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1. Microglia mitochondrial complex I deficiency during development induces glial dysfunction and early lethality

Author

Mora-Romero, Bella, Capelo-Carrasco, Nicolas, Pérez-Moreno, Juan J., Alvarez-Vergara, María I., Trujillo-Estrada, Laura, Romero-Molina, Carmen, Martinez-Marquez, Emilio, Morano-Catalan, Noelia, Vizuete, Marisa, Lopez-Barneo, Jose, Nieto-Gonzalez, Jose L., Garcia-Junco-Clemente, Pablo, Vitorica, Javier, Gutierrez, Antonia, Macias, David, Rosales-Nieves, Alicia E., and Pascual, Alberto

Published
2024
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2. Microglia mitochondrial complex I deficiency during development induces glial dysfunction and early lethality

Author

Universidad de Sevilla. Departamento de Biología Celular, Universidad de Sevilla. Departamento de Bioquímica y Biología Molecular, Universidad de Sevilla. Departamento de Fisiología Médica y Biofísica, Ministerio de Ciencia e Innovación (MICIN). España, Agencia Estatal de Investigación. España, Instituto de Salud Carlos III, European Commission (EC). Fondo Europeo de Desarrollo Regional (FEDER), Junta de Andalucía, Mora Romero, Bella, Capelo Carrasco, Nicolás, Pérez Moreno, Juan José, Álvarez Vergara, María Isabel, Trujillo Estrada, Laura Isabel, Romero Molina, Carmen, Martínez Márquez, Emilio, Morano Catalan, Noelia, Vizuete Chacón, María Luisa, López Barneo, José, Nieto González, José Luis, García-Junco Clemente, Pablo, Vitorica Ferrández, Francisco Javier, Gutiérrez, Antonia, Macías, David, Rosales Nieves, Alicia E., Pascual Bravo, Alberto, Universidad de Sevilla. Departamento de Biología Celular, Universidad de Sevilla. Departamento de Bioquímica y Biología Molecular, Universidad de Sevilla. Departamento de Fisiología Médica y Biofísica, Ministerio de Ciencia e Innovación (MICIN). España, Agencia Estatal de Investigación. España, Instituto de Salud Carlos III, European Commission (EC). Fondo Europeo de Desarrollo Regional (FEDER), Junta de Andalucía, Mora Romero, Bella, Capelo Carrasco, Nicolás, Pérez Moreno, Juan José, Álvarez Vergara, María Isabel, Trujillo Estrada, Laura Isabel, Romero Molina, Carmen, Martínez Márquez, Emilio, Morano Catalan, Noelia, Vizuete Chacón, María Luisa, López Barneo, José, Nieto González, José Luis, García-Junco Clemente, Pablo, Vitorica Ferrández, Francisco Javier, Gutiérrez, Antonia, Macías, David, Rosales Nieves, Alicia E., and Pascual Bravo, Alberto

Abstract

Primary mitochondrial diseases (PMDs) are associated with pediatric neurological disorders and are traditionally related to oxidative phosphorylation system (OXPHOS) defects in neurons. Interestingly, both PMD mouse models and patients with PMD show gliosis, and pharmacological depletion of microglia, the innate immune cells of the brain, ameliorates multiple symptoms in a mouse model. Given that microglia activation correlates with the expression of OXPHOS genes, we studied whether OXPHOS deficits in microglia may contribute to PMDs. We first observed that the metabolic rewiring associated with microglia stimulation in vitro (via IL-33 or TAU treatment) was partially changed by complex I (CI) inhibition (via rotenone treatment). In vivo, we generated a mouse model deficient for CI activity in microglia (MGcCI). MGcCI microglia showed metabolic rewiring and gradual transcriptional activation, which led to hypertrophy and dysfunction in juvenile (1-month-old) and adult (3-month-old) stages, respectively. MGcCI mice presented widespread reactive astrocytes, a decrease of synaptic markers accompanied by an increased number of parvalbumin neurons, a behavioral deficit characterized by prolonged periods of immobility, loss of weight and premature death that was partially rescued by pharmacologic depletion of microglia. Our data demonstrate that microglia development depends on mitochondrial CI and suggest a direct microglial contribution to PMDs.

Published
2024

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