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James E. Schwob - One of the best experts on this subject based on the ideXlab platform.
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primary cilia on horizontal basal cells regulate regeneration of the Olfactory Epithelium
The Journal of Neuroscience, 2015Co-Authors: Ariell M Joiner, James E. Schwob, Warren W Green, Jeremy C Mcintyre, Benjamin L Allen, Jeffrey R MartensAbstract:The Olfactory Epithelium (OE) is one of the few tissues to undergo constitutive neurogenesis throughout the mammalian lifespan. It is composed of multiple cell types including Olfactory sensory neurons (OSNs) that are readily replaced by two populations of basal stem cells, frequently dividing globose basal cells and quiescent horizontal basal cells (HBCs). However, the precise mechanisms by which these cells mediate OE regeneration are unclear. Here, we show for the first time that the HBC subpopulation of basal stem cells uniquely possesses primary cilia that are aligned in an apical orientation in direct apposition to sustentacular cell end feet. The positioning of these cilia suggests that they function in the detection of growth signals and/or differentiation cues. To test this idea, we generated an inducible, cell type-specific Ift88 knock-out mouse line ( K5rtTA;tetOCre;Ift88fl/fl ) to disrupt cilia formation and maintenance specifically in HBCs. Surprisingly, the loss of HBC cilia did not affect the maintenance of the adult OE but dramatically impaired the regeneration of OSNs following lesion. Furthermore, the loss of cilia during development resulted in a region-specific decrease in neurogenesis, implicating HBCs in the establishment of the OE. Together, these results suggest a novel role for primary cilia in HBC activation, proliferation, and differentiation. SIGNIFICANCE STATEMENT We show for the first time the presence of primary cilia on a quiescent population of basal stem cells, the horizontal basal cells (HBCs), in the Olfactory Epithelium (OE). Importantly, our data demonstrate that cilia on HBCs are necessary for regeneration of the OE following injury. Moreover, the disruption of HBC cilia alters neurogenesis during the development of the OE, providing evidence that HBCs participate in the establishment of this tissue. These data suggest that the mechanisms of penetrance for ciliopathies in the OE extend beyond that of defects in Olfactory sensory neurons and may include alterations in OE maintenance and regeneration.
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progenitor cell capacity of neurod1 expressing globose basal cells in the mouse Olfactory Epithelium
The Journal of Comparative Neurology, 2011Co-Authors: Adam Packard, Andrew B Leiter, Maryann Gielmoloney, James E. SchwobAbstract:The basic helix-loop-helix transcription factor NeuroD1 is expressed in embryonic and adult mouse Olfactory Epithelium (OE), as well as during epithelial regeneration, suggesting that it plays an important role in Olfactory neurogenesis. We characterized NEUROD1-expressing progenitors, determined their progeny in the adult OE, and identified a subtle phenotype in ΔNeuroD1-knockout mice. All Olfactory sensory neurons (OSNs) derive from a NeuroD1-expressing progenitor as shown by recombination-mediated lineage tracing, as do other sensory receptors of the nose, including vomeronasal, nasal septal, and Grunenberg ganglion neurons. NEUROD1-expressing cells are found among the globose basal cell population: they are actively proliferating and frequently coexpress Neurog1, but not the transit amplifying cell marker MASH1, nor the neuronal marker NCAM. As a consequence, NEUROD1-expressing globose basal cells are best classified as immediate neuronal precursors. In adolescent ΔNeuroD1-LacZ knock-in null mice the OE displays subtle abnormalities, as compared to wildtype and heterozygous littermates. In some areas of the OE, mature neurons are absent, or sparse, although those same areas retain immature OSNs and LacZ-expressing progenitors, albeit both of these populations are smaller than expected. Our results support the conclusion that most, if not all, nasal chemosensory neurons derive from NeuroD1-expressing globose basal cells of the immediate neuronal precursor variety. Moreover, elimination of NeuroD1 by gene knockout, while it does not disrupt initial OSN differentiation, does compromise the integrity of parts of the Olfactory Epithelium by altering proliferation, neuronal differentiation, or neuronal survival there.
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globose basal cells are required for reconstitution of Olfactory Epithelium after methyl bromide lesion
The Journal of Comparative Neurology, 2003Co-Authors: Woochan Jang, Steven L Youngentob, James E. SchwobAbstract:Despite a remarkable regenerative capacity, recovery of the mammalian Olfactory Epithelium can fail in severely injured areas, which subsequently reconstitute as aneuronal respiratory Epithelium (metaplasia). We contrasted the cellular response of areas of the rat Epithelium that recover as Olfactory after methyl bromide lesion with those undergoing respiratory metaplasia in order to identify stem cells that restore lesioned Epithelium as Olfactory. Ventral Olfactory Epithelium is at particular risk for metaplasia after lesion and patches of it are rendered acellular by methyl bromide exposure. In contrast, globose basal cells (GBCs, marked by staining with GBC-2) are preserved in surrounding ventral areas and uniformly throughout dorsal Epithelium, which consistently and completely recovers as Olfactory after lesion. Over the next few days, neurons reappear, but only in those areas in which GBCs are preserved and multiply. In contrast, parts of the Epithelium in which GBCs are destroyed are repopulated in part by Bowman's gland cells, which pile up above the basal lamina. Electron microscopy confirms the reciprocity between gland cells and globose basal cells. By 14 days after lesion, the areas that are undergoing metaplasia are repopulated by typical respiratory epithelial cells. As horizontal basal cells are eliminated from all parts of the ventral Epithelium, the data suggest that GBC-2(+) cells are ultimately responsible for regenerating Olfactory neuroEpithelium. In contrast, GLA-13(+) cells may give rise to respiratory metaplastic Epithelium where GBCs are eliminated. Thus, we support the idea that a subpopulation of GBCs is the neural stem cell of the Olfactory Epithelium.
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reconstitution of the rat Olfactory Epithelium after methyl bromide induced lesion
The Journal of Comparative Neurology, 1995Co-Authors: James E. Schwob, Steven L Youngentob, Renee C MezzaAbstract:The Olfactory Epithelium and its neuronal population are known to have a substantial capacity to recover after either direct injury or damage to the Olfactory nerve. However, the mechanisms underlying that capacity for recovery, and indeed the limits on the recovery process, are not well understood. The aim of this study is to describe in detail the way in which the Olfactory Epithelium reconstitutes after direct injury. Adult male rats were exposed to 330 ppm methyl bromide (MeBr) gas for a single 6-hour period. The exposure destroys all of the neurons and sustentacular cells in over 95% of the Olfactory Epithelium of food-restricted rats and in over 90% of the Epithelium in ad-libitum-fed rats of the same weight, yet substantial recovery of the Olfactory Epithelium occurs. In response to the lesion, cellular proliferation increases markedly beginning between 24 and 48 hours, peaks at 1 week, and persists at levels higher than the control level for more than 4 weeks after MeBr exposure. Even though proliferation accelerates promptly, the beginning of neuronal reconstitution is delayed; only a few immature neurons are observed 3 days after the lesion, yet they reappear in large numbers by the end of the first week. The first mature neurons emerge between 7 and 14 days after lesion and increase to near normal numbers by 4-6 weeks. In association with the restoration of the neuronal population, basal cell proliferation returns to control levels between 4 and 6 weeks after damage. Likewise, sustentacular cells, identifiable by anticytokeratin 18 labeling, reappear rapidly and reform a distinct lamina in the superficial aspect of the Epithelium. They closely resemble their counterparts in control Epithelium with regard to disposition and shape by 3 weeks after lesion and with regard to expression of Olfactory-specific cytochrome P450s by 8 weeks. Thus, most areas of the Epithelium are restored to a near normal appearance and cellular composition by the end of 8 weeks, suggesting that the MeBr paradigm for lesioning the Epithelium offers significant advantages over techniques such as Triton X-100 or ZnSO4 irrigation. However, not all measures of epithelial status are normal even at 8 weeks. Immature neurons remain slightly more numerous than normal at this time. Furthermore, some areas of the Olfactory Epithelium do not recover after MeBr lesion and are replaced by respiratory Epithelium.(ABSTRACT TRUNCATED AT 400 WORDS)
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cell cycle of globose basal cells in rat Olfactory Epithelium
Developmental Dynamics, 1995Co-Authors: Josee M T Huard, James E. SchwobAbstract:The Olfactory Epithelium of adult mammals has the unique property of generating Olfactory sensory neurons throughout life. Cells of the basal compartment, which include horizontal and globose basal cells, are responsible for the ongoing process of neurogenesis in this system. We report here that the globose basal cells in Olfactory Epithelium of rats, as in mice, are the predominant type of proliferating cell, and account for 97.6% of the actively dividing cells in the basal compartment of the normal Epithelium. Globose basal cells have not been fully characterized in terms of their proliferative properties, and the dynamic aspects of neurogenesis are not well understood. As a consequence, it is uncertain whether cell kinetic properties are under any regulation that could affect the rate of neurogenesis. To address this gap in our knowledge, we have determined the duration of both the synthesis phase (S-phase) and the full cell cycle of globose basal cells in adult rats. The duration of the S-phase was found to be 9 hr in experiments utilizing sequential injections of either IdU followed by BrdU or 3H-thy followed by BrdU. The duration of the cell cycle was determined by varying the time interval between the injections of 3H-thy and BrdU and tracking the set of cells that exit S shortly after the first injection. With this paradigm, the interval required for these cells to traverse G2, M, G1, and a second S-phase, is equivalent to the duration of one mitotic cycle and equals 17 hr. These observations serve as the foundation to assess whether the cell cycle duration is subject to regulation in response to experimental injury, and whether such regulation is partly responsible for changes in the rate of neurogenesis in such settings.
Diego Restrepo - One of the best experts on this subject based on the ideXlab platform.
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transcriptional profiling reveals trpm5 expressing cells involved in viral infection in the Olfactory Epithelium
bioRxiv, 2020Co-Authors: Eric D Larson, Laetitia Merle, Paul Feinstein, Arianna Gentile Polese, Andrew N Bubak, Christy S Niemeyer, Vijay R Ramakrishnan, Douglas P Shepherd, M Nagel, Diego RestrepoAbstract:Understanding viral infection of the Olfactory Epithelium is essential because smell loss can occur with coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus clade 2 (SARS-CoV-2), and because the Olfactory nerve is an important route of entry for viruses to the central nervous system. Specialized chemosensory epithelial cells that express the transient receptor potential cation channel subfamily M member 5 (TRPM5) are found throughout the airways and intestinal Epithelium and are involved in responses to viral infection. Herein we performed deep transcriptional profiling of Olfactory epithelial cells sorted by flow cytometry based on the expression of fluorescent protein markers for Olfactory sensory neurons and TRPM5. We find profuse expression of transcripts involved in inflammation, immunity and viral infection in TRPM5-expressing microvillous cells and Olfactory sensory neurons. These cells express the Tmprss2 transcript that encodes for a serine protease that primes the SARS-CoV-2 spike protein before entry into host cells. Our study provides new insights into a potential role for TRPM5-expressing cells in viral infection of the Olfactory Epithelium.
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trpm5 expressing microvillous cells in the main Olfactory Epithelium
BMC Neuroscience, 2008Co-Authors: Ejiofor Ad Ezekwe, Weihong Lin, Zhen Zhen Zhao, Emily R Liman, Diego RestrepoAbstract:The main Olfactory Epithelium (MOE) in the nasal cavity detects a variety of air borne molecules that provide information regarding the presence of food, predators and other relevant social and environmental factors. Within the Epithelium are ciliated sensory neurons, supporting cells, basal cells and microvillous cells, each of which is distinct in morphology and function. Arguably, the least understood, are the microvillous cells, a population of cells that are small in number and whose function is not known. We previously found that in a mouse strain in which the TRPM5 promoter drives expression of the green fluorescent protein (GFP), a population of ciliated Olfactory sensory neurons (OSNs), as well as a population of cells displaying microvilli-like structures is labeled. Here we examined the morphology and immunocytochemical properties of these microvillous-like cells using immunocytochemical methods. We show that the GFP-positive microvillous cells were morphologically diversified and scattered throughout the entire MOE. These cells immunoreacted to an antibody against TRPM5, confirming the expression of this ion channel in these cells. In addition, they showed a Ca2+-activated non-selective cation current in electrophysiological recordings. They did not immunoreact to antibodies that label cell markers and elements of the transduction pathways from Olfactory sensory neurons and solitary chemosensory cells of the nasal cavity. Further, the TRPM5-expressing cells did not display axon-like processes and were not labeled with a neuronal marker nor did trigeminal peptidergic nerve fibers innervate these cells. We provide morphological and immunocytochemical characterization of the TRPM5-expressing microvillous cells in the main Olfactory Epithelium. Our data demonstrate that these cells are non-neuronal and in terms of chemosensory transduction do not resemble the TRPM5-expressing Olfactory sensory neurons and nasal solitary chemosensory cells.
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heterogeneous expression of connexin 36 in the Olfactory Epithelium and glomerular layer of the Olfactory bulb
The Journal of Comparative Neurology, 2003Co-Authors: Chunbo Zhang, Diego RestrepoAbstract:Gap junctions regulate a variety of cell functions by directly connecting two cells through intercellular channels. Connexins are gap junction channel-forming protein subunits. In this study, we studied the expression of connexin 36 (Cx36) in the Olfactory Epithelium and Olfactory bulb of adult mice. In situ hybridization revealed that mRNA for Cx36 was expressed in the Olfactory sensory Epithelium, main Olfactory bulb and accessory Olfactory bulb. Expression of mRNA encoding Cx36 was observed in the Olfactory Epithelium mainly in ventral and lateral regions of the turbinates. Immunohistochemical determination of Cx36 protein expression showed sparse punctuate staining in the Olfactory epithelial layer. Intense Cx36-like immunostaining was found in the Olfactory nerve bundles underlying the Olfactory Epithelium and in the Olfactory nerve layer and glomerular layer of the Olfactory bulb. Mapping of the intensity of Cx36-like immunofluorescence in glomeruli throughout the main Olfactory bulb indicated a heterogeneous distribution. A set of approximately 50 glomeruli located in the anterior and posterior limits of the Olfactory bulb was more intensely labeled than other glomeruli. There was intense immunofluorescence signal in the glomerular layer of the accessory Olfactory bulb and in the vomeronasal nerve. β-Galactosidase distribution in the Olfactory Epithelium and Olfactory bulb in Cx36 knockout mice (Deans et al. [2001] Neuron 31:477–485) supported the findings with immunofluorescence. Cx36-like immunofluorescence was absent in the Olfactory nerve bundles in Cx36 knockout mice. The immunolocalization of Cx36 to the Olfactory and vomeronasal nerves, and a subset of Olfactory glomeruli suggest a functional role for Cx36 in odor coding. J. Comp. Neurol. 459:426–439, 2003. © 2003 Wiley-Liss, Inc.
Thomas Michiels - One of the best experts on this subject based on the ideXlab platform.
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ifn λ decreases murid herpesvirus 4 infection of the Olfactory Epithelium but fails to prevent virus reactivation in the vaginal mucosa
Viruses, 2019Co-Authors: Sophie Jacobs, Caroline Zeippen, Fanny Wavreil, Laurent Gillet, Thomas MichielsAbstract:Murid herpesvirus-4 (MuHV-4), a natural gammaherpesvirus of rodents, can infect the mouse through the nasal mucosa, where it targets sustentacular cells and Olfactory neurons in the Olfactory Epithelium before it propagates to myeloid cells and then to B cells in lymphoid tissues. After establishment of latency in B cells, viral reactivation occurs in the genital tract in 80% of female mice, which can lead to spontaneous sexual transmission to co-housed males. Interferon-lambda (IFN-λ) is a key player of the innate immune response at mucosal surfaces and is believed to limit the transmission of numerous viruses by acting on epithelial cells. We used in vivo plasmid-mediated IFN-λ expression to assess whether IFN-λ could prophylactically limit MuHV-4 infection in the Olfactory and vaginal mucosae. In vitro, IFN-λ decreased MuHV-4 infection in cells that overexpressed IFN-λ receptor 1 (IFNLR1). In vivo, prophylactic IFN-λ expression decreased infection of the Olfactory Epithelium but did not prevent virus propagation to downstream organs, such as the spleen where the virus establishes latency. In the Olfactory Epithelium, sustentacular cells readily responded to IFN-λ. In contrast, Olfactory neurons did not respond to IFN-λ, thus, likely allowing viral entry. In the female genital tract, columnar epithelial cells strongly responded to IFN-λ, as did most vaginal epithelial cells, although with some variation from mouse to mouse. IFN-λ expression, however, failed to prevent virus reactivation in the vaginal mucosa. In conclusion, IFN-λ decreased MuHV-4 replication in the upper respiratory Epithelium, likely by protecting the sustentacular epithelial cells, but it did not protect Olfactory neurons and failed to block virus reactivation in the genital mucosa.
Ping Wang - One of the best experts on this subject based on the ideXlab platform.
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expansion of murine and human Olfactory Epithelium mucosa colonies and generation of mature Olfactory sensory neurons under chemically defined conditions
Theranostics, 2021Co-Authors: Wenwen Ren, Ping Wang, Li Wang, Xiujuan Zhang, Xiaoyu Feng, Liujing Zhuang, Nan Jiang, Xicai SunAbstract:Olfactory dysfunctions, including hyposmia and anosmia, affect ~100 million people around the world and the underlying causes are not fully understood. Degeneration of Olfactory sensory neurons and incapacity of globose basal cells to generate Olfactory sensory neurons are found in elder people and patients with smell disorders. Thus, Olfactory stem cell may function as a promising tool to replace inactivated globose basal cells and to generate sensory neurons. Methods: We established clonal expansion of cells from the murine Olfactory Epithelium as well as colony growth from human Olfactory mucosa using Matrigel-based three-dimensional system. These colonies were characterized by immunostaining against Olfactory Epithelium cellular markers and by calcium imaging of responses to odors. Chemical addition was optimized to promote Lgr5 expression, colony growth and sensory neuron generation, tested by quantitative PCR and immunostaining against progenitor and neuronal markers. The differential transcriptomes in multiple signaling pathways between colonies under different base media and chemical cocktails were determined by RNA-Seq. Results: In defined culture media, we found that VPA and CHIR99021 induced the highest Lgr5 expression level, while LY411575 resulted in the most abundant yield of OMP+ mature sensory neurons in murine colonies. Different base culture media with drug cocktails led to apparent morphological alteration from filled to cystic appearance, accompanied with massive transcriptional changes in multiple signaling pathways. Generation of sensory neurons in human colonies was affected through TGF-β signaling, while Lgr5 expression and cell proliferation was regulated by VPA. Conclusion: Our findings suggest that targeting expansion of Olfactory Epithelium/mucosa colonies in vitro potentially results in discovery of new source to cell replacement-based therapy against smell loss.
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Olfactory Epithelium biosensor odor discrimination of receptor neurons from a bio hybrid sensing system
Biomedical Microdevices, 2012Co-Authors: Qingjun Liu, Fenni Zhang, Ping Wang, Diming Zhang, Jimmy K HsiaAbstract:Bio-hybrid systems provide an opportunity for integrating a living bio-active unit and a proper biosensing system, to employ the unique properties of the bio-active unit. The biological Olfactory system can sense and identify thousands of trace odors. The purpose of this study is to combine Olfactory Epithelium with microelectrode array (MEA) to establish an Olfactory Epithelium-MEA hybrid system to record the odor-induced electrophysiological activities of the tissue. In our experiments, extracellular potential of Olfactory receptor neurons in intact Epithelium were measured in the presence of ethyl ether, acetic acid, butanedione, and acetone, respectively. After the odor-induced response signals were analyzed in the time and frequency domain, the temporal characteristics of response signals were extracted. We found that Olfactory Epithelium-MEA hybrid system can reflect the in vitro odor information of different signal characteristics and firing modes in vitro. The bio-hybrid sensing system can represent a useful instrument to sense and detect the odorant molecules with well recognizing patterns. With the development of sensor technology, bio-hybrid systems will represent emerging and promising platforms for wide applications, ranging from health care to environmental monitoring.
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odors discrimination by Olfactory Epithelium biosensor
OLFACTION AND ELECTRONIC NOSE: PROCEEDINGS OF THE 14TH INTERNATIONAL SYMPOSIUM ON OLFACTION AND ELECTRONIC NOSE, 2011Co-Authors: Qingjun Liu, Fenni Zhang, Hua Wang, Ping WangAbstract:Humans are exploring the bionic biological olfaction to sense the various trace components of gas or liquid in many fields. For achieving the goal, we endeavor to establish a bioelectronic nose system for odor detection by combining intact bioactive function units with sensors. The bioelectronic nose is based on the Olfactory Epithelium of rat and microelectrode array (MEA). The Olfactory Epithelium biosensor generates extracellular potentials in presence of odor, and presents obvious specificity under different odors condition. The odor response signals can be distinguished with each other effectively by signal sorting. On basis of bioactive MEA hybrid system and the improved signal processing analysis, the bioelectronic nose will realize odor discrimination by the specific feature of signals response to various odors.
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extracellular potentials recording in intact Olfactory Epithelium by microelectrode array for a bioelectronic nose
Biosensors and Bioelectronics, 2010Co-Authors: Qingjun Liu, Ping Wang, Lidan XiaoAbstract:Abstract Human beings and animals have sensitive Olfactory systems that can sense and identify a variety of odors. The purpose of this study is to combine biological cells with micro-chips to establish a novel bioelectronic nose system for odor detection by electrophysiological sensing measurements of Olfactory tissue. In our experiments, 36-channel microelectrode arrays (MEAs) with the diameter of 30 μm were fabricated on the glass substrate, and Olfactory Epithelium was stripped from rats and fixed on the surface of MEA. Electrophysiological activities of Olfactory receptor neurons in intact Epithelium were measured through the multi-channel recording system. The extracellular potentials of cell networks could be effectively analyzed by correlation analysis between different channels. After being stimulated by odorants, such as acetic acid and butanedione, the Olfactory cells generate different firing modes. These firing characteristics can be derived by time-domain and frequency-domain analysis, and they were different from spontaneous potentials. The investigation of Olfactory Epithelium can provide more information of Olfactory system for artificial olfaction biomimetic design.
Weihong Lin - One of the best experts on this subject based on the ideXlab platform.
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skn 1a pou2f3 is required for the generation of trpm5 expressing microvillous cells in the mouse main Olfactory Epithelium
BMC Neuroscience, 2014Co-Authors: Tatsuya Yamaguchi, Weihong Lin, Junpei Yamashita, Makoto Ohmoto, Imad Aoude, Tatsuya Ogura, Wangmei Luo, Alexander A Bachmanov, Ichiro Matsumoto, Junji HirotaAbstract:The main Olfactory Epithelium (MOE) in mammals is a specialized organ to detect odorous molecules in the external environment. The MOE consists of four types of cells: Olfactory sensory neurons, supporting cells, basal cells, and microvillous cells. Among these, development and function of microvillous cells remain largely unknown. Recent studies have shown that a population of microvillous cells expresses the monovalent cation channel Trpm5 (transient receptor potential channel M5). To examine functional differentiation of Trpm5-expressing microvillous cells in the MOE, we investigated the expression and function of Skn-1a, a POU (Pit-Oct-Unc) transcription factor required for functional differentiation of Trpm5-expressing sweet, umami, and bitter taste bud cells in oropharyngeal Epithelium and solitary chemosensory cells in nasal respiratory Epithelium. Skn-1a is expressed in a subset of basal cells and apical non-neuronal cells in the MOE of embryonic and adult mice. Two-color in situ hybridization revealed that a small population of Skn-1a-expressing cells was co-labeled with Mash1/Ascl1 and that most Skn-1a-expressing cells coexpress Trpm5. To investigate whether Skn-1a has an irreplaceable role in the MOE, we analyzed Skn-1a-deficient mice. In the absence of Skn-1a, Olfactory sensory neurons differentiate normally except for a limited defect in terminal differentiation in ectoturbinate 2 of some of MOEs examined. In contrast, the impact of Skn-1a deficiency on Trpm5-expressing microvillous cells is much more striking: Trpm5, villin, and choline acetyltransferase, cell markers previously shown to identify Trpm5-expressing microvillous cells, were no longer detectable in Skn-1a-deficient mice. In addition, quantitative analysis demonstrated that the density of superficial microvillous cells was significantly decreased in Skn-1a-deficient mice. Skn-1a is expressed in a minority of Mash1-positive Olfactory progenitor cells and a majority of Trpm5-expressing microvillous cells in the main Olfactory Epithelium. Loss-of-function mutation of Skn-1a resulted in complete loss of Trpm5-expressing microvillous cells, whereas most of Olfactory sensory neurons differentiated normally. Thus, Skn-1a is a critical regulator for the generation of Trpm5-expressing microvillous cells in the main Olfactory Epithelium in mice.
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trpm5 expressing microvillous cells in the main Olfactory Epithelium
BMC Neuroscience, 2008Co-Authors: Ejiofor Ad Ezekwe, Weihong Lin, Zhen Zhen Zhao, Emily R Liman, Diego RestrepoAbstract:The main Olfactory Epithelium (MOE) in the nasal cavity detects a variety of air borne molecules that provide information regarding the presence of food, predators and other relevant social and environmental factors. Within the Epithelium are ciliated sensory neurons, supporting cells, basal cells and microvillous cells, each of which is distinct in morphology and function. Arguably, the least understood, are the microvillous cells, a population of cells that are small in number and whose function is not known. We previously found that in a mouse strain in which the TRPM5 promoter drives expression of the green fluorescent protein (GFP), a population of ciliated Olfactory sensory neurons (OSNs), as well as a population of cells displaying microvilli-like structures is labeled. Here we examined the morphology and immunocytochemical properties of these microvillous-like cells using immunocytochemical methods. We show that the GFP-positive microvillous cells were morphologically diversified and scattered throughout the entire MOE. These cells immunoreacted to an antibody against TRPM5, confirming the expression of this ion channel in these cells. In addition, they showed a Ca2+-activated non-selective cation current in electrophysiological recordings. They did not immunoreact to antibodies that label cell markers and elements of the transduction pathways from Olfactory sensory neurons and solitary chemosensory cells of the nasal cavity. Further, the TRPM5-expressing cells did not display axon-like processes and were not labeled with a neuronal marker nor did trigeminal peptidergic nerve fibers innervate these cells. We provide morphological and immunocytochemical characterization of the TRPM5-expressing microvillous cells in the main Olfactory Epithelium. Our data demonstrate that these cells are non-neuronal and in terms of chemosensory transduction do not resemble the TRPM5-expressing Olfactory sensory neurons and nasal solitary chemosensory cells.
