Hyperglycemia increases SCO-spondin and Wnt5a secretion into the cerebrospinal fluid to regulate ependymal cell beating and glucose sensing

Hyperglycemia increases glucose concentrations in the cerebrospinal fluid (CSF), activating glucose-sensing mechanisms and feeding behavior in the hypothalamus. Here, we discuss how hyperglycemia temporarily modifies ependymal cell ciliary beating to increase hypothalamic glucose sensing. A high lev...

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Veröffentlicht in:PLoS biology 2023-09, Vol.21 (9), p.e3002308-e3002308
Hauptverfasser: Nualart, Francisco, Cifuentes, Manuel, Ramírez, Eder, Martínez, Fernando, Barahona, María José, Ferrada, Luciano, Saldivia, Natalia, Bongarzone, Ernesto R, Thorens, Bernard, Salazar, Katterine
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container_title PLoS biology
container_volume 21
creator Nualart, Francisco
Cifuentes, Manuel
Ramírez, Eder
Martínez, Fernando
Barahona, María José
Ferrada, Luciano
Saldivia, Natalia
Bongarzone, Ernesto R
Thorens, Bernard
Salazar, Katterine
description Hyperglycemia increases glucose concentrations in the cerebrospinal fluid (CSF), activating glucose-sensing mechanisms and feeding behavior in the hypothalamus. Here, we discuss how hyperglycemia temporarily modifies ependymal cell ciliary beating to increase hypothalamic glucose sensing. A high level of glucose in the rat CSF stimulates glucose transporter 2 (GLUT2)-positive subcommissural organ (SCO) cells to release SCO-spondin into the dorsal third ventricle. Genetic inactivation of mice GLUT2 decreases hyperglycemia-induced SCO-spondin secretion. In addition, SCO cells secrete Wnt5a-positive vesicles; thus, Wnt5a and SCO-spondin are found at the apex of dorsal ependymal cilia to regulate ciliary beating. Frizzled-2 and ROR2 receptors, as well as specific proteoglycans, such as glypican/testican (essential for the interaction of Wnt5a with its receptors) and Cx43 coupling, were also analyzed in ependymal cells. Finally, we propose that the SCO-spondin/Wnt5a/Frizzled-2/Cx43 axis in ependymal cells regulates ciliary beating, a cyclic and adaptive signaling mechanism to control glucose sensing.
doi_str_mv 10.1371/journal.pbio.3002308
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Here, we discuss how hyperglycemia temporarily modifies ependymal cell ciliary beating to increase hypothalamic glucose sensing. A high level of glucose in the rat CSF stimulates glucose transporter 2 (GLUT2)-positive subcommissural organ (SCO) cells to release SCO-spondin into the dorsal third ventricle. Genetic inactivation of mice GLUT2 decreases hyperglycemia-induced SCO-spondin secretion. In addition, SCO cells secrete Wnt5a-positive vesicles; thus, Wnt5a and SCO-spondin are found at the apex of dorsal ependymal cilia to regulate ciliary beating. Frizzled-2 and ROR2 receptors, as well as specific proteoglycans, such as glypican/testican (essential for the interaction of Wnt5a with its receptors) and Cx43 coupling, were also analyzed in ependymal cells. 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subjects Analysis
Biology and Life Sciences
Cerebrospinal fluid
Chemoreception
Cilia
Connexin 43
Dextrose
Endoplasmic reticulum
Ependymal cells
Feeding behavior
Frizzled protein
Glucose
Glucose transporter
Glycoproteins
Heparan sulfate proteoglycans
Hyperglycemia
Hypothalamus
Inactivation
Independent sample
Kinases
Medicine and Health Sciences
Morphogenesis
Physical Sciences
Proteoglycans
Quantitative analysis
Receptors
Research and Analysis Methods
Secretion
Subcommissural organ
Ventricle
Ventricles (cerebral)
Wnt protein
title Hyperglycemia increases SCO-spondin and Wnt5a secretion into the cerebrospinal fluid to regulate ependymal cell beating and glucose sensing
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