2026-05-30T09:33:44Zhttps://riuma.uma.es/rest/oai/request

oai:riuma.uma.es:10630/345382026-02-03T11:25:45Zcom_10630_2254col_10630_37953

00925njm 22002777a 4500 dc Estivill-Torrús, Guillermo author Llebrez Zayas, Pedro author Matas-Rico, Elisa author Rodriguez-de-Fonseca, Fernando author Chun, Jerold author Santín-Núñez, Luis Javier author Pedraza-Benítez, María del Carmen author De-Diego-Barbado, Isabel author Del Arco-Herrera, Ignacio author Fernández-Llebrez, Pedro author 2008-04 Lysophosphatidic acid (LPA) is a simple phospholipid with extracellular signaling properties mediated by specific G protein-coupled receptors. At least 2 LPA receptors, LPA(1) and LPA(2), are expressed in the developing brain, the former enriched in the neurogenic ventricular zone (VZ), suggesting a normal role in neurogenesis. Despite numerous studies reporting the effects of exogenous LPA using in vitro neural models, the first LPA(1) loss-of-function mutants reported did not show gross cerebral cortical defects in the 50% that survived perinatal demise. Here, we report a role for LPA(1) in cortical neural precursors resulting from analysis of a variant of a previously characterized LPA(1)-null mutant that arose spontaneously during colony expansion. These LPA(1)-null mice, termed maLPA(1), exhibit almost complete perinatal viability and show a reduced VZ, altered neuronal markers, and increased cortical cell death that results in a loss of cortical layer cellularity in adults. These data support LPA(1) function in normal cortical development and suggest that the presence of genetic modifiers of LPA(1) influences cerebral cortical development. Guillermo Estivill-Torrús, Pedro Llebrez-Zayas, Elisa Matas-Rico, Luis Santín, Carmen Pedraza, Isabel De Diego, Ignacio Del Arco, Pedro Fernández-Llebrez, Jerold Chun, Fernando Rodríguez De Fonseca, Absence of LPA1 Signaling Results in Defective Cortical Development, Cerebral Cortex, Volume 18, Issue 4, April 2008, Pages 938–950, https://doi.org/10.1093/cercor/bhm132 https://hdl.handle.net/10630/34538 10.1093/cercor/bhm132 Cerebro - Evolución Absence of LPA1 signaling results in defective cortical development