The Experts below are selected from a list of 279 Experts worldwide ranked by ideXlab platform
Tatsuya Yamasoba - One of the best experts on this subject based on the ideXlab platform.
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Caloric restriction reduces basal cell proliferation and results in the deterioration of neuroepithelial regeneration following olfactotoxic mucosal damage in mouse olfactory mucosa
Cell and Tissue Research, 2019Co-Authors: Hitoshi Iwamura, Kenji Kondo, Keigo Suzukawa, Shu Kikuta, Hironobu Nishijima, Ryoji Kagoya, Mizuo Ando, Chisato Fujimoto, Makiko Toma-hirano, Tatsuya YamasobaAbstract:The effects of caloric restriction (CR) on cell dynamics and gene expression in the mouse olfactory Neuroepithelium are evaluated. Eight-week-old male C57BL/6 mice were fed either control pellets (104 kcal/week) or CR pellets (67 kcal/week). The cytoarchitecture of the olfactory Neuroepithelium in the uninjured condition and its regeneration after injury by an olfactotoxic chemical, methimazole, were compared between mice fed with the control and CR diets. In the uninjured condition, there were significantly fewer olfactory marker protein (OMP)-positive olfactory receptor neurons and Ki67-positive proliferating basal cells at 3 months in the CR group than in the control group. The number of Ki67-positive basal cells increased after methimazole-induced mucosal injury in both the control and the CR groups, but the increase was less robust in the CR group. The recovery of the Neuroepithelium at 2 months after methimazole administration was less complete in the CR group than in the control group. These histological changes were region-specific. The decrease in the OMP-positive neurons was prominent in the anterior region of the olfactory mucosa. Gene expression analysis using a DNA microarray and quantitative real-time polymerase chain reaction demonstrated that the expression levels of two inflammatory cytokines, interleukin-6 and chemokine ligand 1, were elevated in the olfactory mucosa of the CR group compared with the control group. These findings suggest that CR may be disadvantageous to the maintenance of the olfactory Neuroepithelium, especially when it is injured.
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innate immune responses and neuroepithelial degeneration and regeneration in the mouse olfactory mucosa induced by intranasal administration of poly i c
Cell and Tissue Research, 2014Co-Authors: Kaori Kanaya, Kenji Kondo, Keigo Suzukawa, Takashi Sakamoto, Shu Kikuta, Kazunari Okada, Tatsuya YamasobaAbstract:The pathogenesis of postviral olfactory disorder (PVOD) has not been fully elucidated. We investigated morphological changes and innate immune responses in the mouse olfactory mucosa induced by intranasal administration of polyinosinic-polycytidylic acid [Poly(I:C)], a synthetic analog of viral double-stranded RNA. Mice received three administrations of saline with or without Poly(I:C), once every 24 h. The olfactory mucosa was harvested at various intervals after the first administration (8 h, 3, 9 and 24 days). In the Poly(I:C) group, the number of apoptotic cells in the olfactory Neuroepithelium had increased at 8 h. At 9 days, the olfactory Neuroepithelium had severely degenerated and behavioral tests demonstrated that the mice showed signs of olfactory deterioration. At 24 days, the structure of the Neuroepithelium had regenerated almost completely. Regarding the innate immune responses, many neutrophils had infiltrated the olfactory Neuroepithelium at 8 h and had exuded into the nasal cavity by 3 days. Macrophages had also infiltrated the olfactory Neuroepithelium at 8 h although to a lesser extent, but they still remained in the Neuroepithelium at 24 days. Poly(I:C)-induced neuroepithelial damage was significantly inhibited by a neutrophil elastase inhibitor and was suppressed in neutropenic model mice. These findings suggest that the secondary damage caused by the neutrophil-mediated innate immune response plays an important role in the pathogenesis of PVOD.
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age related changes in cell dynamics of the postnatal mouse olfactory Neuroepithelium cell proliferation neuronal differentiation and cell death
The Journal of Comparative Neurology, 2010Co-Authors: Kenji Kondo, Ken-ichi Nibu, Kaori Kanaya, Keigo Suzukawa, Takashi Sakamoto, Kenta Watanabe, Munetaka Ushio, Takuhiro Yamaguchi, Kimitaka Kaga, Tatsuya YamasobaAbstract:Age-related changes in cell proliferation, neuronal differentiation, and cell death in mouse olfactory Neuroepithelium were investigated. Mice at the age of 10 days through 16 months were given a single injection of bromodeoxyuridine (BrdU). The olfactory mucosae were fixed at 9 timepoints ranging from 2 hours to 3 months after the injection and examined using double immunostaining for BrdU and olfactory marker protein (OMP), and double staining with terminal deoxynucleotidyl transferase-mediated biotinylated dUTP nick end labeling (TUNEL) and immunostaining for OMP. The number of BrdU-labeled cells/mm epithelial length initially increased, peaked at 2–3 days after the BrdU injection, then declined at each age. The number of BrdU- and TUNEL-labeled neuronal cells both decreased with increasing age, suggesting that the rates of both cell proliferation and cell death in the olfactory Neuroepithelium decrease with increasing age. Double-labeled cells for BrdU and OMP appeared at 7 days after injection in all age groups, suggesting that the time required for neuronal differentiation is broadly similar irrespective of age. In older age groups, smaller amounts of the newly produced cohort are integrated into the OMP-positive ORN population, and even once it is integrated it is eliminated from the population more rapidly compared to the younger age groups. Furthermore, TUNEL assay showed that the fraction of apoptotic cells distributed in the OMP-positive layer/total apoptotic cells decreased with age. This observation suggests that the turnover of mature ORNs is slower in the older Neuroepithelium compared to the younger Neuroepithelium. J. Comp. Neurol. 518:1962–1975, 2010. © 2010 Wiley-Liss, Inc.
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Distribution and severity of spontaneous lesions in the Neuroepithelium and Bowman’s glands in mouse olfactory mucosa: age-related progression
Cell and Tissue Research, 2009Co-Authors: Kenji Kondo, Ken-ichi Nibu, Keigo Suzukawa, Takashi Sakamoto, Kenta Watanabe, Kimitaka Kaga, Tatsuya YamasobaAbstract:Age-related changes were examined in the distribution and severity of spontaneous lesions in the Neuroepithelium and Bowman’s glands in mouse olfactory mucosa. The olfactory mucosa of female ICR mice at postnatal ages from 10 days to 16 months were investigated histologically by hematoxylin and eosin staining, high-iron diamine-Alcian blue (HID-AB) staining, and immunohistochemistry for olfactory marker protein (OMP), βIII tubulin (βIIIT), and Ki67. The lesions in the Neuroepithelium and Bowman’s glands were quantitatively assessed by morphometric analyses of sections stained with anti-OMP antibody or HID-AB. The first appearance of neuroepithelial abnormality was observed in the dorsomedial portion of the olfactory mucosa in 5-month-old mice. The distribution and severity of lesions progressed with increasing age. In mildly affected epithelium in which OMP-positive olfactory receptor neurons (ORNs) were present but in smaller amounts, the numbers of βIIIT-positive and Ki67-positive neuroepithelial cells tended to be increased, indicating that neurogenesis was upregulated in these areas. In contrast, severely affected epithelium in which OMP-positive ORNs were virtually absent showed high variability in the numbers of βIIIT- and Ki67-positive cells among the areas examined, probably reflecting differences in the capacity of the basal cells remaining in the affected area to generate new neuronal cells. Histological analysis with HID-AB revealed that spontaneous lesions in Bowman’s glands also occurred in aged mouse olfactory mucosa. Lesions in the Neuroepithelium and underlying Bowman’s glands tended to be spatially co-localized, suggesting a close association between pathogeneses in these two structures. Moreover, lesions in Bowman’s glands were associated with changes in the biochemical composition of mucus on the olfactory mucosa. This information should prove useful in improving the understanding of the pathogenetic mechanisms underlying age-related changes in the peripheral olfactory system.
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distribution and severity of spontaneous lesions in the Neuroepithelium and bowman s glands in mouse olfactory mucosa age related progression
Cell and Tissue Research, 2009Co-Authors: Kenji Kondo, Ken-ichi Nibu, Keigo Suzukawa, Takashi Sakamoto, Kenta Watanabe, Kimitaka Kaga, Tatsuya YamasobaAbstract:Age-related changes were examined in the distribution and severity of spontaneous lesions in the Neuroepithelium and Bowman’s glands in mouse olfactory mucosa. The olfactory mucosa of female ICR mice at postnatal ages from 10 days to 16 months were investigated histologically by hematoxylin and eosin staining, high-iron diamine-Alcian blue (HID-AB) staining, and immunohistochemistry for olfactory marker protein (OMP), βIII tubulin (βIIIT), and Ki67. The lesions in the Neuroepithelium and Bowman’s glands were quantitatively assessed by morphometric analyses of sections stained with anti-OMP antibody or HID-AB. The first appearance of neuroepithelial abnormality was observed in the dorsomedial portion of the olfactory mucosa in 5-month-old mice. The distribution and severity of lesions progressed with increasing age. In mildly affected epithelium in which OMP-positive olfactory receptor neurons (ORNs) were present but in smaller amounts, the numbers of βIIIT-positive and Ki67-positive neuroepithelial cells tended to be increased, indicating that neurogenesis was upregulated in these areas. In contrast, severely affected epithelium in which OMP-positive ORNs were virtually absent showed high variability in the numbers of βIIIT- and Ki67-positive cells among the areas examined, probably reflecting differences in the capacity of the basal cells remaining in the affected area to generate new neuronal cells. Histological analysis with HID-AB revealed that spontaneous lesions in Bowman’s glands also occurred in aged mouse olfactory mucosa. Lesions in the Neuroepithelium and underlying Bowman’s glands tended to be spatially co-localized, suggesting a close association between pathogeneses in these two structures. Moreover, lesions in Bowman’s glands were associated with changes in the biochemical composition of mucus on the olfactory mucosa. This information should prove useful in improving the understanding of the pathogenetic mechanisms underlying age-related changes in the peripheral olfactory system.
Thomas E Willnow - One of the best experts on this subject based on the ideXlab platform.
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lrp2 megalin is required for patterning of the ventral telencephalon
Development, 2005Co-Authors: Robert Spoelgen, Uwe Anzenberger, Dietmar Zechner, Olav M Andersen, Boris Jerchow, Annette Hammes, Thomas E WillnowAbstract:Megalin is a low-density lipoprotein receptor-related protein (LRP2) expressed in the Neuroepithelium and the yolk sac of the early embryo. Absence of megalin expression in knockout mice results in holoprosencephaly, indicating an essential yet unidentified function in forebrain development. We used mice with complete or conditional megalin gene inactivation in the embryo to demonstrate that expression of megalin in the Neuroepithelium but not in the yolk sac is crucial for brain development. During early forebrain development, megalin deficiency leads to an increase in bone morphogenic protein (Bmp) 4 expression and signaling in the rostral dorsal Neuroepithelium, and a subsequent loss of sonic hedgehog (Shh) expression in the ventral forebrain. As a consequence of absent SHH activity, ventrally derived oligodendroglial and interneuronal cell populations are lost in the forebrain of megalin-/- embryos. Similar defects are seen in models with enhanced signaling through BMPs, central regulators of neural tube patterning. Because megalin mediates endocytic uptake and degradation of BMP4, these findings indicate a role for megalin in neural tube specification, possibly by acting as BMP4 clearance receptor in the Neuroepithelium.
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LRP2/megalin is required for patterning of the ventral telencephalon
Development, 2005Co-Authors: Robert Spoelgen, Uwe Anzenberger, Dietmar Zechner, Olav M Andersen, Boris Jerchow, Annette Hammes, Thomas E WillnowAbstract:Megalin is a low-density lipoprotein receptor-related protein (LRP2) expressed in the Neuroepithelium and the yolk sac of the early embryo. Absence of megalin expression in knockout mice results in holoprosencephaly, indicating an essential yet unidentified function in forebrain development. We used mice with complete or conditional megalin gene inactivation in the embryo to demonstrate that expression of megalin in the Neuroepithelium but not in the yolk sac is crucial for brain development. During early forebrain development, megalin deficiency leads to an increase in bone morphogenic protein (Bmp) 4 expression and signaling in the rostral dorsal Neuroepithelium, and a subsequent loss of sonic hedgehog (Shh) expression in the ventral forebrain. As a consequence of absent SHH activity, ventrally derived oligodendroglial and interneuronal cell populations are lost in the forebrain of megalin-/- embryos. Similar defects are seen in models with enhanced signaling through BMPs, central regulators of neural tube patterning. Because megalin mediates endocytic uptake and degradation of BMP4, these findings indicate a role for megalin in neural tube specification, possibly by acting as BMP4 clearance receptor in the Neuroepithelium.
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defective forebrain development in mice lacking gp330 megalin
Proceedings of the National Academy of Sciences of the United States of America, 1996Co-Authors: Thomas E Willnow, Jan Hilpert, Scott A Armstrong, Astrid Rohlmann, Robert E Hammer, Dennis K Burns, Joachim HerzAbstract:gp330/megalin, a member of the low density lipoprotein (LDL) receptor gene family, is expressed on the apical surfaces of epithelial tissues, including the Neuroepithelium, where it mediates the endocytic uptake of diverse macromolecules, such as cholesterol-carrying lipoproteins, proteases, and antiproteinases. Megalin knockout mice manifest abnormalities in epithelial tissues including lung and kidney that normally express the protein and they die perinatally from respiratory insufficiency. In brain, impaired proliferation of Neuroepithelium produces a holoprosencephalic syndrome, characterized by lack of olfactory bulbs, forebrain fusion, and a common ventricular system. Similar syndromes in humans and animals are caused by insufficient supply of cholesterol during development. Because megalin can bind lipoproteins, we propose that the receptor is part of the maternal-fetal lipoprotein transport system and mediates the endocytic uptake of essential nutrients in the postgastrulation stage.
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Defective forebrain development in mice lacking gp330/megalin
Proceedings of the National Academy of Sciences of the United States of America, 1996Co-Authors: Thomas E Willnow, Jan Hilpert, Scott A Armstrong, Astrid Rohlmann, Robert E Hammer, Dennis K Burns, Joachim HerzAbstract:gp330/megalin, a member of the low density lipoprotein (LDL) receptor gene family, is expressed on the apical surfaces of epithelial tissues, including the Neuroepithelium, where it mediates the endocytic uptake of diverse macromolecules, such as cholesterol-carrying lipoproteins, proteases, and antiproteinases. Megalin knockout mice manifest abnormalities in epithelial tissues including lung and kidney that normally express the protein and they die perinatally from respiratory insufficiency. In brain, impaired proliferation of Neuroepithelium produces a holoprosencephalic syndrome, characterized by lack of olfactory bulbs, forebrain fusion, and a common ventricular system. Similar syndromes in humans and animals are caused by insufficient supply of cholesterol during development. Because megalin can bind lipoproteins, we propose that the receptor is part of the maternal-fetal lipoprotein transport system and mediates the endocytic uptake of essential nutrients in the postgastrulation stage.
Yutaka Yoshida - One of the best experts on this subject based on the ideXlab platform.
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left right locomotor circuitry depends on rhoa driven organization of the Neuroepithelium in the developing spinal cord
The Journal of Neuroscience, 2012Co-Authors: Keiichi Katayama, Jennifer R Leslie, Richard A Lang, Yi Zheng, Yutaka YoshidaAbstract:RhoA is a key regulator of cytoskeletal dynamics with a variety of effects on cellular processes. Loss of RhoA in neural progenitor cells disrupts adherens junctions and causes disorganization of the Neuroepithelium in the developing nervous system. However, it remains essentially unknown how the loss of RhoA physiologically affects neural circuit formation. Here we show that proper neuroepithelial organization maintained by RhoA GTPase in both the ventral and dorsal spinal cord is critical for left–right locomotor behavior. We examined the roles of RhoA in the ventral and dorsal spinal cord by deleting the gene in neural progenitors using Olig2–Cre and Wnt1–Cre mice, respectively. RhoA-deleted neural progenitors in both mutants exhibit defects in the formation of apical adherens junctions and disorganization of the Neuroepithelium. Consequently, the ventricular zone and lumen of the dysplastic region are lost, causing the left and right sides of the gray matter to be directly connected. Furthermore, the dysplastic region lacks ephrinB3 expression at the midline that is required for preventing EphA4-expressing corticospinal neurons and spinal interneurons from crossing the midline. As a result, aberrant neuronal projections are observed in that region. Finally, both RhoA mutants develop a rabbit-like hopping gait. These results demonstrate that RhoA functions to maintain neuroepithelial structures in the developing spinal cord and that proper organization of the Neuroepithelium is required for appropriate left–right motor behavior.
Renata Basto - One of the best experts on this subject based on the ideXlab platform.
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The microcephaly protein Asp regulates Neuroepithelium morphogenesis by controlling the spatial distribution of myosin II
Nature Cell Biology, 2013Co-Authors: Maria A. Rujano, Luis Sanchez-pulido, Carole Pennetier, Renata BastoAbstract:The microcephaly protein ASPM is required for correct spindle positioning in neuroepithelial cells. Basto and colleagues demonstrate that, in addition to having a role in cell division, the fly ASPM orthologue Asp is important for the maintenance of Neuroepithelium integrity by mediating myosin II apico-basal polarity. Mutations in ASPM are the most frequent cause of microcephaly, a disorder characterized by reduced brain size at birth. ASPM is recognized as a major regulator of brain size, yet its role during neural development remains poorly understood. Moreover, the role of ASPM proteins in invertebrate brain morphogenesis has never been investigated. Here, we characterized the function of the Drosophila ASPM orthologue, Asp, and found that asp mutants present severe defects in brain size and Neuroepithelium morphogenesis. We show that size reduction depends on the mitotic function of Asp, whereas regulation of tissue shape depends on an uncharacterized function. Asp interacts with myosin II regulating its polarized distribution along the apico-basal axis. In the absence of Asp, mislocalization of myosin II results in interkinetic nuclear migration and tissue architecture defects. We propose that Asp regulates Neuroepithelium morphogenesis through myosin-II-mediated structural and mechanical processes to maintain force balance and tissue cohesiveness.
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the microcephaly protein asp regulates Neuroepithelium morphogenesis by controlling the spatial distribution of myosin ii
Nature Cell Biology, 2013Co-Authors: Maria A. Rujano, Carole Pennetier, Luis Sanchezpulido, Renata BastoAbstract:Mutations in ASPM are the most frequent cause of microcephaly, a disorder characterized by reduced brain size at birth. ASPM is recognized as a major regulator of brain size, yet its role during neural development remains poorly understood. Moreover, the role of ASPM proteins in invertebrate brain morphogenesis has never been investigated. Here, we characterized the function of the Drosophila ASPM orthologue, Asp, and found that asp mutants present severe defects in brain size and Neuroepithelium morphogenesis. We show that size reduction depends on the mitotic function of Asp, whereas regulation of tissue shape depends on an uncharacterized function. Asp interacts with myosin II regulating its polarized distribution along the apico-basal axis. In the absence of Asp, mislocalization of myosin II results in interkinetic nuclear migration and tissue architecture defects. We propose that Asp regulates Neuroepithelium morphogenesis through myosin-II-mediated structural and mechanical processes to maintain force balance and tissue cohesiveness.
Kenji Kondo - One of the best experts on this subject based on the ideXlab platform.
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Caloric restriction reduces basal cell proliferation and results in the deterioration of neuroepithelial regeneration following olfactotoxic mucosal damage in mouse olfactory mucosa
Cell and Tissue Research, 2019Co-Authors: Hitoshi Iwamura, Kenji Kondo, Keigo Suzukawa, Shu Kikuta, Hironobu Nishijima, Ryoji Kagoya, Mizuo Ando, Chisato Fujimoto, Makiko Toma-hirano, Tatsuya YamasobaAbstract:The effects of caloric restriction (CR) on cell dynamics and gene expression in the mouse olfactory Neuroepithelium are evaluated. Eight-week-old male C57BL/6 mice were fed either control pellets (104 kcal/week) or CR pellets (67 kcal/week). The cytoarchitecture of the olfactory Neuroepithelium in the uninjured condition and its regeneration after injury by an olfactotoxic chemical, methimazole, were compared between mice fed with the control and CR diets. In the uninjured condition, there were significantly fewer olfactory marker protein (OMP)-positive olfactory receptor neurons and Ki67-positive proliferating basal cells at 3 months in the CR group than in the control group. The number of Ki67-positive basal cells increased after methimazole-induced mucosal injury in both the control and the CR groups, but the increase was less robust in the CR group. The recovery of the Neuroepithelium at 2 months after methimazole administration was less complete in the CR group than in the control group. These histological changes were region-specific. The decrease in the OMP-positive neurons was prominent in the anterior region of the olfactory mucosa. Gene expression analysis using a DNA microarray and quantitative real-time polymerase chain reaction demonstrated that the expression levels of two inflammatory cytokines, interleukin-6 and chemokine ligand 1, were elevated in the olfactory mucosa of the CR group compared with the control group. These findings suggest that CR may be disadvantageous to the maintenance of the olfactory Neuroepithelium, especially when it is injured.
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innate immune responses and neuroepithelial degeneration and regeneration in the mouse olfactory mucosa induced by intranasal administration of poly i c
Cell and Tissue Research, 2014Co-Authors: Kaori Kanaya, Kenji Kondo, Keigo Suzukawa, Takashi Sakamoto, Shu Kikuta, Kazunari Okada, Tatsuya YamasobaAbstract:The pathogenesis of postviral olfactory disorder (PVOD) has not been fully elucidated. We investigated morphological changes and innate immune responses in the mouse olfactory mucosa induced by intranasal administration of polyinosinic-polycytidylic acid [Poly(I:C)], a synthetic analog of viral double-stranded RNA. Mice received three administrations of saline with or without Poly(I:C), once every 24 h. The olfactory mucosa was harvested at various intervals after the first administration (8 h, 3, 9 and 24 days). In the Poly(I:C) group, the number of apoptotic cells in the olfactory Neuroepithelium had increased at 8 h. At 9 days, the olfactory Neuroepithelium had severely degenerated and behavioral tests demonstrated that the mice showed signs of olfactory deterioration. At 24 days, the structure of the Neuroepithelium had regenerated almost completely. Regarding the innate immune responses, many neutrophils had infiltrated the olfactory Neuroepithelium at 8 h and had exuded into the nasal cavity by 3 days. Macrophages had also infiltrated the olfactory Neuroepithelium at 8 h although to a lesser extent, but they still remained in the Neuroepithelium at 24 days. Poly(I:C)-induced neuroepithelial damage was significantly inhibited by a neutrophil elastase inhibitor and was suppressed in neutropenic model mice. These findings suggest that the secondary damage caused by the neutrophil-mediated innate immune response plays an important role in the pathogenesis of PVOD.
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age related changes in cell dynamics of the postnatal mouse olfactory Neuroepithelium cell proliferation neuronal differentiation and cell death
The Journal of Comparative Neurology, 2010Co-Authors: Kenji Kondo, Ken-ichi Nibu, Kaori Kanaya, Keigo Suzukawa, Takashi Sakamoto, Kenta Watanabe, Munetaka Ushio, Takuhiro Yamaguchi, Kimitaka Kaga, Tatsuya YamasobaAbstract:Age-related changes in cell proliferation, neuronal differentiation, and cell death in mouse olfactory Neuroepithelium were investigated. Mice at the age of 10 days through 16 months were given a single injection of bromodeoxyuridine (BrdU). The olfactory mucosae were fixed at 9 timepoints ranging from 2 hours to 3 months after the injection and examined using double immunostaining for BrdU and olfactory marker protein (OMP), and double staining with terminal deoxynucleotidyl transferase-mediated biotinylated dUTP nick end labeling (TUNEL) and immunostaining for OMP. The number of BrdU-labeled cells/mm epithelial length initially increased, peaked at 2–3 days after the BrdU injection, then declined at each age. The number of BrdU- and TUNEL-labeled neuronal cells both decreased with increasing age, suggesting that the rates of both cell proliferation and cell death in the olfactory Neuroepithelium decrease with increasing age. Double-labeled cells for BrdU and OMP appeared at 7 days after injection in all age groups, suggesting that the time required for neuronal differentiation is broadly similar irrespective of age. In older age groups, smaller amounts of the newly produced cohort are integrated into the OMP-positive ORN population, and even once it is integrated it is eliminated from the population more rapidly compared to the younger age groups. Furthermore, TUNEL assay showed that the fraction of apoptotic cells distributed in the OMP-positive layer/total apoptotic cells decreased with age. This observation suggests that the turnover of mature ORNs is slower in the older Neuroepithelium compared to the younger Neuroepithelium. J. Comp. Neurol. 518:1962–1975, 2010. © 2010 Wiley-Liss, Inc.
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Distribution and severity of spontaneous lesions in the Neuroepithelium and Bowman’s glands in mouse olfactory mucosa: age-related progression
Cell and Tissue Research, 2009Co-Authors: Kenji Kondo, Ken-ichi Nibu, Keigo Suzukawa, Takashi Sakamoto, Kenta Watanabe, Kimitaka Kaga, Tatsuya YamasobaAbstract:Age-related changes were examined in the distribution and severity of spontaneous lesions in the Neuroepithelium and Bowman’s glands in mouse olfactory mucosa. The olfactory mucosa of female ICR mice at postnatal ages from 10 days to 16 months were investigated histologically by hematoxylin and eosin staining, high-iron diamine-Alcian blue (HID-AB) staining, and immunohistochemistry for olfactory marker protein (OMP), βIII tubulin (βIIIT), and Ki67. The lesions in the Neuroepithelium and Bowman’s glands were quantitatively assessed by morphometric analyses of sections stained with anti-OMP antibody or HID-AB. The first appearance of neuroepithelial abnormality was observed in the dorsomedial portion of the olfactory mucosa in 5-month-old mice. The distribution and severity of lesions progressed with increasing age. In mildly affected epithelium in which OMP-positive olfactory receptor neurons (ORNs) were present but in smaller amounts, the numbers of βIIIT-positive and Ki67-positive neuroepithelial cells tended to be increased, indicating that neurogenesis was upregulated in these areas. In contrast, severely affected epithelium in which OMP-positive ORNs were virtually absent showed high variability in the numbers of βIIIT- and Ki67-positive cells among the areas examined, probably reflecting differences in the capacity of the basal cells remaining in the affected area to generate new neuronal cells. Histological analysis with HID-AB revealed that spontaneous lesions in Bowman’s glands also occurred in aged mouse olfactory mucosa. Lesions in the Neuroepithelium and underlying Bowman’s glands tended to be spatially co-localized, suggesting a close association between pathogeneses in these two structures. Moreover, lesions in Bowman’s glands were associated with changes in the biochemical composition of mucus on the olfactory mucosa. This information should prove useful in improving the understanding of the pathogenetic mechanisms underlying age-related changes in the peripheral olfactory system.
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distribution and severity of spontaneous lesions in the Neuroepithelium and bowman s glands in mouse olfactory mucosa age related progression
Cell and Tissue Research, 2009Co-Authors: Kenji Kondo, Ken-ichi Nibu, Keigo Suzukawa, Takashi Sakamoto, Kenta Watanabe, Kimitaka Kaga, Tatsuya YamasobaAbstract:Age-related changes were examined in the distribution and severity of spontaneous lesions in the Neuroepithelium and Bowman’s glands in mouse olfactory mucosa. The olfactory mucosa of female ICR mice at postnatal ages from 10 days to 16 months were investigated histologically by hematoxylin and eosin staining, high-iron diamine-Alcian blue (HID-AB) staining, and immunohistochemistry for olfactory marker protein (OMP), βIII tubulin (βIIIT), and Ki67. The lesions in the Neuroepithelium and Bowman’s glands were quantitatively assessed by morphometric analyses of sections stained with anti-OMP antibody or HID-AB. The first appearance of neuroepithelial abnormality was observed in the dorsomedial portion of the olfactory mucosa in 5-month-old mice. The distribution and severity of lesions progressed with increasing age. In mildly affected epithelium in which OMP-positive olfactory receptor neurons (ORNs) were present but in smaller amounts, the numbers of βIIIT-positive and Ki67-positive neuroepithelial cells tended to be increased, indicating that neurogenesis was upregulated in these areas. In contrast, severely affected epithelium in which OMP-positive ORNs were virtually absent showed high variability in the numbers of βIIIT- and Ki67-positive cells among the areas examined, probably reflecting differences in the capacity of the basal cells remaining in the affected area to generate new neuronal cells. Histological analysis with HID-AB revealed that spontaneous lesions in Bowman’s glands also occurred in aged mouse olfactory mucosa. Lesions in the Neuroepithelium and underlying Bowman’s glands tended to be spatially co-localized, suggesting a close association between pathogeneses in these two structures. Moreover, lesions in Bowman’s glands were associated with changes in the biochemical composition of mucus on the olfactory mucosa. This information should prove useful in improving the understanding of the pathogenetic mechanisms underlying age-related changes in the peripheral olfactory system.