2021
DOI: 10.1016/j.ibneur.2021.07.003
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Mid-pregnancy maternal immune activation increases Pax6-positive and Tbr2-positive neural progenitor cells and causes integrated stress response in the fetal brain in a mouse model of maternal viral infection

Abstract: Maternal immune activation (MIA) in midpregnancy is a risk factor for neurodevelopmental disorders. Improper brain development may cause malformations of the brain; maldevelopment induced by MIA may lead to a pathology-related phenotype. In this study, a single intraperitoneal injection of 20 mg/kg polyriboinosinic–polyribocytidylic acid [poly(I:C)] was administered to C57BL/6J mice on embryonic day (E) 12.5 to mimic maternal viral infection. Histopathological analysis of neurogenesis was performed using marke… Show more

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Cited by 10 publications
(12 citation statements)
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“…In our mouse model, which is based on calorie deprivation by restricting access to food, it is impossible to distinguish whether the effects seen are due to calorie restriction per se or due to the lack of specific nutrients such as proteins, vitamins etc. The ISR is known to be implicated in the pathogenesis of preeclampsia [ 60 ] and in neurodevelopmental deficits [ 61 , 62 ], to name a few of prenatal pathologies. Given that there are some indications that Nrf2 can possibly co-operate with Atf4 signaling in order to induce an antioxidant-cytoprotective response [ 63 ], it would be plausible that such an interaction may also be present in life in utero and consist one of the mechanisms of embryonic protection.…”
Section: Discussionmentioning
confidence: 99%
“…In our mouse model, which is based on calorie deprivation by restricting access to food, it is impossible to distinguish whether the effects seen are due to calorie restriction per se or due to the lack of specific nutrients such as proteins, vitamins etc. The ISR is known to be implicated in the pathogenesis of preeclampsia [ 60 ] and in neurodevelopmental deficits [ 61 , 62 ], to name a few of prenatal pathologies. Given that there are some indications that Nrf2 can possibly co-operate with Atf4 signaling in order to induce an antioxidant-cytoprotective response [ 63 ], it would be plausible that such an interaction may also be present in life in utero and consist one of the mechanisms of embryonic protection.…”
Section: Discussionmentioning
confidence: 99%
“…Timing of MIA induction may be particularly important in this case due to the rapid and precise nature of embryonic neurogenesis (Urbán and Guillemot, 2014). The majority of studies referenced in this review expose pregnant mice to MIA at E12.5-13.5 (Maekawa et al, 2005;Osumi et al, 2008;Carpentier et al, 2011;Stolp et al, 2011;Gallagher et al, 2013;Choi et al, 2016;Braun et al, 2019;Ben-Reuven and Reiner, 2021;Canales et al, 2021;Tsukada et al, 2021), which, in typical murine neurodevelopment, coincides with significant changes in The impact of MIA on murine corticogenesis. Exposure to MIA whilst in utero causes an acute neurogenesis defect, associated with a decreased proportion of symmetric, proliferative divisions and increased number of asymmetric, neurogenic divisions.…”
Section: Neurogenesismentioning
confidence: 91%
“…This is demonstrated by cell cycle parameter changes recorded acutely following MIA, including a shortening of S-phase, which has been associated with a commitment to neuron production (Salomoni and Calegari, 2010;Arai et al, 2011;Mi et al, 2018;Ben-Reuven and Reiner, 2021). In accordance, it appears more NECs are dividing asymmetrically to form RGCs, IPCs or neurons, which is demonstrated by increased expansion of the RGC (PAX6) population (De Miranda et al, 2010;Tsukada et al, 2021) and elevated proportion of newly formed IPCs (Tsukada et al, 2021), contributing to indirect neurogenesis. Furthermore, studies report increased number of RGCs giving rise to a post-mitotic neuron and RGC, otherwise known as direct neurogenesis (Ben-Reuven and Reiner, 2021).…”
Section: Neurogenesismentioning
confidence: 96%
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