Journal articles: '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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10

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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Das, V. Shruthi, V. Prarthana Bhushan, and Charumathy Kathireshan. "Choroid plexus carcinoma: A case report." Indian Journal of Pathology and Oncology 9, no. 4 (December 15, 2022): 382–85. http://dx.doi.org/10.18231/j.ijpo.2022.093.

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Choroid plexus carcinoma is a rare aggressive malignant epithelial neoplasm (WHO grade III) arising from choroid plexus epithelium. It commonly occurs in children arising in lateral ventricles. This tumour has a tendency for recurrence and metastatic dissemination along cerebrospinal fluid (CSF) pathway. We report a case of 11 month old boy presenting with hydrocephalus, irritability and vomiting. Contrast enhanced computed tomography (CECT) brain and magnetic resonance imaging (MRI) brain with contrast revealed a mass lesion within right lateral ventricle and hydrocephalus. Surgical resection was done and the excised tissue was sent for cytology and histopathological examination and a diagnosis of choroid plexus carcinoma was made.

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Thomas, T., and M. Dziadek. "Capacity to form choroid plexus-like cells in vitro is restricted to specific regions of the mouse neural ectoderm." Development 117, no. 1 (January 1, 1993): 253–62. http://dx.doi.org/10.1242/dev.117.1.253.

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Neural ectoderm was dissected from 9.5-day and 8.5-day gestation mouse embryos and divided into forebrain, midbrain, hindbrain and spinal cord regions. Forebrain and hindbrain material from 9.5-day neural ectoderm was further divided into presumptive choroid plexus regions and regions that would normally form nervous tissue in vivo. All tissues were plated onto a basement membrane substratum for culture in vitro. It was found that explants of neural ectoderm that would normally form choroid plexus in vivo, readily differentiated to form choroid plexus-like cells in culture. Cells from hindbrain segments and forebrain regions, which would normally form nervous tissue, also had the potential to differentiate into cells resembling the choroid plexus epithelium in culture, provided that the normal cell-cell interactions were disrupted. Cells from the midbrain neuromeres of 9.5-day embryos, which do not form a choroid plexus in vivo, did not form this lineage in vitro. However, cells cultured from the earlier head-fold stage midbrain neural ectoderm could develop into choroid plexus epithelium. There was no evidence that neural ectoderm from the spinal cord had the developmental potential to form choroid plexus epithelial cells at either of these two developmental stages. These studies show that the restrictions in the potential of neural ectoderm stem cells to form different lineages proceeds according to morphological divisions that appear along the anterior-posterior axis during the early stages of brain development. These results suggest that the division of neural ectoderm into segments which contain discrete stem cell populations may be a general feature of the early phase of development of the central nervous system.

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Damkier, Helle H., Peter D. Brown, and Jeppe Praetorius. "Epithelial Pathways in Choroid Plexus Electrolyte Transport." Physiology 25, no. 4 (August 2010): 239–49. http://dx.doi.org/10.1152/physiol.00011.2010.

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A stable intraventricular milieu is crucial for maintaining normal neuronal function. The choroid plexus epithelium produces the cerebrospinal fluid and in doing so influences the chemical composition of the interstitial fluid of the brain. Here, we review the molecular pathways involved in transport of the electrolytes Na+, K+, Cl−, and HCO3− across the choroid plexus epithelium.

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Bouzinova, Elena V., Jeppe Praetorius, Leila V. Virkki, Søren Nielsen, Walter F. Boron, and Christian Aalkjaer. "Na+-dependent HCO3− uptake into the rat choroid plexus epithelium is partially DIDS sensitive." American Journal of Physiology-Cell Physiology 289, no. 6 (December 2005): C1448—C1456. http://dx.doi.org/10.1152/ajpcell.00313.2005.

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Several studies suggest the involvement of Na+ and HCO3− transport in the formation of cerebrospinal fluid. Two Na+-dependent HCO3− transporters were recently localized to the epithelial cells of the rat choroid plexus (NBCn1 and NCBE), and the mRNA for a third protein was also detected (NBCe2) (Praetorius J, Nejsum LN, and Nielsen S. Am J Physiol Cell Physiol 286: C601–C610, 2004). Our goal was to immunolocalize the NBCe2 to the choroid plexus by immunohistochemistry and immunogold electronmicroscopy and to functionally characterize the bicarbonate transport in the isolated rat choroid plexus by measurements of intracellular pH (pHi) using a dual-excitation wavelength pH-sensitive dye (BCECF). Both antisera derived from COOH-terminal and NH2-terminal NBCe2 peptides localized NBCe2 to the brush-border membrane domain of choroid plexus epithelial cells. Steady-state pHi in choroidal cells increased from 7.03 ± 0.02 to 7.38 ± 0.02 ( n = 41) after addition of CO2/HCO3− into the bath solution. This increase was Na+ dependent and inhibited by the Cl− and HCO3− transport inhibitor DIDS (200 μM). This suggests the presence of Na+-dependent, partially DIDS-sensitive HCO3− uptake. The pHi recovery after acid loading revealed an initial Na+ and HCO3−-dependent net base flux of 0.828 ± 0.116 mM/s ( n = 8). The initial flux in the presence of CO2/HCO3− was unaffected by DIDS. Our data support the existence of both DIDS-sensitive and -insensitive Na+- and HCO3−-dependent base loader uptake into the rat choroid plexus epithelial cells. This is consistent with the localization of the three base transporters NBCn1, Na+-driven Cl− bicarbonate exchanger, and NBCe2 in this tissue.

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Praetorius, J., L. N. Nejsum, and S. Nielsen. "A SCL4A10 gene product maps selectively to the basolateral plasma membrane of choroid plexus epithelial cells." American Journal of Physiology-Cell Physiology 286, no. 3 (March 2004): C601—C610. http://dx.doi.org/10.1152/ajpcell.00240.2003.

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The choroid plexus epithelium of the brain ventricular system produces the majority of the cerebrospinal fluid and thereby defines the ionic composition of the interstitial fluid in the brain. The transepithelial movement of Na+ and water in the choroid plexus depend on a yet-unidentified basolateral stilbene-sensitive [Formula: see text]-[Formula: see text] uptake protein. Reverse transcriptase-polymerase chain reaction (RT-PCR) analysis revealed the expression in the choroid plexus of SLC4A10 mRNA, which encodes a stilbene-sensitive [Formula: see text]-[Formula: see text] transporter. Anti-COOH-terminal antibodies were developed to determine the specific expression and localization of this [Formula: see text]-[Formula: see text] transport protein. Immunoblotting demonstrated antibody binding to a 180-kDa protein band from mouse and rat brain preparations enriched with choroid plexus. The immunoreactive band migrated as a 140-kDa protein after N-deglycosylation, consistent with the predicted molecular size of the SLC4A10 gene product. Bright-field immunohistochemistry and immunoelectron microscopy demonstrated strong labeling confined to the basolateral plasma membrane domain of the choroid plexus epithelium. Furthermore, the stilbene-insensitive [Formula: see text]-[Formula: see text] cotransporter, NBCn1, was also localized to the basolateral plasma membrane domain of the choroid plexus epithelium. Hence, we propose that the SLC4A10 gene product and NBCn1 both function as basolateral [Formula: see text] entry pathways and that the SLC4A10 gene product may be responsible for the stilbene-sensitive [Formula: see text]-[Formula: see text] uptake that is essential for cerebrospinal fluid production.

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Marrs, J. A., E. W. Napolitano, C. Murphy-Erdosh, R. W. Mays, L. F. Reichardt, and W. J. Nelson. "Distinguishing roles of the membrane-cytoskeleton and cadherin mediated cell-cell adhesion in generating different Na+,K(+)-ATPase distributions in polarized epithelia." Journal of Cell Biology 123, no. 1 (October 1, 1993): 149–64. http://dx.doi.org/10.1083/jcb.123.1.149.

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In simple epithelia, the distribution of ion transporting proteins between the apical or basal-lateral domains of the plasma membrane is important for determining directions of vectorial ion transport across the epithelium. In the choroid plexus, Na+,K(+)-ATPase is localized to the apical plasma membrane domain where it regulates sodium secretion and production of cerebrospinal fluid; in contrast, Na+,K(+)-ATPase is localized to the basal-lateral membrane of cells in the kidney nephron where it regulates ion and solute reabsorption. The mechanisms involved in restricting Na+,K(+)-ATPase distribution to different membrane domains in these simple epithelia are poorly understood. Previous studies have indicated a role for E-cadherin mediated cell-cell adhesion and membrane-cytoskeleton (ankyrin and fodrin) assembly in regulating Na+,K(+)-ATPase distribution in absorptive kidney epithelial cells. Confocal immunofluorescence microscopy reveals that in chicken and rat choroid plexus epithelium, fodrin, and ankyrin colocalize with Na+,K(+)-ATPase at the apical plasma membrane, but fodrin, ankyrin, and adducin also localize at the lateral plasma membrane where Na+,K(+)-ATPase is absent. Biochemical analysis shows that fodrin, ankyrin, and Na+,K(+)-ATPase are relatively resistant to extraction from cells in buffers containing Triton X-100. The fractions of Na+,K(+)-ATPase, fodrin, and ankyrin that are extracted from cells cosediment in sucrose gradients at approximately 10.5 S. Further separation of the 10.5 S peak of proteins by electrophoresis in nondenaturing polyacrylamide gels revealed that fodrin, ankyrin, and Na+,K(+)-ATPase comigrate, indicating that these proteins are in a high molecular weight complex similar to that found previously in kidney epithelial cells. In contrast, the anion exchanger (AE2), a marker protein of the basal-lateral plasma membrane in the choroid plexus, did not cosediment in sucrose gradients or comigrate in nondenaturing polyacrylamide gels with the complex of Na+,K(+)-ATPase, ankyrin, and fodrin. Ca(++)-dependent cell adhesion molecules (cadherins) were detected at lateral membranes of the choroid plexus epithelium and colocalized with a distinct fraction of ankyrin, fodrin, and adducin. Cadherins did not colocalize with Na+,K(+)-ATPase and were absent from the apical membrane. The fraction of cadherins that was extracted with buffers containing Triton X-100 cosedimented with ankyrin and fodrin in sucrose gradients and comigrated in nondenaturing gels with ankyrin and fodrin in a high molecular weight complex. Since a previous study showed that E-cadherin is an instructive inducer of Na+,K(+)-ATPase distribution, we examined protein distributions in fibroblasts transfected with B-cadherin, a prominent cadherin expressed in the choroid plexus epithelium.(ABSTRACT TRUNCATED AT 400 WORDS)

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Cornford, Eain M., John B. Varesi, Shigeyo Hyman, Raymond T. Damian, and Michael J. Raleigh. "Mitochondrial content of choroid plexus epithelium." Experimental Brain Research 116, no. 3 (October 6, 1997): 399–405. http://dx.doi.org/10.1007/pl00005768.

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Breeze, Robert E., J. Gordon McComb, Shigeyo Hyman, and Floyd H. Gilles. "CSF production in acute ventriculitis." Journal of Neurosurgery 70, no. 4 (April 1989): 619–22. http://dx.doi.org/10.3171/jns.1989.70.4.0619.

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✓ Clinically, there appears to be a significant reduction in cerebrospinal fluid (CSF) formation during acute ventriculitis — an observation that has not been well documented by experimental studies. To examine this phenomenon, an inoculum of Escherichia coli was injected into the lateral ventricles of New Zealand White rabbits. Approximately 18 hours later, the survivors (64%) underwent a 3-hour ventriculocisternal perfusion of carbon-14-dextran (MW 7 × 104) as a reference marker for CSF formation. On the average, CSF formation in this experimental group was reduced by one-half to two-thirds of normal, confirming the clinical observation. Histologically, the stroma of the choroid plexus was the site of an extensive inflammatory infiltrate. Meningitis, ependymitis, and focal encephalitis completed the picture. Vasculitis was not present in the choroid plexus. The epithelium of the choroid plexus underwent patchy cellular swelling or frank necrosis and destruction. It is postulated that the changes in the choroid plexus caused by the inflammatory process were responsible for the diminished CSF formation in this acute setting. Reduced choroidal blood flow and/or enterotoxin may play a role in these alterations.

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Philp, Nancy J., Heeyong Yoon, and Lorraine Lombardi. "Mouse MCT3 gene is expressed preferentially in retinal pigment and choroid plexus epithelia." American Journal of Physiology-Cell Physiology 280, no. 5 (May 1, 2001): C1319—C1326. http://dx.doi.org/10.1152/ajpcell.2001.280.5.c1319.

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Monocarboxylate transporters (MCTs) are a family of highly homologous membrane proteins that mediate the 1:1 transport of a proton and a lactate ion. In chicken, MCT3 is preferentially expressed in the retinal pigment epithelium (RPE). We have isolated the mouse MCT3 cDNA and gene and characterized the pattern of tissue expression. MCT3 is a single copy gene with a 1.8-kb transcript that encodes a protein with a predicted molecular mass of 51.5 kDa. Based on Northern hybridization analysis, MCT3 transcript was expressed in only two tissues: RPE and choroid plexus epithelium (CPE). The choroid plexus forms a barrier between the cerebrospinal fluid and fenestrated capillaries, similar to the organization of the RPE and choroidal vessels. Immunohistochemical staining demonstrated that MCT3 was restricted to the basolateral membranes of both epithelia but was more abundant in RPE than CPE. Differences in the level of protein expression were confirmed by Western blot analysis. The cloning of MCT3 identifies a specific transporter that could regulate lactate levels in fluid-bathing neuronal tissues.

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Hossain, Mohammad, Nazmin Ahmed, Narendra Shalike, Md Rokibul Islam, Soumen Samadder, Mohammad Shahnawaz Bari, and Satish Kumar Shah. "Choroid Plexus Papilloma with Dandy Walker Variant: Co-existence or Association- A Case Report." Bangladesh Medical Journal 46, no. 2 (February 14, 2019): 61–65. http://dx.doi.org/10.3329/bmj.v46i2.40222.

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Choroid plexus tumors are rare intracranial tumors which account for 0.4-0.6% of all brain tumors. Choroid plexus tumors represent a spectrum of neoplasms derived from papillary epithelium of normal choroid plexus, including well-differentiated papilloma (WHO grade I), intermediate form as atypical Choroid Plexus Papilloma (WHO grade II) and highly aggressive choroid plexus carcinomas (WHO grade III). Though rare, it is responsible for the communicating hydrocephalus in children due to overproduction of cerebrospinal fluid. Due to advances in molecular biology and better understanding of the tumorigenesis of choroid plexus papilloma, now it is established that several genetic syndromes and central nervous sytem abnormalities are associated with this tumor. Here, we reported a case of a 10 months old child who presented with sudden deterioration of consciousness level and after thorough evaluation, diagnosed as a case of Choroid Plexus Papilloma with Dandy Walker Variant. Till date, this is the first reported case of the association/ co-existence of such two conditions which needs further evaluation. Bangladesh Med J. 2017 May; 46 (2): 61-65

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TAMEGA, OISENYL JOSÉ, LUÍS FERNANDO TIRAPELLI, and SIDNEI PETRONI. "Scanning electron microscopy study of the choroid plexus in the monkey (Cebus apella apella)." Arquivos de Neuro-Psiquiatria 58, no. 3B (September 2000): 820–25. http://dx.doi.org/10.1590/s0004-282x2000000500005.

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The cells of the choroid plexus of the lateral ventricles of the monkey Cebus apella apella were examined through scanning electron microscopy at contributing to the description of such structures in primates. The animals were anesthetized previously with 3% hypnol intraperitoneally and after perfusion with 2.5% glutaraldehyde, samples of the choroid plexus were collected after exhibition of the central portion and inferior horn of the lateral ventricles. The ventricular surface of those cells presents globose form as well as fine interlaced protrusions named microvilli. Among those, it is observed the presence of some cilia. Resting on the choroid epithelial cells there is a variable number of free cells, with fine prolongations which extend from them. They are probably macrophages and have been compared to Kolmer cells or epiplexus cells, located on choroid epithelium. The choroid plexus of the encephalic lateral ventricles of the monkey Cebus apella apella at scanning electron microscopy is similar to that of other primates, as well as to that of other species of mammals mainly cats and rats, and also humans.

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Merve, Ashirwad, Xinyu Zhang, Nicola Pomella, Serena Acquati, Joerg Hoeck, Anaelle Dumas, Gabriel Rosser, et al. "Choroid plexus papillomas are induced by c-Myc overexpression in the choroid plexus via a T-cell inflammatory mechanism." Neuro-Oncology 21, Supplement_4 (October 2019): iv9—iv10. http://dx.doi.org/10.1093/neuonc/noz167.040.

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Abstract Choroid plexus tumours (CPT) account for up to 20% of brain tumours in children under 2 years of age. Histologically CPTs are classified into three categories - Choroid Plexus Papilloma (CPP), Atypical Choroid Plexus Papilloma (ACPP) and Choroid Plexus Carcinoma (CPC). Recent literature demonstrates that CPP and ACPP are molecularly distinct from CPC. Initial management for CPT include surgery followed by adjuvant therapy in selected patients. Currently there are no disease-specific chemotherapeutic agents available, possibly because of their rarity and paucity of faithful pre-clinical experimental models. In this study we show that c-Myc overexpression in the choroid plexus epithelium induces T-cell inflammation-dependent choroid plexus papillomas in a mouse model. We demonstrate that c-MYC is expressed in a substantial proportion of human choroid plexus tumours and that this subgroup of tumours is characterised by an inflammatory transcriptome and significant inflammatory infiltrates. We observed that triple transgenic compound mutant mouse model with c-Myc overexpression in an immune-suppressed background led to a decreased incidence of CPP and reduced tumour bulk. A reduced tumour size was also observed when c-Myc overexpressing mice were treated with anti-CD3 antibodies. Our data raise the possibility that benign choroid plexus tumours expressing c-MYC could be amenable to medical therapy with anti-inflammatory drugs.

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Baasch Christensen, Inga, Lei Cheng, Jonathan R. Brewer, Udo Bartsch, Robert A. Fenton, Helle H. Damkier, and Jeppe Praetorius. "Multiple Na,K-ATPase Subunits Colocalize in the Brush Border of Mouse Choroid Plexus Epithelial Cells." International Journal of Molecular Sciences 22, no. 4 (February 4, 2021): 1569. http://dx.doi.org/10.3390/ijms22041569.

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(1) Background: The unusual accumulation of Na,K-ATPase complexes in the brush border membrane of choroid plexus epithelial cells have intrigued researchers for decades. However, the full range of the expressed Na,K-ATPase subunits and their relation to the microvillus cytoskeleton remains unknown. (2) Methods: RT-PCR analysis, co-immunoprecipitation, native PAGE, mass spectrometry, and differential centrifugation were combined with high-resolution immunofluorescence histochemistry, proximity ligase assays, and stimulated emission depletion (STED) microscopy on mouse choroid plexus cells or tissues in order to resolve these issues. (3) Results: The choroid plexus epithelium expresses Na,K-ATPase subunits α1, α2, β1, β2, β3, and phospholemman. The α1, α2, β1, and β2, subunits are all localized to the brush border membrane, where they appear to form a complex. The ATPase complexes may stabilize in the brush border membrane via anchoring to microvillar actin indirectly through ankyrin-3 or directly via other co-precipitated proteins. Aquaporin 1 (AQP1) may form part of the proposed multi-protein complexes in contrast to another membrane protein, the Na-K-2Cl cotransporter 1 (NKCC1). NKCC1 expression seems necessary for full brush border membrane accumulation of the Na,K-ATPase in the choroid plexus. (4) Conclusion: A multitude of Na,K-ATPase subunits form molecular complexes in the choroid plexus brush border, which may bind to the cytoskeleton by various alternative actin binding proteins.

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REDZIC, Z., and M. SEGAL. "The structure of the choroid plexus and the physiology of the choroid plexus epithelium." Advanced Drug Delivery Reviews 56, no. 12 (October 14, 2004): 1695–716. http://dx.doi.org/10.1016/j.addr.2004.07.005.

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Young, Robin K., and Alice R. A. Villalobos. "Stress-induced stimulation of choline transport in cultured choroid plexus epithelium exposed to low concentrations of cadmium." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 306, no. 5 (March 1, 2014): R291—R303. http://dx.doi.org/10.1152/ajpregu.00252.2013.

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The choroid plexus epithelium forms the blood-cerebrospinal fluid barrier and accumulates essential minerals and heavy metals. Choroid plexus is cited as being a “sink” for heavy metals and excess minerals, serving to minimize accumulation of these potentially toxic agents in the brain. An understanding of how low doses of contaminant metals might alter transport of other solutes in the choroid plexus is limited. Using primary cultures of epithelial cells isolated from neonatal rat choroid plexus, our objective was to characterize modulation of apical uptake of the model organic cation choline elicited by low concentrations of the contaminant metal cadmium (CdCl2). At 50–1,000 nM, cadmium did not directly decrease or increase 30-min apical uptake of 10 μM [3H]choline. However, extended exposure to 250–500 nM cadmium increased [3H]choline uptake by as much as 75% without marked cytotoxicity. In addition, cadmium induced heat shock protein 70 and heme oxygenase-1 protein expression and markedly induced metallothionein gene expression. The antioxidant N-acetylcysteine attenuated stimulation of choline uptake and induction of stress proteins. Conversely, an inhibitor of glutathione synthesis l-buthionine-sulfoximine (BSO) enhanced stimulation of choline uptake and induction of stress proteins. Cadmium also activated ERK1/2 MAP kinase. The MEK1 inhibitor PD98059 diminished ERK1/2 activation and attenuated stimulation of choline uptake. Furthermore, inhibition of ERK1/2 activation abated stimulation of choline uptake in cells exposed to cadmium with BSO. These data indicate that in the choroid plexus, exposure to low concentrations of cadmium may induce oxidative stress and consequently stimulate apical choline transport through activation of ERK1/2 MAP kinase.

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Karimy, Jason K., Daniel Duran, Jamie K. Hu, Charuta Gavankar, Jonathan R. Gaillard, Yasar Bayri, Hunter Rice, et al. "Cerebrospinal fluid hypersecretion in pediatric hydrocephalus." Neurosurgical Focus 41, no. 5 (November 2016): E10. http://dx.doi.org/10.3171/2016.8.focus16278.

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Hydrocephalus, despite its heterogeneous causes, is ultimately a disease of disordered CSF homeostasis that results in pathological expansion of the cerebral ventricles. Our current understanding of the pathophysiology of hydrocephalus is inadequate but evolving. Over this past century, the majority of hydrocephalus cases has been explained by functional or anatomical obstructions to bulk CSF flow. More recently, hydrodynamic models of hydrocephalus have emphasized the role of abnormal intracranial pulsations in disease pathogenesis. Here, the authors review the molecular mechanisms of CSF secretion by the choroid plexus epithelium, the most efficient and actively secreting epithelium in the human body, and provide experimental and clinical evidence for the role of increased CSF production in hydrocephalus. Although the choroid plexus epithelium might have only an indirect influence on the pathogenesis of many types of pediatric hydrocephalus, the ability to modify CSF secretion with drugs newer than acetazolamide or furosemide would be an invaluable component of future therapies to alleviate permanent shunt dependence. Investigation into the human genetics of developmental hydrocephalus and choroid plexus hyperplasia, and the molecular physiology of the ion channels and transporters responsible for CSF secretion, might yield novel targets that could be exploited for pharmacotherapeutic intervention.

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Beschorner, Rudi, Georgios Pantazis, Astrid Jeibmann, Jana Boy, Richard Meyermann, Michel Mittelbronn, and Jens Schittenhelm. "Expression of EAAT-1 distinguishes choroid plexus tumors from normal and reactive choroid plexus epithelium." Acta Neuropathologica 117, no. 6 (March 13, 2009): 667–75. http://dx.doi.org/10.1007/s00401-009-0519-y.

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Zivkovic, Vladimir, Milica Stanojkovic, and Milorad Antic. "Psammoma bodies as signs of choroid plexus ageing: A morphometric analysis." Vojnosanitetski pregled 74, no. 11 (2017): 1054–59. http://dx.doi.org/10.2298/vsp160321205z.

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Background/Aim. Psammoma bodies (PB) are regarded as benign consequences of ageing in choroid plexus stroma. The aim of this study was to assess the morphometric characteristics of psammoma bodies of all four choroid plexuses during the ageing process. Our intention was to find the possible relations between psammoma bodies and choroid plexus and blood vessels parameters. Methods. This study was conducted on the material taken from 15 cadavers during routine autopsies. Tissue samples were collected from both lateral, third and forth ventricles? choroid plexus. Slices were stained with Mallory trichrome stains. In each image, we analyzed morphometrically the epithelium, blood vessels present and all the psammoma bodies. Results. With age, right choroid plexus surface density decreases (p < 0.05), while the psammoma bodies volume density increases (p < 0.05). A decrease in the blood vessels volume density was observed in the third ventricle?s choroid plexus (p < 0.05), as well as an age-related decrease in the psammoma bodies perimeter (p < 0.01). Not associated with ageing, the increase in psammoma bodies perimeter and volume density predicts a decrease in choroid plexus surface density (p < 0.05 and p < 0.001, respectively). There was a decrease in the volume density of blood vessels with age and with the increase in Feret?s diameter of psammoma bodies, (p < 0.001 and p < 0.05, respectively). Conclusion. We want to point out that there is an association between ageing and increased size and volume density of psammoma bodies. More important is the fact that psammoma bodies? presence and their morphometric characteristics are good predictors of changes occurring on the level of choroid plexus structure and vascularization, which may have crucial effects on the choroid plexus physiology.

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Mahajan, Tanvi, and Subha Ganguly. "Developmental Changes in Choroid Plexus Epithelium: A Review." International Journal of Contemporary Pathology 1, no. 2 (2015): 33. http://dx.doi.org/10.5958/2395-1184.2015.00036.4.

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Mayer, S., and E. Sanders-Bush. "Na+/H+ antiport in cultured choroid plexus epithelium." European Journal of Pharmacology 183, no. 4 (July 1990): 1172. http://dx.doi.org/10.1016/0014-2999(90)94261-u.

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Shintaku, Masayuki. "Tubular (acinar) transformation of the choroid plexus epithelium." Brain Tumor Pathology 19, no. 1 (March 2002): 31–34. http://dx.doi.org/10.1007/bf02482453.

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Valiakhmetova, A. F., L. I. Papusha, L. A. Yasko, A. E. Druy, S. K. Gorelyshev, and A. I. Karachunskiy. "Choroid plexus carcinoma: review of literature." Russian Journal of Pediatric Hematology and Oncology 7, no. 1 (March 2, 2020): 51–61. http://dx.doi.org/10.21682/2311-1267-2020-7-1-51-61.

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Choroid plexus carcinoma (CPC) is a rare malignant tumor arising from the epithelium of the choroid plexus of the brain. More than 80 % of CPCs occur in children. Mutations in the TP53 gene is played the main role in the pathogenesis of these tumors. Choroid plexus carcinomas in 40 % of cases are associated with Li–Fraumeni syndrome. Survival rates in patients with CPC and Li–Fraumeni syndrome are extremely low. The standards of the therapy for patients with CPC are not defined. The extent of surgical resection and treatment modality correlate with prognosis. The role of adjuvant therapy in CPC remains unclear: doses and volumes of radiation therapy (RT), combinations of chemotherapeutic drugs, timing, and a combination of RT and chemotherapy (CT) have not been identified. Also, there is neither a standard CT regimen nor a prospective international study assessing the efficacy and toxicity of various combinations of cytostatics in patients with CPC. The article presents an overview of the existing molecular genetic changes, existing methods for the diagnosis and treatment of choroid plexus carcinoma.

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Johanson, C. E., and V. A. Murphy. "Acetazolamide and insulin alter choroid plexus epithelial cell [Na+], pH, and volume." American Journal of Physiology-Renal Physiology 258, no. 6 (June 1, 1990): F1538—F1546. http://dx.doi.org/10.1152/ajprenal.1990.258.6.f1538.

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Agents that inhibit or stimulate Na+ transport were tested for their effects on the ionic composition and volume of the in vivo choroid plexus (CP) epithelium. Ketamine-anesthetized adult Sprague-Dawley rats treated 1 h with acetazolamide or insulin were analyzed for choroid cell [Na+]i, [HCO3-]i, and pHi (dimethadione method); for transmembrane Na+ and H+ gradients; and for the kinetics of penetration of 22Na from plasma to plexus epithelium to CSF. Acetazolamide (25 mg/kg) reduced [Na+]i by 5-10 mmol/l and substantially elevated [HCO3-]i and pHi; the concurrent 22Na uptake by the in vivo choroid plexus and CSF, as quantified by the transfer coefficient, Kin (ml.g-1.h-1), was curtailed by 55-60%. Such effects on Na+ transport and distribution are likely secondary to the alkalinization of pHi induced by carbonic anhydrase inhibition. Conversely, insulin (3 U/kg ip) stimulated Na+ transport, i.e., manifested as enhanced uptake of 22Na from plasma to choroid cell and increased [Na+]i. For various treatments altering the basolateral membrane H+ gradient, the regression analysis of the 22Na Kin vs. log [H+]i/[H+]ISF (where ISF is interstitial fluid) was significant at P less than 0.01. This is consistent with effects mediated by Na(+)-H+ exchange. K+ and Cl- redistribution phenomena were coincident with altered Na+ transport, as choroidal cells retained K+, Cl-, and H2O after acetazolamide but lost K+, Cl-, and H2O with insulin treatment. A model is presented relating alterations in CP Na+ transport, KCl content, and cell volume. Overall, the findings encourage the postulate for effects of these drugs on Na+ transport basolaterally, either indirectly by attenuating [H+]i/[H+]ISF (acetazolamide) or directly by accelerating Na+ transport (insulin).

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Villalobos, Alice R., Judith T. Parmelee, and J. Larry Renfro. "Choline uptake across the ventricular membrane of neonate rat choroid plexus." American Journal of Physiology-Cell Physiology 276, no. 6 (June 1, 1999): C1288—C1296. http://dx.doi.org/10.1152/ajpcell.1999.276.6.c1288.

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The uptake of [3H]choline from the cerebrospinal fluid (CSF) side of the rat neonatal choroid plexus was characterized in primary cultures of the choroidal epithelium grown on solid supports. Cell-to-medium concentration ratios were ∼5 at 1 min and as high as 70 at 30 min. Apical choline uptake was facilitated; the K m was ∼50 μM. Several organic cations (e.g., hemicholinium-3 and N 1-methylnicotinamide) inhibited uptake. The reduction or removal of external Na+ or the addition of 5 mM LiCl had no effect on uptake. However, increasing external K+ concentration from 3 to 30 mM depolarized ventricular membrane potential (−70 to −15 mV) and reduced uptake to 45% of that for the control. Treatment with 1 mM ouabain or 2 mM BaCl2 reduced uptake 45%, and intracellular acidification reduced uptake to ∼90% of that for controls. These data indicate that the uptake of choline from CSF across the ventricular membrane of the neonatal choroidal epithelium is not directly coupled to Na+ influx but is sensitive to plasma membrane electrical potential.

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Dai, Chun-Fu, and Naoyuki Kanoh. "Cytochemical Localization of Ouabain-sensitive, K+-dependent p-Nitrophenylphosphatase Activity in the Choroid Plexus of Normal and Reserpinized Guinea Pigs." Journal of Histochemistry & Cytochemistry 46, no. 8 (August 1998): 975–76. http://dx.doi.org/10.1177/002215549804600812.

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SUMMARY High doses of reserpine induce depletion of biogenic amines. The K-NPPase activity of choroid plexus was determined after one-shot reserpine administration using cerium-based cytochemistry. In normal untreated animals, reaction product was found on the microvilli of the choroidal epithelium but was almost undetectable 3 and 7 days after reserpinization. At 20 days after reserpinization, however, it was detectable. These findings suggested that reserpine decreased the choroidal Na,K-ATPase activity, and that catecholamines might be essential to maintain normal choroidal Na,K-ATPase activity.

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Szmydynger-Chodobska, Joanna, Nathalie Strazielle, Brian J. Zink, Jean-François Ghersi-Egea, and Adam Chodobski. "The Role of the Choroid Plexus in Neutrophil Invasion after Traumatic Brain Injury." Journal of Cerebral Blood Flow & Metabolism 29, no. 9 (May 27, 2009): 1503–16. http://dx.doi.org/10.1038/jcbfm.2009.71.

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Traumatic brain injury (TBI) frequently results in neuroinflammation, which includes the invasion of neutrophils. After TBI, neutrophils infiltrate the choroid plexus (CP), a site of the blood—cerebrospinal fluid (CSF) barrier (BCSFB), and accumulate in the CSF space near the injury, from where these inflammatory cells may migrate to brain parenchyma. We have hypothesized that the CP functions as an entry point for neutrophils to invade the injured brain. Using the controlled cortical impact model of TBI in rats and an in vitro model of the BCSFB, we show that the CP produces CXC chemokines, such as cytokine-induced neutrophil chemoattractant (CINC)-1 or CXCL1, CINC-2α or CXCL3, and CINC-3 or CXCL2. These chemokines are secreted both apically and basolaterally from the choroidal epithelium, a prerequisite for neutrophil migration across epithelial barriers. Consistent with these findings, we also provide electron microscopic evidence that neutrophils infiltrate the choroidal stroma and subsequently reach the intercellular space between choroidal epithelial cells. This is the first detailed analysis of the BCSFB function related to neutrophil trafficking. Our observations support the role of this barrier in posttraumatic neutrophil invasion.

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Tanji, Kurenai, Eric A. Schon, Salvatore DiMauro, and Eduardo Bonilla. "Kearns–Sayre syndrome: oncocytic transformation of choroid plexus epithelium." Journal of the Neurological Sciences 178, no. 1 (September 2000): 29–36. http://dx.doi.org/10.1016/s0022-510x(00)00354-3.

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De Spiegelaere, W., C. Casteleyn, W. Van Den Broeck, and P. Simoens. "Electron Microscopic Study of the Porcine Choroid Plexus Epithelium." Anatomia, Histologia, Embryologia 37, no. 6 (December 2008): 458–63. http://dx.doi.org/10.1111/j.1439-0264.2008.00882.x.

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Knuckey, N. W., J. Preston, D. Palm, M. H. Epstein, and C. Johanson. "Hydrocephalus decreases chloride efflux from the choroid plexus epithelium." Brain Research 618, no. 2 (August 1993): 313–17. http://dx.doi.org/10.1016/0006-8993(93)91282-w.

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Langford, Michael B., Conor J. O’Leary, Lenin Veeraval, Amanda White, Vanessa Lanoue, and Helen M. Cooper. "WNT5a Regulates Epithelial Morphogenesis in the Developing Choroid Plexus." Cerebral Cortex 30, no. 6 (January 8, 2020): 3617–31. http://dx.doi.org/10.1093/cercor/bhz330.

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Abstract The choroid plexus (CP) is the predominant supplier of cerebral spinal fluid (CSF) and the site of the blood–CSF barrier and is thus essential for brain development and central nervous system homeostasis. Despite these crucial roles, our understanding of the molecular and cellular processes giving rise to the CPs within the ventricles of the mammalian brain is very rudimentary. Here, we identify WNT5a as an important regulator of CP development, where it acts as a pivotal factor driving CP epithelial morphogenesis in all ventricles. We show that WNT5a is essential for the establishment of a cohesive epithelium in the developing CP. We find that in its absence all CPs are substantially reduced in size and complexity and fail to expand into the ventricles. Severe defects were observed in the epithelial cytoarchitecture of all Wnt5a−/− CPs, exemplified by loss of apicobasally polarized morphology and detachment from the ventricular surface and/or basement membrane. We also present evidence that the WNT5a receptor, RYK, and the RHOA kinase, ROCK, are required for normal CP epithelial morphogenesis. Our study, therefore, reveals important insights into the molecular and cellular mechanisms governing CP development.

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Szmydynger-Chodobska, Joanna, Nathalie Strazielle, Jessica R. Gandy, Timothy H. Keefe, Brian J. Zink, Jean-François Ghersi-Egea, and Adam Chodobski. "Posttraumatic Invasion of Monocytes across the Blood—Cerebrospinal Fluid Barrier." Journal of Cerebral Blood Flow & Metabolism 32, no. 1 (August 10, 2011): 93–104. http://dx.doi.org/10.1038/jcbfm.2011.111.

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The invasion of inflammatory cells occurring after ischemic or traumatic brain injury (TBI) has a detrimental effect on neuronal survival and functional recovery after injury. We have recently demonstrated that not only the blood-brain barrier, but also the blood-cerebrospinal fluid (CSF) barrier (BCSFB), has a role in posttraumatic recruitment of neutrophils. Here, we show that TBI results in a rapid increase in synthesis and release into the CSF of a major chemoattractant for monocytes, CCL2, by the choroid plexus epithelium, a site of the BCSFB. Using an in vitro model of the BCSFB, we also show that CCL2 is released across the apical and basolateral membranes of the choroidal epithelium, a pattern of chemokine secretion that promotes leukocyte migration across epithelial barriers. Immunohistochemical and electron microscopic analyses of choroidal tissue provide evidence for the movement of monocytes, sometimes in tandem with neutrophils, along the paracellular pathways between adjacent epithelial cells. These data further support the pathophysiological role of BCSFB in promoting the recruitment of inflammatory cells to the injured brain.

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Ho, Khang-Loon, and Julio H. Garcia. "New observations of colloid cysts of the third ventricle: An ultrastructural study of the lining epithelium and the wall." Proceedings, annual meeting, Electron Microscopy Society of America 49 (August 1991): 94–95. http://dx.doi.org/10.1017/s0424820100084776.

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Colloid cysts of the third ventricle represent one of the variety of the epithelial-lined cysts of the neuraxis. Their histogenesis remains unsettled. Ultrastructural and immunohistochemical analyses have suggested the following possible origins: (a) neuroectoderm, including paraphysis, ependyma, choroid plexus, and tela choroidea and (b) endoderm, including respiratory and enteric epithelium.This report describes the ultrastructure of the lining epithelium and the wall of four cases of colloid cyst. Six distinct cell types were recognized in the epithelium (Fig.1,2): (1) ciliated cells with various types of ciliary abnormalities, (2) non-ciliated cells with microvilli coated with granulo-fibrillary material, (3) goblet cells showing discharge of secretory granules, (4) basal cells with prominent tonofilaments, (5) basal-located cells with elongated cell bodies parallel to the basement membrane and electron-lucent cytoplasm containing sparse, membrane-bound dense core granules (150-250 nm) and (6) small undifferentiated cells with scanty organelles.

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Schwerk, Christian, Kasia Rybarczyk, Frank Essmann, Annette Seibt, Marie-Louise Mölleken, Patrick Zeni, Horst Schroten, and Tobias Tenenbaum. "TNF Induces Choroid Plexus Epithelial Cell Barrier Alterations by Apoptotic and Nonapoptotic Mechanisms." Journal of Biomedicine and Biotechnology 2010 (2010): 1–10. http://dx.doi.org/10.1155/2010/307231.

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The choroid plexus epithelium constitutes the structural basis of the blood-cerebrospinal fluid barrier. Since the cytokine TNF is markedly increased during inflammatory diseases in the blood and the central nervous system, we investigated by which mechanisms TNF induces barrier alteration in porcine choroid plexus epithelial cells. We found a dose-dependent decrease of transepithelial electrical resistance, increase of paracellular inulin-flux, and induction of histone-associated DNA fragmentation and caspase-3 activation after TNF stimulation. This response was strongly aggravated by the addition of cycloheximide and could partially be inhibited by the NF-B inhibitor CAPE, but most effectively by the pan-caspase-inhibitor zVAD-fmk and not by the JNK inhibitor SP600125. Partial loss of cell viability could also be attenuated by CAPE. Immunostaining showed cell condensation and nuclear binding of high-mobility group box 1 protein as a sign of apoptosis after TNF stimulation. Taken together our findings indicate that TNF compromises PCPEC barrier function by caspase and NF-B dependent mechanisms.

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Leggas, Markos, Masashi Adachi, George L. Scheffer, Daxi Sun, Peter Wielinga, Guoqing Du, Kelly E. Mercer, et al. "Mrp4 Confers Resistance to Topotecan and Protects the Brain from Chemotherapy." Molecular and Cellular Biology 24, no. 17 (September 1, 2004): 7612–21. http://dx.doi.org/10.1128/mcb.24.17.7612-7621.2004.

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ABSTRACT The role of the multidrug resistance protein MRP4/ABCC4 in vivo remains undefined. To explore this role, we generated Mrp4-deficient mice. Unexpectedly, these mice showed enhanced accumulation of the anticancer agent topotecan in brain tissue and cerebrospinal fluid (CSF). Further studies demonstrated that topotecan was an Mrp4 substrate and that cells overexpressing Mrp4 were resistant to its cytotoxic effects. We then used new antibodies to discover that Mrp4 is unique among the anionic ATP-dependent transporters in its dual localization at the basolateral membrane of the choroid plexus epithelium and in the apical membrane of the endothelial cells of the brain capillaries. Microdialysis sampling of ventricular CSF demonstrated that localization of Mrp4 at the choroid epithelium is integral to its function in limiting drug penetration into the CSF. The topotecan resistance of cells overexpressing Mrp4 and the polarized expression of Mrp4 in the choroid plexus and brain capillary endothelial cells indicate that Mrp4 has a dual role in protecting the brain from cytotoxins and suggest that the therapeutic efficacy of central nervous system-directed drugs that are Mrp4 substrates may be improved by developing Mrp4 inhibitors.

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Murphy, V. A., and C. E. Johanson. "Na(+)-H+ exchange in choroid plexus and CSF in acute metabolic acidosis or alkalosis." American Journal of Physiology-Renal Physiology 258, no. 6 (June 1, 1990): F1528—F1537. http://dx.doi.org/10.1152/ajprenal.1990.258.6.f1528.

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Basolateral Na(+)-H+ exchange was analyzed with an in vivo model of choroid plexus (CP) epithelium in nephrectomized adult rats anesthetized with ketamine. Acid-base balance in blood was altered for 1 h over a pH continuum of 7.19 to 7.53 by equimolar intraperitoneal injections of HCl, NH4Cl, NaCl, or NaHCO3. Compartmental analysis enabled determination of CP intracellular pH (pHi) [dimethadione (DMO) method] and the choroid cellular concentration of 23Na (stable) and 22Na (tracer). HCl acidosis reduced the outwardly directed transmembrane basolateral H+ gradient, lowered the [23Na]i by 25%, and decreased the influx coefficient (Kin) for 22Na from blood into CP parenchyma (by 45% from 0.211 to 0.117 ml.g-1.h-1) and into cerebrospinal fluid (CSF) (by 43%, from 0.897 to 0.516). Compared with acid-loaded rats (HCl or NH4Cl), the NaHCO3-alkalotic animals had significantly enhanced uptake of 22Na into the CP-CSF system. This pH-dependent transport of Na+ from blood to CP was abolished by pretreatment with amiloride, an inhibitor of Na(+)-H+ exchange. Except in severe acidosis (HCl), the choroid cell pHi (7.05 +/- 0.02 in NaCl controls) and [HCO3-] (11-12 mM) remained stable in the face of acidemic and alkalemic challenges. With respect to reaction of the blood-CSF barrier to plasma acid-base perturbations, the responses of the fourth ventricle plexus pHi, [Na+]i, and 22Na uptake were similar to corresponding ones in lateral plexuses. We conclude that in the choroidal epithelium there is a Na(+)-H+ exchange activity capable of modulating Na+ flux into the CSF by approximately 50% as arterial pH is varied from 7.2 to 7.5.

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Tirapelli, Daniela Pretti da Cunha, Luiza da Silva Lopes, João José Lachat, Benedicto Oscar Colli, and Luís Fernando Tirapelli. "Ultrastructural study of the lateral ventricle choroid plexus in experimental hydrocephalus in Wistar rats." Arquivos de Neuro-Psiquiatria 65, no. 4a (December 2007): 974–77. http://dx.doi.org/10.1590/s0004-282x2007000600010.

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Hydrocephalus is one of the most frequent and complex neurological diseases characterized by the abnormal buildup of cerebrospinal fluid (CSF) in the ventricles of the brain, due to an altered CSF dynamics. To detect possible ultrastructural alterations of the lateral ventricles choroid plexus (responsible for the CSF production), rats seven days after birth were submitted to an intracisternal injection of 20% kaolim (hydrated aluminum silicate) for the hydrocephalus induction. Twenty-eight or 35 days after injection, injected animals and respective controls were processed for observation under a transmission electron microscopy. Alterations found: presence of concentric cell membrane fragments, larger number of primary and secondary lysossomes, vacuoles, and cytoplasmic vesicles, and an enlargement of the intercellular space and between the basolateral interdigitation of the choroid epithelium. The alterations observed are probably associated to an increase of the ventricular pressure, inducing morpho-functional effects on the choroid plexus integrity.

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Damkier, Helle Hasager, Søren Nielsen, and Jeppe Praetorius. "Molecular expression of SLC4-derived Na+-dependent anion transporters in selected human tissues." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 293, no. 5 (November 2007): R2136—R2146. http://dx.doi.org/10.1152/ajpregu.00356.2007.

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NaHCO3 transporters are involved in maintenance of intracellular pH and transepithelial HCO3− movement in many rodent tissues. To establish the human relevance of the many investigations on rodents, this study aimed to map these transporters and a related polypeptide, NaBC1 [solute carrier 4 (SLC4)A11], to several human tissues by using PCR on reverse transcribed human mRNA and immunoperoxidase histochemistry. The mRNA encoding the electroneutral Na+:HCO3− cotransporter (NBCe1; SLC4A4), was expressed in renal cortex, renal medulla, stomach, duodenum, jejunum, ileum, colon, pancreas, choroid plexus, cerebellum, cerebrum, and hippocampus. NBCe2 (SLC4A5) and NBCn1 (SLC4A7) mRNAs were mainly found in kidney and brain tissues, as was mRNA encoding the Na+-dependent anion exchangers NCBE (SLC4A10) and NDCBE1 (SLC4A8). In addition to previous findings, NBCn1 protein was localized to human renal medullary thick ascending limbs and duodenal epithelial villus cells and NBCe2 protein to renal collecting ducts. Finally, the message encoding NaBC1 was found in kidney, stomach, duodenum, pancreas, and brain, and the corresponding protein in the anterior and posterior corneal epithelia, renal corpuscules, proximal tubules, collecting ducts, pancreatic ducts, and the choroid plexus epithelium. In conclusion, the selected human tissues display distinct expression patterns of HCO3− transporters, which closely resemble that of rodent tissues.

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International, BioMed Research. "Retracted: Gelsolin Restores Aβ-Induced Alterations in Choroid Plexus Epithelium." BioMed Research International 2021 (April 14, 2021): 1. http://dx.doi.org/10.1155/2021/9815368.

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Franzén, Annika M., Ke-zhou Zhang, Johan A. Westberg, Wan-Ming Zhang, Johanna Arola, Henrik S. Olsen, and Leif C. Andersson. "Expression of stanniocalcin in the epithelium of human choroid plexus." Brain Research 887, no. 2 (December 2000): 440–43. http://dx.doi.org/10.1016/s0006-8993(00)03029-8.

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Kasahara, M., T. Matsuzawa, M. Kokubo, Y. Gushiken, K. Tashiro, T. Koide, H. Watanabe, and N. Katunuma. "Immunohistochemical localization of ornithine aminotransferase in normal rat tissues by Fab'-horseradish peroxidase conjugates." Journal of Histochemistry & Cytochemistry 34, no. 11 (November 1986): 1385–88. http://dx.doi.org/10.1177/34.11.3534076.

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Immunohistochemical localization of ornithine aminotransferase (L-ornithine: 2-oxo-acid aminotransferase, EC 2.6.1.13), a mitochondrial enzyme whose hereditary absence induces gyrate atrophy of the choroid and retina, was elucidated by a direct immunoperoxidase method using Fab'-horseradish peroxidase conjugates. In immunodiffusion studies, the antibodies raised with the re-crystallized enzyme were highly specific to ornithine aminotransferase. To show localization of ornithine aminotransferase in normal rat tissues, clear immunohistochemical staining of this enzyme through the inner mitochondrial membrane in paraffin sections was achieved with Fab'-horseradish peroxidase conjugates. Strong immunoreactivity was present in cerebral neurons, hepatocytes, and epithelial cells of renal tubuli, gut mucous membranes, and ocular tissues. Specific distribution of ornithine aminotransferase was found in ependymal cell groups: namely, epithelial cells of the choroid plexus, pigmented and nonpigmented epithelial cells of the ciliary body. and Müller cells and pigment epithelium of the retina.

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Journal articles on the topic 'Choroid Plexus Epithelium'

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