Relevant bibliographies by topics / Choroid Plexus Epithelium

Academic literature on the topic 'Choroid Plexus Epithelium'

Author: Grafiati
Published: 10 December 2022
Last updated: 29 January 2023

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Journal articles on the topic "Choroid Plexus Epithelium"

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Damkier, Helle H., Peter D. Brown, and Jeppe Praetorius. "Cerebrospinal Fluid Secretion by the Choroid Plexus." Physiological Reviews 93, no. 4 (October 2013): 1847–92. http://dx.doi.org/10.1152/physrev.00004.2013.

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The choroid plexus epithelium is a cuboidal cell monolayer, which produces the majority of the cerebrospinal fluid. The concerted action of a variety of integral membrane proteins mediates the transepithelial movement of solutes and water across the epithelium. Secretion by the choroid plexus is characterized by an extremely high rate and by the unusual cellular polarization of well-known epithelial transport proteins. This review focuses on the specific ion and water transport by the choroid plexus cells, and then attempts to integrate the action of specific transport proteins to formulate a model of cerebrospinal fluid secretion. Significant emphasis is placed on the concept of isotonic fluid transport across epithelia, as there is still surprisingly little consensus on the basic biophysics of this phenomenon. The role of the choroid plexus in the regulation of fluid and electrolyte balance in the central nervous system is discussed, and choroid plexus dysfunctions are described in a very diverse set of clinical conditions such as aging, Alzheimer's disease, brain edema, neoplasms, and hydrocephalus. Although the choroid plexus may only have an indirect influence on the pathogenesis of these conditions, the ability to modify epithelial function may be an important component of future therapies.
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Banizs, Boglarka, Peter Komlosi, Mark O. Bevensee, Erik M. Schwiebert, Phillip D. Bell, and Bradley K. Yoder. "Altered pHi regulation and Na+/HCO3− transporter activity in choroid plexus of cilia-defective Tg737orpk mutant mouse." American Journal of Physiology-Cell Physiology 292, no. 4 (April 2007): C1409—C1416. http://dx.doi.org/10.1152/ajpcell.00408.2006.

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Tg737 orpk mice have defects in cilia assembly and develop hydrocephalus in the perinatal period of life. Hydrocephalus is progressive and is thought to be initiated by abnormal ion and water transport across the choroid plexus epithelium. The pathology is further aggravated by the slow and disorganized beating of motile cilia on ependymal cells that contribute to decreased cerebrospinal fluid movement through the ventricles. Previously, we demonstrated that the hydrocephalus phenotype is associated with a marked increase in intracellular cAMP levels in choroid plexus epithelium, which is known to have regulatory effects on ion and fluid movement in many secretory epithelia. To evaluate whether the hydrocephalus in Tg737 orpk mutants is associated with defects in ion transport, we compared the steady-state pHi and Na+-dependent transport activities of isolated choroid plexus epithelium tissue from Tg737 orpk mutant and wild-type mice. The data indicate that Tg737 orpk mutant choroid plexus epithelium have lower pHi and higher Na+-dependent HCO3− transport activity compared with wild-type choroid plexus epithelium. In addition, wild-type choroid plexus epithelium could be converted to a mutant phenotype with regard to the activity of Na+-dependent HCO3− transport by addition of dibutyryl-cAMP and mutant choroid plexus epithelium toward the wild-type phenotype by inhibiting PKA activity with H-89. Together, these data suggest that cilia have an important role in regulating normal physiology of choroid plexus epithelium and that ciliary dysfunction in Tg737 orpk mutants disrupts a signaling pathway leading to elevated intracellular cAMP levels and aberrant regulation of pHi and ion transport activity.
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Kondziolka, Douglas, and Juan M. Bilbao. "An immunohistochemical study of neuroepithelial (colloid) cysts." Journal of Neurosurgery 71, no. 1 (July 1989): 91–97. http://dx.doi.org/10.3171/jns.1989.71.1.0091.

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✓ Monoclonal and polyclonal antisera were used against 12 cases of neuroepithelial (colloid) cysts to determine the specific antigenic profile of the cyst epithelium. Intermediate filament markers (cytokeratin, vimentin, neurofilament, and glial fibrillary acidic protein) and epithelial markers (epithelial membrane antigen and monoclonal antibody lu-5) demonstrated that colloid cyst epithelium has a unique antigenic profile in contrast to that of choroid plexus or glial tissue. Theories raised to explain the etiology of colloid cysts have included derivation from the embryonic paraphysis, detachments of developing neuroepithelium from the tela choroidea, and remnants of respiratory epithelium; a more recent theory suggests that these cysts are products of developing choroid plexus or ependyma. The present study shows that colloid cyst epithelium is distinct from that of choroid plexus or ependyma and therefore does not represent a product of their formation, nor does it represent a form of immature glia. This finding supports the conclusion that colloid cysts in any ventricular location represent a developmental anomaly of primitive neuroectoderm in the embryo, which remains unique from other products of neuroectodermal derivation.
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Damkier, Helle H., Henriette L. Christensen, Inga B. Christensen, Qi Wu, Robert A. Fenton, and Jeppe Praetorius. "The murine choroid plexus epithelium expresses the 2Cl−/H+ exchanger ClC-7 and Na+/H+ exchanger NHE6 in the luminal membrane domain." American Journal of Physiology-Cell Physiology 314, no. 4 (April 1, 2018): C439—C448. http://dx.doi.org/10.1152/ajpcell.00145.2017.

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The choroid plexus epithelium within the brain ventricles secretes the majority of the cerebrospinal fluid (CSF). The luminal Na+-K+-ATPase acts in concert with a host of other transport proteins to mediate efficient fluid secretion across the epithelium. The CSF contains little protein buffer, but the pH value seems nonetheless maintained within narrow limits, even when faced with acid-base challenges. The involvement of choroid plexus acid-base transporters in CSF pH regulation is highlighted by the expression of several acid-base transporters in the epithelium. The aim of the present study was to identify novel acid-base transporters expressed in the luminal membrane of the choroid plexus epithelium to pave the way for systematic investigations of each candidate transporter in the regulation of CSF pH. Mass spectrometry analysis of proteins from epithelial cells isolated by fluorescence-activated cell sorting identified the Cl−/H+ exchangers ClC-3, -4, -5, and -7 in addition to known choroid plexus acid-base transporters. RT-PCR on FACS isolated epithelial cells confirmed the expression of the corresponding mRNAs, as well as Na+/H+ exchanger NHE6 mRNA. Both NHE6 and ClC-7 were immunolocalized to the luminal plasma membrane domain of the choroid plexus epithelial cells. Dynamic imaging of intracellular pH and membrane potential changes in isolated choroid plexus epithelial cells demonstrated Cl− gradient-driven changes in intracellular pH and membrane potential that are consistent with Cl−/H+ exchange. In conclusion, we have detected for the first time NHE6 and ClC-7 in the choroid plexus, which are potentially involved in pH regulation of the CSF.
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Praetorius, Jeppe, and Søren Nielsen. "Distribution of sodium transporters and aquaporin-1 in the human choroid plexus." American Journal of Physiology-Cell Physiology 291, no. 1 (July 2006): C59—C67. http://dx.doi.org/10.1152/ajpcell.00433.2005.

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The choroid plexus epithelium secretes electrolytes and fluid in the brain ventricular lumen at high rates. Several channels and ion carriers have been identified as likely mediators of this transport in rodent choroid plexus. This study aimed to map several of these proteins to the human choroid plexus. Immunoperoxidase-histochemistry was employed to determine the cellular and subcellular localization of the proteins. The water channel, aquaporin (AQP) 1, was predominantly situated in the apical plasma membrane domain, although distinct basolateral and endothelial immunoreactivity was also observed. The Na+-K+-ATPase α1-subunit was exclusively localized apically in the human choroid plexus epithelial cells. Immunoreactivity for the Na+-K+-2Cl− cotransporter, NKCC1, was likewise confined to the apical plasma membrane domain of the epithelium. The Cl−/HCO3− exchanger, AE2, was localized basolaterally, as was the Na+-dependent Cl−/HCO3− exchanger, NCBE, and the electroneutral Na+-HCO3− cotransporter, NBCn1. No immunoreactivity was found toward the Na+-dependent acid/base transporters NHE1 or NBCe2. Hence, the human choroid plexus epithelium displays an almost identical distribution pattern of water channels and Na+ transporters as the rat and mouse choroid plexus. This general cross species pattern suggests central roles for these transporters in choroid plexus functions such as cerebrospinal fluid production.
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Praetorius, Jeppe, and Helle Hasager Damkier. "Transport across the choroid plexus epithelium." American Journal of Physiology-Cell Physiology 312, no. 6 (June 1, 2017): C673—C686. http://dx.doi.org/10.1152/ajpcell.00041.2017.

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The choroid plexus epithelium is a secretory epithelium par excellence. However, this is perhaps not the most prominent reason for the massive interest in this modest-sized tissue residing inside the brain ventricles. Most likely, the dominant reason for extensive studies of the choroid plexus is the identification of this epithelium as the source of the majority of intraventricular cerebrospinal fluid. This finding has direct relevance for studies of diseases and conditions with deranged central fluid volume or ionic balance. While the concept is supported by the vast majority of the literature, the implication of the choroid plexus in secretion of the cerebrospinal fluid was recently challenged once again. Three newer and promising areas of current choroid plexus-related investigations are as follows: 1) the choroid plexus epithelium as the source of mediators necessary for central nervous system development, 2) the choroid plexus as a route for microorganisms and immune cells into the central nervous system, and 3) the choroid plexus as a potential route for drug delivery into the central nervous system, bypassing the blood-brain barrier. Thus, the purpose of this review is to highlight current active areas of research in the choroid plexus physiology and a few matters of continuous controversy.
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Chiba, Yoichi, Ryuta Murakami, Koichi Matsumoto, Keiji Wakamatsu, Wakako Nonaka, Naoya Uemura, Ken Yanase, Masaki Kamada, and Masaki Ueno. "Glucose, Fructose, and Urate Transporters in the Choroid Plexus Epithelium." International Journal of Molecular Sciences 21, no. 19 (September 30, 2020): 7230. http://dx.doi.org/10.3390/ijms21197230.

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The choroid plexus plays a central role in the regulation of the microenvironment of the central nervous system by secreting the majority of the cerebrospinal fluid and controlling its composition, despite that it only represents approximately 1% of the total brain weight. In addition to a variety of transporter and channel proteins for solutes and water, the choroid plexus epithelial cells are equipped with glucose, fructose, and urate transporters that are used as energy sources or antioxidative neuroprotective substrates. This review focuses on the recent advances in the understanding of the transporters of the SLC2A and SLC5A families (GLUT1, SGLT2, GLUT5, GLUT8, and GLUT9), as well as on the urate-transporting URAT1 and BCRP/ABCG2, which are expressed in choroid plexus epithelial cells. The glucose, fructose, and urate transporters repertoire in the choroid plexus epithelium share similar features with the renal proximal tubular epithelium, although some of these transporters exhibit inversely polarized submembrane localization. Since choroid plexus epithelial cells have high energy demands for proper functioning, a decline in the expression and function of these transporters can contribute to the process of age-associated brain impairment and pathophysiology of neurodegenerative diseases.
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Fukuda, Hidekazu, Taku Hirata, Nobuhiro Nakamura, Akira Kato, Katsumasa Kawahara, Shigeo Wakabayashi, Min-Hwang Chang, Michael F. Romero, and Shigehisa Hirose. "Identification and properties of a novel variant of NBC4 (Na+/HCO3− co-transporter 4) that is predominantly expressed in the choroid plexus." Biochemical Journal 450, no. 1 (January 24, 2013): 179–87. http://dx.doi.org/10.1042/bj20121515.

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Secretion of HCO3− at the apical side of the epithelial cells of the choroid plexus is an essential step in the formation of cerebrospinal fluid. Anion conductance with a high degree of HCO3− permeability has been observed and suggested to be the major pathway for HCO3− transport across the apical membrane. Recently, it was found that NBC (Na+/HCO3− co-transporter) 4, an electrogenic member of the NBC family, was expressed in the choroid plexus. We found that a novel variant of the NBC4 [NBC4g/Slc4a5 (solute carrier family 4, sodium bicarbonate co-transporter, member 5)] is almost exclusively expressed in the apical membrane of rat choroid plexus epithelium at exceptionally high levels. RNA interference-mediated knockdown allowed the functional demonstration that NBC4g is the major player in the HCO3− transport across the apical membrane of the choroid plexus epithelium. When combined with a recent observation that in choroid plexus epithelial cells electrogenic NBC operates with a stoichiometry of 3:1, the results of the present study suggest that NBC4g mediates the efflux of HCO3− and contributes to cerebrospinal fluid production.
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Vargas, Teo, Desiree Antequera, Cristina Ugalde, Carlos Spuch, and Eva Carro. "Gelsolin Restores Aβ-Induced Alterations in Choroid Plexus Epithelium." Journal of Biomedicine and Biotechnology 2010 (2010): 1–7. http://dx.doi.org/10.1155/2010/805405.

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Histologically, Alzheimer's disease (AD) is characterized by senile plaques and cerebrovascular amyloid deposits. In previous studies we demonstrated that in AD patients, amyloid-β(Aβ) peptide also accumulates in choroid plexus, and that this process is associated with mitochondrial dysfunction and epithelial cell death. However, the molecular mechanisms underlying Aβaccumulation at the choroid plexus epithelium remain unclear. Aβclearance, from the brain to the blood, involves Aβcarrier proteins that bind to megalin, including gelsolin, a protein produced specifically by the choroid plexus epithelial cells. In this study, we show that treatment with gelsolin reduces Aβ-induced cytoskeletal disruption of blood-cerebrospinal fluid (CSF) barrier at the choroid plexus. Additionally, our results demonstrate that gelsolin plays an important role in decreasing Aβ-induced cytotoxicity by inhibiting nitric oxide production and apoptotic mitochondrial changes. Taken together, these findings make gelsolin an appealing tool for the prophylactic treatment of AD.
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Lach, Boleslaw, Bernd W. Scheithauer, Alistair Gregor, and Mark R. Wick. "Colloid cyst of the third ventricle." Journal of Neurosurgery 78, no. 1 (January 1993): 101–11. http://dx.doi.org/10.3171/jns.1993.78.1.0101.

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✓ In an effort to shed light upon the nature of the colloid cyst, the immunohistochemical properties of 21 examples of this lesion were compared with those of other neuraxial cysts and choroid plexus epithelium. The neuraxial cysts included the following: eight Rathke's cleft cysts, 25 pituitaries containing follicular cysts of the pars intermedia, and four enterogenous cysts. Fifteen examples of normal choroid plexus and 12 choroid plexus papillomas were studied as well. These lesions were examined for localization of the following antigens: cytokeratins, epithelial membrane antigen, secretory component, carcinoembryonic antigen, prealbumin, vimentin, glial fibrillary acidic protein (GFAP), S-100 protein, neuron-specific enolase, 68-kD neurofilament protein, chromogranin, serotonin, and lysozyme, and with Leu-7 monoclonal antibodies. Five colloid cysts were immunostained with monoclonal antibodies that were specific for Clara-cell antigens and surfactant, respectively. Sugar moieties were localized using Ulex europaeus I, and Ricinus communis agglutinin I lectins. All Rathke's cleft cysts and follicular cysts of the pars intermedia as well as three selected colloid cysts were examined for pituitary hormones. The epithelial cells of colloid and enterogenous cysts, as well as those lining follicular and Rathke's cleft cyst, showed uniformly strong reactivity for cytokeratins, epithelial membrane antigen, secretory component, and vimentin, and bound Ulex europaeus lectin. Occasional cells in colloid cysts were positive for Clara cell-specific antigens. Reaction for carcinoembryonic antigen was present on the apical surface of scattered cells of colloid, follicular, and Rathke's cleft cysts. Many cells of follicles in the pars intermedia as well as individual cells of five Rathke's cleft cysts were also immunoreactive for chromogranin, S-100 protein, GFAP, and pituitary hormones. Colloid and enterogenous cysts were negative for prealbumin, S-100 protein, GFAP, and neuron-specific enolase; in all but a few instances, they failed to bind Ricinus communis agglutinin. In contrast, normal choroid plexus and choroid plexus papillomas were positive for prealbumin, S-100 protein, neuron-specific enolase, cytokeratin, vimentin, and Ricinus communis agglutinin receptors; they lacked Ulex europaeus lectin, 56/66-kD cytokeratins, and epithelial membrane antigen. Unlike normal choroid plexus, choroid plexus papillomas were often GFAP-positive. All tissues studied were nonreactive for lysosome, serotonin, and neurofilament, and with Leu-7 antibodies. This study indicates that the immunophenotype of epithelium lining colloid cysts is similar to that of other cysts showing endodermal or ectodermal differentiation and to respiratory tract mucosa. Epithelium of colloid cysts is immunohistochemically different from that of normal or neoplastic choroid plexus. These findings indicate an endodermal rather than neuroepithelial nature for colloid cysts.
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Dissertations / Theses on the topic "Choroid Plexus Epithelium"

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Yang, Peter. "Central role for Sonic hedgehog-triggered pericytes in hindbrain choroid plexus development." Thesis, Harvard University, 2013. http://dissertations.umi.com/gsas.harvard:11225.

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The choroid plexus is an organ within each brain ventricle comprised of elaborate folds of epithelium (CPe) and vasculature. It performs numerous functions essential for brain development and health, including secretion of cerebrospinal fluid (CSF) and acting as the blood-CSF barrier. Functionality requires: (1) that CPe and vasculature develop in register and in close proximity, so that the CPe ensheaths the vasculature at a high surface area to volume ratio, which permits efficient CSF secretion; and (2) that CPe barrier integrity is sustained throughout choroid plexus expansion. Genetic experiments in mouse embryos have identified a central role for Sonic hedgehog (Shh) in coordinating these developmental challenges. Specifically, Shh is secreted by differentiated CPe and drives choroid plexus expansion. In the absence of Shh, a hypoplastic choroid plexus forms, which is deficient in CPe, vasculature, and villous folds. Two choroid plexus cell populations respond to Shh: (1) rhombic lip-resident CPe progenitor cells and (2) vascular pericytes. Here, I present evidence that canonical Shh signaling to CPe progenitors alone is insufficient to fully drive their proliferation at normal rates. Rather, Shh-triggered pericytes appear to secondarily boost CPe progenitor cell proliferation, in addition to acting in vascular development. Shh-triggered pericytes also appear necessary for formation of the characteristic folds of the choroid plexus. Thus, pericytes coordinate the expansion of choroid plexus epithelium and vasculature. Notch signaling was also explored and was found to inhibit the differentiation of CPe progenitors, maintaining them in a proliferative state. Notch activation in CPe progenitors leads to invaginated tubules from the overproliferating CPe progenitor domain, without associated vascular growth or villous folds. Folding morphogenesis may thus be regulated by vascular components such as pericytes, and require that vascular growth match CPe growth. To identify Shh-induced pericyte signaling programs that might underlie these developmental processes, expression profiling was performed on dsRed-labeled pericytes isolated from Shh-deficient versus wild-type choroid plexuses. Candidate genes, including several involved in lipid metabolism, were identified. Collectively, this work points to pericytes as central in orchestrating the coordinated elaboration of multiple choroid plexus cell types, producing the complex tissue architecture required for efficient CSF production.
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Hughes, Alexandra. "Mechanisms of volume regulation in murine choroid plexus epithelial cells." Thesis, University of Manchester, 2010. https://www.research.manchester.ac.uk/portal/en/theses/mechanisms-of-volume-regulation-in-murine-choroid-plexus-epithelial-cells(66cb068e-0e38-4773-83ca-a7867aaff66c).html.

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The choroid plexuses are largely responsible for cerebrospinal fluid (CSF) secretion and therefore play a fundamental role in brain homeostasis. The membrane proteins involved in CSF secretion are not fully known. Several electroneutral transporters have been identified by molecular methods in choroid plexus epithelial cells but there is a lack of functional data to support their expression making it impossible to elucidate their role in CSF secretion fully. The activity of many of these transporters can be observed in cell volume regulation. Thus, the main aim of the present study was to determine the ability of mammalian choroid plexus epithelial cells to regulate their volume in response to anisosmotic challenge and to investigate the transporters involved.Experiments were performed on cells isolated from the mouse fourth ventricle choroid plexus. Cells were isolated using a combination of manual perturbation, the enzyme dispase and a Ca2+ free incubation to disrupt tight junctions. Cell volume was measured using a video-imaging method. Cells used in this study were all of a similar morphology and had a mean volume of 0.71 pL.Cells exhibited a HCO3- dependent regulatory volume increase (RVI) in response to hypertonic challenge. Strong evidence is presented that the Na+/H+ exchanger (NHE1) and the Cl-/HCO3- exchanger (AE2) contribute to the RVI but the Na+K+2Cl- cotransporter (NKCC1) and the epithelial Na+ channel (ENaC) do not. Choroid plexus cells exhibit a HCO3- dependent regulatory volume decrease (RVD) in response to hypotonic challenge. The RVD was unaffected by DIOA (an inhibitor of KCC activity), the K+ channel inhibitors TEA+, Ba2+ or 4AP or the Cl- channel inhibitors DIDS or NPPB. However removal of extracellular Ca2+ completely abolished cell swelling in response to hypotonic challenge. This sensitivity of volume change to Ca2+ was specific to cell swelling as cell shrinkage in hypertonic artificial CSF was unaffected by removal of extracellular Ca2+.Thus functional evidence is presented to further elucidate the role of several proteins in the choroid plexus cell volume regulatory response to anisosmotic challenge.
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Gellrich, Dorothee [Verfasser], Horst [Akademischer Betreuer] Schroten, and Colin [Akademischer Betreuer] Mackenzie. "Bacterial invasion of Streptococcus suis in porcine choroid plexus epithelial cells / Dorothee Gellrich. Gutachter: Horst Schroten ; Colin MacKenzie." Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2012. http://d-nb.info/1025337557/34.

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Gregoriades, Jeannine Marie Crum. "Functions of the apical Na+/ K+/ 2Cl- Cotransporter 1 in choroid plexus epithelial cells." Wright State University / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=wright150367502359194.

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Preston, Daniel. "TRPV4 in the Choroid Plexus Epithelium: Pathway Analysis and Implications for Cerebrospinal Fluid Production." Thesis, 2019. http://hdl.handle.net/1805/21335.

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Indiana University-Purdue University Indianapolis (IUPUI)
Hydrocephalus is a disease characterized by an increase in cerebrospinal fluid (CSF) in the ventricles of the brain. This manifests as a result of either overproduction or underabsorption of CSF leading to increases in pressure, swelling and loss of brain matter. Current treatments for this disease include surgical interventions via the introduction of shunts or endoscopic third ventriculostomy, both of which aim to redirect flow of CSF in to another cavity for absorption. Limited pharmacotherapies are available in the treatment of hydrocephalus, and there exists a clinical need for drug therapies, which can ameliorate the pathophysiology associated with hydrocephalus and ventriculomegaly. CSF is produced primarily by the choroid plexus (CP), found in the ventricles of the brain. Composed of a high resistance epithelium surrounding a capillary network, the CP epithelium acts as a barrier, regulating ion transport between the CSF and blood. Transient Receptor Potential Vanilloid-4 (TRPV4) is a nonselective Ca2+-permeable cation channel expressed in the CP which is being investigated for its role in CSF production. To study hydrocephalus, we utilize two model systems; the TMEM67-/- Wpk rat, and the PCP-R cell line. The Wpk rat model is used to study the effects of drug intervention on the development and progression of hydrocephalus. The PCP-R cell line is utilized for studies which aim to understand the mechanisms by which CSF is produced. Using Ussing chamber electrophysiology, we are able to study the role of specific channels, transporters and modulators in driving epithelial ion flux across the CP. This research aims to establish a role for TRPV4 in production and regulation of CSF, and to interrogate a mechanism by which this ion transport occurs. The chapters that follow describe components of the pathway by which TRPV4 is activated and ion flux is stimulated.
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Costabile, Brianna Kay. "Structural and functional characterization of the retinol-binding protein receptor STRA6." Thesis, 2021. https://doi.org/10.7916/d8-07wx-8189.

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Vitamin A is an essential nutrient; it is not synthesized by mammals and therefore must be obtained through the diet. During times of fasting or dietary vitamin A insufficiency, retinol, the alcohol form of the vitamin is released from the liver, its main storage tissue, for circulation in complex with retinol-binding protein 4 (RBP) to provide an adequate supply to peripheral tissues. Stimulated by Retinoic Acid 6 (STRA6), the transmembrane RBP receptor, mediates retinol uptake across blood-tissue barriers such as the retinal pigment epithelium of the eye, the placenta and the choroid plexus of the brain. Our understanding as to how this protein functions has been greatly enhanced by the high-resolution 3D structure of zebrafish STRA6 in complex with calmodulin (CaM) solved by single-particle cryogenic-electron microscopy. However, the nature of the interaction of STRA6 with retinol remains unclear. Here, I present the high-resolution structures of zebrafish and sheep STRA6 reconstituted in nanodisc lipid bilayers in the presence and absence of retinol. The nanodisc reconstitution system has allowed us to study this protein in a close to physiological environment and examine its interaction with the cell membrane and relationship with its ligand, retinol. We also present the structure of sheep STRA6 in complex with human RBP. The structure of the STRA6-RBP complex confirms predictions in the literature as to the nature of the protein-protein interaction needed for retinol transport. Calcium-bound CaM is bound to STRA6 in the RBP-STRA6 structure, consistent with a regulatory role of this calcium binding protein in STRA6-RBP interaction. The analysis of the three states of STRA6 – pre, post and during interaction with retinol – provide unique insights into the mechanism of STRA6-mediated cellular retinol uptake.
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Books on the topic "Choroid Plexus Epithelium"

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Santos, Maria, Eric Bouffet, Carolyn Freeman, and Mark M. Souweidane. Choroid plexus tumours. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199651870.003.0006.

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Choroid plexus tumours are rare, intraventricular, primary central nervous system tumours derived from the choroid plexus epithelium. They occur predominantly in children and are classified based on histological criteria as choroid plexus papilloma, atypical choroid plexus papilloma, and choroid plexus carcinoma. Choroid plexus carcinomas can occur in the context of Li–Fraumeni syndrome, where the TP53 germline mutation predisposes patients to a wide range of neoplasms. Treatment of these tumours is challenging, due to their high vascularity and the young age of the patients. While surgery is the mainstay of treatment of all choroid plexus tumours, the exact role of adjuvant therapy, particularly in choroid plexus carcinoma, is still unclear. For incompletely resected tumours, there is evidence that neoadjuvant chemotherapy can facilitate second-look surgery and reduce the risk of intraoperative bleeding. However, the role of adjuvant radiation after complete resection remains unclear.
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Book chapters on the topic "Choroid Plexus Epithelium"

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Johnsen, Laura Øllegaard, Helle Hasager Damkier, and Jeppe Praetorius. "Ion Transport in the Choroid Plexus Epithelium." In Ion Transport Across Epithelial Tissues and Disease, 333–61. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-55310-4_10.

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Krstić, Radivoj V. "Surface Epithelia. Simple Cuboidal Epithelium from the Rat Choroid Plexus." In General Histology of the Mammal, 26–27. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70420-8_12.

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Steffensen, Annette B., and Thomas Zeuthen. "Cotransport of Water in the Choroid Plexus Epithelium: From Amphibians to Mammals." In Physiology in Health and Disease, 99–124. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0536-3_4.

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Menheniott, Trevelyan R., Marika Charalambous, and Andrew Ward. "Derivation of Primary Choroid Plexus Epithelial Cells from the Mouse." In Methods in Molecular Biology, 207–20. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-59745-019-5_15.

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Thanos, Christopher G., Briannan Bintz, and Dwaine F. Emerich. "Microencapsulated Choroid Plexus Epithelial Cell Transplants for Repair of the Brain." In Advances in Experimental Medicine and Biology, 80–91. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-5786-3_8.

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Monnot, Andrew D., and Wei Zheng. "Culture of Choroid Plexus Epithelial Cells and In Vitro Model of Blood–CSF Barrier." In Methods in Molecular Biology, 13–29. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-125-7_2.

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Wijdicks, Eelco F. M., and William D. Freeman. "Intracranial Pressure." In Mayo Clinic Critical and Neurocritical Care Board Review, edited by Eelco F. M. Wijdicks, James Y. Findlay, William D. Freeman, and Ayan Sen, 69–73. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780190862923.003.0008.

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Cerebrospinal fluid (CSF) fills the subarachnoid space, spinal canal, and ventricles of the brain. CSF is enclosed within the brain by the pial layer, ependymal cells lining the ventricles, and the epithelial surface of the choroid plexus, where it is largely produced. Choroid plexus is present throughout the ventricular system with the exception of the frontal and occipital horns of the lateral ventricle and the cerebral aqueduct. The vascular smooth muscle and the epithelium of the choroid plexus receive both sympathetic and parasympathetic input. In an adult, CSF is normally acellular. A normal spinal sample may contain up to 5 white blood cells (WBCs) or red blood cells (RBCs). CSF allows for a route of delivery and removal of nutrients, hormones, and transmitters for the brain.
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Conter, Cecile Faure, Didier Frappaz, Kristian W. Pajtler, and Stefan M. Pfister. "Other Central Nervous System Tumours of Childhood." In Oxford Textbook of Cancer in Children, 198–205. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198797210.003.0024.

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This chapter discusses a number of central nervous system (CNS) tumours of childhood. It details the diagnosis, radiology, molecular pathology, biology, and current treatment strategies for germ-cell tumours (both intracranial and extracranial) and craniopharyngiomas (WHO grade I tumours of the intra/suprasellar region). It also outlines the histopathology, molecular classification, risk stratification, surgery, and outlook for ependymomas. Ependymomas are the third most common paediatric tumour of the CNS, accounting for 10% of brain tumours in children. The chapter also covers choroid plexus tumours (CPT). These rare intraventricular neoplasms derive from the choroid plexus epithelium and represent 0.2% of all CNS neoplasms.
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Johnsen, Laura Ø., Kathrine A. Friis, and Helle H. Damkier. "Transport of ions across the choroid plexus epithelium." In Cerebrospinal Fluid and Subarachnoid Space, 257–71. Elsevier, 2023. http://dx.doi.org/10.1016/b978-0-12-819509-3.00010-9.

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Weaver, Charles E., Paul N. McMillan, John A. Duncan, Edward G. Stopa, and Conrad E. Johanson∗. "Hydrocephalus disorders: their biophysical and neuroendocrine impact on the choroid plexus epithelium." In Advances in Molecular and Cell Biology, 269–93. Elsevier, 2003. http://dx.doi.org/10.1016/s1569-2558(03)31012-4.

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Conference papers on the topic "Choroid Plexus Epithelium"

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Li, Li, Katie Picotte, Brian Westerhuis, and Haotian Zhao. "Abstract B3: Notch 1 signaling-induced choroid plexus tumor arises from epithelial progenitor via Sonic Hedgehog pathway." In Abstracts: AACR Special Conference: Pediatric Cancer at the Crossroads: Translating Discovery into Improved Outcomes; November 3-6, 2013; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.pedcan-b3.

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Zhao, Haotian, Li Li, and Katie Picotte. "Abstract 3095: Notch-induced choroid plexus tumor arises from epithelial progenitor and depends on sonic hedgehog signaling for growth." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3095.

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Cambianica, I., M. Bossi, P. Gasco, W. Gonzalez, J. M. Idee, G. Miserocchi, R. Rigolio, et al. "Targeting Cells With MR Imaging Probes: Cellular Interaction And Intracellular Magnetic Iron Oxide Nanoparticles Uptake In Brain Capillary Endothelial and Choroidal Plexus Epithelial Cells." In BONSAI PROJECT SYMPOSIUM: BREAKTHROUGHS IN NANOPARTICLES FOR BIO-IMAGING. AIP, 2010. http://dx.doi.org/10.1063/1.3505065.

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You might also be interested in the extended bibliographies on the topic 'Choroid Plexus Epithelium' for particular source types:
Journal articles
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