2026-06-03T01:32:34Zhttps://riuma.uma.es/rest/oai/request

oai:riuma.uma.es:10630/358702026-02-03T11:13:39Zcom_10630_2254col_10630_37953

Hyperglycemia increases SCO-spondin and Wnt5a secretion into the cerebrospinal fluid to regulate ependymal cell beating and glucose sensing Nualart, Francisco Cifuentes-Rueda, Manuel Ramírez, Eder Martínez, Fernando Barahona, M José Ferrada, Luciano Saldivia, N Borgonzone, Ernesto R Thorens, B Salazar, Katterine Glucemia 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. 2025-01-07T10:26:09Z 2025-01-07T10:26:09Z 2023-09 journal article Nualart F, Cifuentes M, Ramírez E, Martínez F, Barahona MJ, Ferrada L, Saldivia N, Bongarzone ER, Thorens B, Salazar K. Hyperglycemia increases SCO-spondin and Wnt5a secretion into the cerebrospinal fluid to regulate ependymal cell beating and glucose sensing. PLoS Biol. 2023 Sep 21;21(9):e3002308. doi: 10.1371/journal.pbio.3002308. PMID: 37733692; PMCID: PMC10513282. https://hdl.handle.net/10630/35870 https://doi.org/10.1371/journal.pbio.3002308 eng http://creativecommons.org/licenses/by-nc-nd/4.0/ open access Attribution-NonCommercial-NoDerivatives 4.0 Internacional Public Library of Science