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Updated: Jun 18, 2026
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Observation of the Ciliary Movement of Choroid Plexus Epithelial Cells Ex Vivo
Published on: July 13, 2015
Multiple primary cilia modulate the fluid transcytosis in choroid plexus epithelium
Keishi Narita1, Toyoko Kawate, Naoto Kakinuma
1Department of Anatomy and Cell Biology, Interdisciplinary School of Medicine & Engineering, University of Yamanashi, 1110 Shimo-Kateau, Chuo, Yamanashi 409-3898, Japan.
Traffic (Copenhagen, Denmark)
|December 5, 2009
Summary
Defects in primary cilia of brain cells increase cerebrospinal fluid (CSF) production by disrupting neuropeptide FF (NPFF) signaling. This cilia dysfunction may cause diseases like congenital hydrocephalus.
Area of Science:
- Neuroscience
- Cell Biology
- Physiology
Background:
- Ciliary dysfunction is linked to human diseases, including congenital hydrocephalus.
- Previous research suggests ciliary defects disrupt cerebrospinal fluid (CSF) flow and increase CSF production.
Purpose of the Study:
- To investigate the molecular mechanisms underlying increased CSF production due to ciliary dysfunction.
- To explore the role of primary cilia in choroid plexus epithelial cells (CPECs) in regulating CSF production.
Main Methods:
- Isolation of porcine choroid plexus epithelial cells (CPECs).
- Experimental deciliation of CPECs to assess functional changes.
- Measurement of intracellular cyclic AMP (cAMP) levels and fluid transcytosis.
- Analysis of neuropeptide FF (NPFF) receptor 2 (NPFFR2) expression and function.
- Pharmacological inhibition of NPFF receptor signaling.
Main Results:
- Deciliation of CPECs elevated intracellular cAMP levels and stimulated fluid transcytosis.
- Primary cilia on CPECs expressed NPFFR2, and deciliation reduced NPFF responsiveness.
- CPECs expressed NPFF precursor and NPFFR2, indicating autocrine signaling.
- NPFF receptor antagonism increased fluid transcytosis, suggesting tonic inhibition by NPFF.
Conclusions:
- Primary cilia in CPECs function as chemosensors regulating CSF production.
- Dysfunctional cilia disrupt NPFF signaling, leading to increased fluid transcytosis and potentially contributing to hydrocephalus.
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