scholarly journals TRIP6 functions in brain ciliogenesis

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Shalmali Shukla ◽  
Ronny Haenold ◽  
Pavel Urbánek ◽  
Lucien Frappart ◽  
Shamci Monajembashi ◽  
...  
Keyword(s):  
Choroid Plexus ◽  
Super Resolution ◽  
Epithelial Cell Line ◽  
Lim Domain ◽  
Choroid Plexus Epithelial Cell ◽  
Interaction Sites ◽  
Assembly Factor ◽  
Pericentriolar Material ◽  
Choroid Plexus Epithelial

AbstractTRIP6, a member of the ZYXIN-family of LIM domain proteins, is a focal adhesion component. Trip6 deletion in the mouse, reported here, reveals a function in the brain: ependymal and choroid plexus epithelial cells are carrying, unexpectedly, fewer and shorter cilia, are poorly differentiated, and the mice develop hydrocephalus. TRIP6 carries numerous protein interaction domains and its functions require homodimerization. Indeed, TRIP6 disruption in vitro (in a choroid plexus epithelial cell line), via RNAi or inhibition of its homodimerization, confirms its function in ciliogenesis. Using super-resolution microscopy, we demonstrate TRIP6 localization at the pericentriolar material and along the ciliary axoneme. The requirement for homodimerization which doubles its interaction sites, its punctate localization along the axoneme, and its co-localization with other cilia components suggest a scaffold/co-transporter function for TRIP6 in cilia. Thus, this work uncovers an essential role of a LIM-domain protein assembly factor in mammalian ciliogenesis.

scholarly journals Novel function of TRIP6, in brain ciliogenesis

2019 ◽  
Author(s):  
Shalmali Shukla ◽  
Pavel Urbanek ◽  
Lucien Frappart ◽  
Ronny Hänold ◽  
Sigrun Nagel ◽  
...  
Keyword(s):  
Choroid Plexus ◽  
Super Resolution ◽  
Molecular Assembly ◽  
Epithelial Cell Line ◽  
Choroid Plexus Epithelial Cell ◽  
Interaction Sites ◽  
Assembly Factor ◽  
Pericentriolar Material ◽  
Interaction Domains ◽  
Choroid Plexus Epithelial

AbstractTRIP6, a member of the zyxin-family of LIM domain proteins, is a focal adhesion component. trip6 deletion in the mouse revealed, unexpectedly, in view of its ubiquitous expression, a function in the brain: ependymal and choroid plexus epithelial cells were poorly developed, carrying fewer and shorter cilia, and the mice developed hydrocephalus. TRIP6 disruption, via RNAi or inhibition of its homodimerization, in a choroid plexus epithelial cell line, confirmed its function in ciliogenesis. Zyxin-family members carry numerous protein interaction domains. In common with assembly of other multiprotein complexes, ciliogenesis may be facilitated by molecular assembly factors. Super-resolution microscopy demonstrated TRIP6 localization at the pericentriolar material and along the ciliary axoneme. The requirement for homodimerization which doubles its interaction sites, its punctate localization along the axoneme, and its co-localization with other cilia components suggest a scaffold/co-transporter function for TRIP6 in cilia. This is the first discovery of a protein assembly factor essential for mammalian ciliogenesis.

scholarly journals Expression of junctional proteins in choroid plexus epithelial cell lines: a comparative study

2007 ◽  
Vol 4 (1) ◽  
pp. 11 ◽  
Author(s):  
Joanna Szmydynger-Chodobska ◽  
Crissey L Pascale ◽  
Andrew N Pfeffer ◽  
Cassaundra Coulter ◽  
Adam Chodobski
Keyword(s):  
Epithelial Cell ◽  
Comparative Study ◽  
Choroid Plexus ◽  
Cell Lines ◽  
Choroid Plexus Epithelial Cell ◽  
Junctional Proteins ◽  
Epithelial Cell Lines ◽  
Choroid Plexus Epithelial

scholarly journals Porcine Choroid Plexus Epithelial Cells Induce Streptococcus suis Bacteriostasis In Vitro

2004 ◽  
Vol 72 (5) ◽  
pp. 3084-3087 ◽  
Author(s):  
Rüdiger A. Adam ◽  
Tobias Tenenbaum ◽  
Peter Valentin-Weigand ◽  
Maurice Laryea ◽  
Bernd Schwahn ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Bacterial Meningitis ◽  
Choroid Plexus ◽  
Host Defense ◽  
Streptococcus Suis ◽  
Active Role ◽  
Necrosis Factor Alpha ◽  
Ifn Γ ◽  
Choroid Plexus Epithelial

ABSTRACT The involvement of the choroid plexus in host defense during bacterial meningitis is unclear. Aiming to elucidate possible antibacterial mechanisms, we stimulated primary porcine choroid plexus epithelial cells (pCPEC) with proinflammatory cytokines and challenged them with various Streptococcus suis strains. In the supernatant of gamma interferon (IFN-γ)-stimulated pCPEC, streptococcal growth was markedly suppressed. Costimulation with tumor necrosis factor alpha enhanced this bacteriostatic effect, while supplementation of l-tryptophan completely eliminated it. We also demonstrate that an activation of indoleamine 2,3-dioxygenase in the pCPEC seems to be responsible for the IFN-γ-induced bacteriostasis. This supports the hypothesis of an active role of the choroid plexus in host defense against bacterial meningitis.

scholarly journals Genetic and pharmacological inactivation of apical Na+-K+-2Cl− cotransporter 1 in choroid plexus epithelial cells reveals the physiological function of the cotransporter

2019 ◽  
Vol 316 (4) ◽  
pp. C525-C544 ◽  
Author(s):  
Jeannine M. C. Gregoriades ◽  
Aaron Madaris ◽  
Francisco J. Alvarez ◽  
Francisco J. Alvarez-Leefmans
Keyword(s):  
Epithelial Cells ◽  
Choroid Plexus ◽  
Basolateral Membrane ◽  
Water Volume ◽  
Water Fluxes ◽  
Membrane Location ◽  
Flux Mode ◽  
Choroid Plexus Epithelial

Choroid plexus epithelial cells (CPECs) secrete cerebrospinal fluid (CSF). They express Na+-K+-ATPase and Na+-K+-2Cl− cotransporter 1 (NKCC1) on their apical membrane, deviating from typical basolateral membrane location in secretory epithelia. Given this peculiarity, the direction of basal net ion fluxes mediated by NKCC1 in CPECs is controversial, and cotransporter function is unclear. Determining the direction of basal NKCC1-mediated fluxes is critical to understanding the function of apical NKCC1. If NKCC1 works in the net efflux mode, it may be directly involved in CSF secretion. Conversely, if NKCC1 works in the net influx mode, it would have an absorptive function, contributing to intracellular Cl− concentration ([Cl−]i) and cell water volume (CWV) maintenance needed for CSF secretion. We resolve this long-standing debate by electron microscopy (EM), live-cell-imaging microscopy (LCIM), and intracellular Na+ and Cl− measurements in single CPECs of NKCC1+/+ and NKCC1−/− mouse. NKCC1-mediated ion and associated water fluxes are tightly linked, thus their direction is inferred by measuring CWV changes. Genetic or pharmacological NKCC1 inactivation produces CPEC shrinkage. EM of NKCC1−/− CPECs in situ shows they are shrunken, forming large dilations of their basolateral extracellular spaces, yet remaining attached by tight junctions. Normarski LCIM shows in vitro CPECs from NKCC1−/− are ~17% smaller than NKCC1+/+. CWV measurements in calcein-loaded CPECs show that bumetanide (10 μM) produces ~16% decrease in CWV in NKCC1+/+ but not in NKCC1−/− CPECs. Our findings suggest that under basal conditions apical NKCC1 is continuously active and works in the net inward flux mode maintaining [Cl−]i and CWV needed for CSF secretion.

scholarly journals The Polarity of Choroid Plexus Epithelial Cells In Vitro Is Improved in Serum-Free Medium

2002 ◽  
Vol 71 (3) ◽  
pp. 1141-1150 ◽  
Author(s):  
Ansgar Hakvoort ◽  
Matthias Haselbach ◽  
Joachim Wegener ◽  
Dirk Hoheisel ◽  
Hans-Joachim Galla
Keyword(s):  
Epithelial Cells ◽  
Choroid Plexus ◽  
Serum Free Medium ◽  
Free Medium ◽  
Serum Free ◽  
Choroid Plexus Epithelial

In Vitro Exposure of Cultured Porcine Choroid Plexus Epithelial Cells to Immunosuppressant, Anti-Inflammatory, and Psychoactive Drugs

2007 ◽  
Vol 16 (4) ◽  
pp. 435-440 ◽  
Author(s):  
Dwaine F. Emerich ◽  
Patricia Schneider ◽  
Briannan Bintz ◽  
Jebecka Hudak ◽  
Christopher G. Thanos
Keyword(s):  
Epithelial Cells ◽  
Choroid Plexus ◽  
Psychoactive Drugs ◽  
In Vitro Exposure ◽  
Anti Inflammatory ◽  
Choroid Plexus Epithelial

scholarly journals TNF Induces Choroid Plexus Epithelial Cell Barrier Alterations by Apoptotic and Nonapoptotic Mechanisms

2010 ◽  
Vol 2010 ◽  
pp. 1-10 ◽  
Author(s):  
Christian Schwerk ◽  
Kasia Rybarczyk ◽  
Frank Essmann ◽  
Annette Seibt ◽  
Marie-Louise Mölleken ◽  
...  
Keyword(s):  
Choroid Plexus ◽  
Inflammatory Diseases ◽  
High Mobility ◽  
Structural Basis ◽  
Choroid Plexus Epithelial Cell ◽  
The Central Nervous System ◽  
Cell Condensation ◽  
Dose Dependent Decrease ◽  
Dose Dependent ◽  
Choroid Plexus Epithelial

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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