces (i.e., serous cavities) found at other locations in the body. It is concluded that there is no evidence of a subdural space (actual or potential) in the region of the dura-arachnoid junction and it is suggested that the term spatium subdurale be removed from Nomina Anatomica.
