scholarly journals Localization of metallothionein in the brain of rat and mouse.

1992 ◽  
Vol 40 (2) ◽  
pp. 309-315 ◽  
Author(s):  
N Nishimura ◽  
H Nishimura ◽  
A Ghaffar ◽  
C Tohyama
Keyword(s):  
Endothelial Cells ◽  
Choroid Plexus ◽  
Glial Cells ◽  
Adult Mouse ◽  
Ependymal Cells ◽  
Choroid Plexus Epithelium ◽  
Pia Mater ◽  
Adult Mouse Brain ◽  
Adult Rats ◽  
The Brain

Metallothionein (MT) is a low molecular mass protein inducible by heavy metals such as cadmium (Cd), zinc, and copper, and having high affinity for these metals. In the present study, we investigated the immunohistological localization of MT in the brains of rats and mice. In adult rat brain, almost no MT immunostaining was observed, whereas in adult mouse brain strong MT immunostaining was found in the ependymal cells, some glial cells, arachnoid, and pia mater. No immunostaining was detected in neurons and endothelial cells. In younger rats (1-3 weeks old), strong MT immunostaining was observed in ependymal cells, choroid plexus epithelium, arachnoid, and pia mater. The overall MT concentration in adult mouse brain appeared higher than that of the brains of young and adult rats. When adult rats were administered Cd, MT was induced not only in some glial cells, ependymal cells, arachnoid, and pia mater but also in endothelial cells. Although Cd treatment resulted in an increase in the MT immunostaining in the specific cells described above, the MT induction was not great enough to significantly affect the overall MT level in the brain. The present result suggest a possible link of MT with cell growth of choroid plexus epithelium and ependymal cells, as well as a detoxifying role of MT in the blood-brain barrier and the cerebrospinal fluid-brain barrier.

scholarly journals EPAC2: A new and promising protein for glioma pathogenesis and therapy

2020 ◽  
Vol 14 (1) ◽  
Author(s):  
Seidu A. Richard
Keyword(s):  
Neurological Disorders ◽  
Adult Mouse ◽  
Ependymal Cells ◽  
Low Grade ◽  
Guanine Nucleotide ◽  
Nucleotide Exchange ◽  
Adult Mouse Brain ◽  
Guanine Nucleotide Exchange ◽  
Nucleotide Exchange Factor ◽  
The Brain

Gliomas are prime brain cancers which are initiated by malignant modification of neural stem cells, progenitor cells and differentiated glial cells such as astrocyte, oligodendrocyte as well as ependymal cells. Exchange proteins directly activated by cAMP (EPACs) are crucial cyclic adenosine 3’,5’-monophosphate (cAMP)-determined signaling pathways. Cyclic AMP-intermediated signaling events were utilized to transduce protein kinase A (PKA) leading to the detection of EPACs or cAMP-guanine exchange factors (cAMP-GEFs). EPACs have been detected as crucial proteins associated with the pathogenesis of neurological disorders as well as numerous human diseases. EPAC proteins have two isoforms. These isoforms are EPAC1 and EPAC2. EPAC2 also known as Rap guanine nucleotide exchange factor 4 (RAPGEF4) is generally expression in all neurites. Higher EAPC2 levels was detected in the cortex, hippocampus as well as striatum of adult mouse brain. Activation as well as over-secretion of EPAC2 triggers apoptosis in neurons and EPAC-triggered apoptosis was intermediated via the modulation of Bcl-2 interacting member protein (BIM). EPAC2 secretory levels has proven to be more in low-grade clinical glioma than high-grade clinical glioma. This review therefore explores the effects of EPAC2/RAPGEF4 on the pathogenesis of glioma instead of EPAC1 because EPAC2 and not EPAC1 is predominately expressed in the brain. Therefore, EPAC2 is most likely to modulate glioma pathogenesis rather than EPAC1.

scholarly journals T-Lymphocytes Traffic into the Brain across the Blood-CSF Barrier: Evidence Using a Reconstituted Choroid Plexus Epithelium

PLoS ONE ◽  
2016 ◽  
Vol 11 (3) ◽  
pp. e0150945 ◽  
Author(s):  
Nathalie Strazielle ◽  
Rita Creidy ◽  
Christophe Malcus ◽  
José Boucraut ◽  
Jean-François Ghersi-Egea
Keyword(s):  
T Lymphocytes ◽  
Choroid Plexus ◽  
Choroid Plexus Epithelium ◽  
The Brain

Altered pHi regulation and Na+/HCO3− transporter activity in choroid plexus of cilia-defective Tg737orpk mutant mouse

2007 ◽  
Vol 292 (4) ◽  
pp. C1409-C1416 ◽  
Author(s):  
Boglarka Banizs ◽  
Peter Komlosi ◽  
Mark O. Bevensee ◽  
Erik M. Schwiebert ◽  
Phillip D. Bell ◽  
...  
Keyword(s):  
Ion Transport ◽  
Choroid Plexus ◽  
Perinatal Period ◽  
Ependymal Cells ◽  
Intracellular Camp ◽  
Transport Activity ◽  
Wild Type ◽  
Choroid Plexus Epithelium ◽  
Fluid Movement ◽  
Camp Levels

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.

scholarly journals Brain spectrin(240/235) and brain spectrin(240/235E): two distinct spectrin subtypes with different locations within mammalian neural cells.

1986 ◽  
Vol 102 (6) ◽  
pp. 2088-2097 ◽  
Author(s):  
B M Riederer ◽  
I S Zagon ◽  
S R Goodman
Keyword(s):  
Blood Cell ◽  
Mouse Brain ◽  
Glial Cells ◽  
Red Blood Cell ◽  
Adult Mouse ◽  
Neuronal Cell ◽  
Neural Cells ◽  
Adult Mouse Brain ◽  
Neuronal Cell Bodies ◽  
Brain Spectrin

Adult mouse brain contains at least two distinct spectrin subtypes, both consisting of 240-kD and 235-kD subunits. Brain spectrin(240/235) is found in neuronal axons, but not dendrites, when immunohistochemistry is performed with antibody raised against brain spectrin isolated from enriched synaptic/axonal membranes. A second spectrin subtype, brain spectrin(240/235E), is exclusively recognized by red blood cell spectrin antibody. Brain spectrin(240/235E) is confined to neuronal cell bodies and dendrites, and some glial cells, but is not present in axons or presynaptic terminals.

scholarly journals A cellular and spatial map of the choroid plexus across brain ventricles and ages

2019 ◽  
Author(s):  
Neil Dani ◽  
Rebecca H. Herbst ◽  
Naomi Habib ◽  
Joshua Head ◽  
Danielle Dionne ◽  
...  
Keyword(s):  
Choroid Plexus ◽  
Adult Mouse ◽  
Cell Types ◽  
Rna Seq ◽  
Adult Mouse Brain ◽  
Brain Ventricles ◽  
Future Studies ◽  
Brain Ventricle ◽  
Macrophage Populations ◽  
And Function

AbstractThe choroid plexus (ChP), located in each brain ventricle, produces cerebrospinal fluid (CSF) and forms the blood-CSF barrier, but is under-characterized. Here, we combine single cell RNA-Seq and spatial mapping of RNA and proteins to construct an atlas of each ChP in the developing and adult mouse brain. Each ChP comprises of epithelial, endothelial, mesenchymal, immune, neuronal, and glial cells, with distinct subtypes, differentiation states and anatomical locations. Epithelial, fibroblast, and macrophage populations had ventricle-specific, regionalized gene expression programs across the developing brain. Key cell types are retained in adult, with loss of developmental signatures and maturation of ventricle-specific regionalization in the epithelial cells. Expression of cognate ligand-receptor pairs across cell subtypes suggests substantial cell-cell interactions within the ChP. Our atlas sheds new light on the development and function of the ChP brain barrier system, and will facilitate future studies on its role in brain development, homeostasis and disease.

Majority of alpha2,6-sialylated glycans in the adult mouse brain exist in O-glycans: SALSA-MS analysis for knockout mice of alpha2,6-sialyltransferase genes

Glycobiology ◽  
2020 ◽  
Author(s):  
Yuhsuke Ohmi ◽  
Takashi Nishikaze ◽  
Yoko Kitaura ◽  
Takako Ito ◽  
Satoko Yamamoto ◽  
...  
Keyword(s):  
Sialic Acid ◽  
Mouse Brain ◽  
Adult Mouse ◽  
Expression Profiles ◽  
T Antigen ◽  
Mass Spectrometry Analysis ◽  
Gene Products ◽  
Adult Mouse Brain ◽  
The Brain ◽  
Brain Tissues

Abstract Sialic acids are unique sugars with negative charge and exert various biological functions such as regulation of immune systems, maintenance of nerve tissues and expression of malignant properties of cancers. Alpha 2,6 sialylated N-glycans, one of representative sialylation forms, are synthesized by St6gal1 or St6gal2 gene products in humans and mice. Previously, it has been reported that St6gal1 gene is ubiquitously expressed in almost all tissues. On the other hand, St6gal2 gene is expressed mainly in the embryonic and perinatal stages of brain tissues. However, roles of St6gal2 gene have not been clarified. Expression profiles of N-glycans with terminal α2,6 sialic acid generated by St6gal gene products in the brain have never been directly studied. Using conventional lectin blotting and novel sialic acid linkage-specific alkylamidationmass spectrometry method (SALSA-MS), we investigated the function and expression of St6gal genes and profiles of their products in the adult mouse brain by establishing KO mice lacking St6gal1 gene, St6gal2 gene, or both of them (double knockout). Consequently, α2,6-sialylated N-glycans were scarcely detected in adult mouse brain tissues, and a majority of α2,6-sialylated glycans found in the mouse brain were O-linked glycans. The majority of these α2,6-sialylated O-glycans were shown to be disialyl-T antigen and sialyl-(6)T antigen by mass spectrometry analysis. Moreover, it was revealed that a few α2,6-sialylated N-glycans were produced by the action of St6gal1 gene, despite both St6gal1 and St6gal2 genes being expressed in the adult mouse brain. In the future, where and how sialylated O-linked glycoproteins function in the brain tissue remains to be clarified.

scholarly journals Spontaneous Ectopic Choroid Plexus with Sclerosis in Adult Beagle Dogs

2018 ◽  
Vol 46 (5) ◽  
pp. 608-609
Author(s):  
Ingrid D. Pardo ◽  
Ahmed M. Shoieb ◽  
Robert Garman ◽  
Michael Mirsky ◽  
Rosemary Santos ◽  
...  
Keyword(s):  
Connective Tissue ◽  
Choroid Plexus ◽  
Neural Development ◽  
Clinical Signs ◽  
Ependymal Cells ◽  
Tubular Structures ◽  
Beagle Dogs ◽  
The Brain ◽  
Morphologic Appearance ◽  
Adjacent Brain

Microscopic examination of the brain of adult Beagle dogs from four different general toxicity studies revealed the presence of ectopic choroid plexus tissue in six individual dogs (4 females and 2 males) with ages ranging from 12 to 18 months. In each dog, this finding was characterized by a well-circumscribed mass localized to a region above and along the corpus callosum without any apparent compression of adjacent brain tissue. Each mass was composed of columnar ependymal cells forming tubular structures surrounded by variable amounts of fibrovascular connective tissue and had the appearance of small rests of ependymal cells that had been penetrated by the leptomeninges during neural development. There were no associated clinical signs or macroscopic correlates. Based on morphologic appearance, a diagnosis of spontaneous ectopic choroid plexus with secondary sclerosis was made. To the authors’ knowledge, ectopic choroid plexus has not been reported in Beagle dogs and is rare in humans and horses.

scholarly journals Blood-Brain Barrier Dysfunction Amplifies the Development of Neuroinflammation: Understanding of Cellular Events in Brain Microvascular Endothelial Cells for Prevention and Treatment of BBB Dysfunction

2021 ◽  
Vol 15 ◽  
Author(s):  
Fuyuko Takata ◽  
Shinsuke Nakagawa ◽  
Junichi Matsumoto ◽  
Shinya Dohgu
Keyword(s):  
Endothelial Cells ◽  
Signaling Pathways ◽  
Blood Brain Barrier ◽  
Glial Cells ◽  
Inflammatory Mediators ◽  
Brain Barrier ◽  
Brain Endothelial Cells ◽  
Perivascular Cells ◽  
Cellular Components ◽  
The Brain

Neuroinflammation is involved in the onset or progression of various neurodegenerative diseases. Initiation of neuroinflammation is triggered by endogenous substances (damage-associated molecular patterns) and/or exogenous pathogens. Activation of glial cells (microglia and astrocytes) is widely recognized as a hallmark of neuroinflammation and triggers the release of proinflammatory cytokines, leading to neurotoxicity and neuronal dysfunction. Another feature associated with neuroinflammatory diseases is impairment of the blood-brain barrier (BBB). The BBB, which is composed of brain endothelial cells connected by tight junctions, maintains brain homeostasis and protects neurons. Impairment of this barrier allows trafficking of immune cells or plasma proteins into the brain parenchyma and subsequent inflammatory processes in the brain. Besides neurons, activated glial cells also affect BBB integrity. Therefore, BBB dysfunction can amplify neuroinflammation and act as a key process in the development of neuroinflammation. BBB integrity is determined by the integration of multiple signaling pathways within brain endothelial cells through intercellular communication between brain endothelial cells and brain perivascular cells (pericytes, astrocytes, microglia, and oligodendrocytes). For prevention of BBB disruption, both cellular components, such as signaling molecules in brain endothelial cells, and non-cellular components, such as inflammatory mediators released by perivascular cells, should be considered. Thus, understanding of intracellular signaling pathways that disrupt the BBB can provide novel treatments for neurological diseases associated with neuroinflammation. In this review, we discuss current knowledge regarding the underlying mechanisms involved in BBB impairment by inflammatory mediators released by perivascular cells.

Intracranial Pressure

2019 ◽  
pp. 69-73
Author(s):  
Eelco F. M. Wijdicks ◽  
William D. Freeman
Keyword(s):  
Cerebrospinal Fluid ◽  
Smooth Muscle ◽  
Choroid Plexus ◽  
Blood Cells ◽  
White Blood Cells ◽  
Ependymal Cells ◽  
Cerebral Aqueduct ◽  
Epithelial Surface ◽  
The Brain ◽  
Route Of Delivery

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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