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Published on: May 10, 2017
Lithium protects against glucocorticoid induced neural progenitor cell apoptosis in the developing cerebellum
Omar Cabrera1, Joseph Dougherty2, Sukrit Singh2
1Washington University in Saint Louis, School of Medicine, Department of Genetics, Saint Louis, MO 63110, USA.
Insights
Glucocorticoids (GCs) can harm brain development in premature infants. This study found that lithium pretreatment effectively protects neural progenitor cells (NPCs) from GC-induced cell death, offering a potential neuroprotective strategy.
Area of Science:
- Neuroscience
- Developmental Biology
- Pharmacology
Background:
- Respiratory dysfunction is a leading cause of death in premature infants.
- Antenatal and postnatal glucocorticoid (GC) therapy is common but linked to neurodevelopmental deficits.
- GC treatment may cause cerebellar neuropathology via neural progenitor cell (NPC) apoptosis.
Purpose of the Study:
- To investigate the neuroprotective potential of lithium against GC-induced NPC apoptosis.
- To determine if lithium can prevent GC-mediated toxicity in vivo and in vitro.
Main Methods:
- Utilized in vivo and in vitro models to assess GC toxicity on NPCs.
- Administered acute lithium pretreatment before GC exposure.
- Quantified NPC apoptosis and neuroprotection.
Main Results:
- Lithium pretreatment significantly attenuated GC-induced NPC toxicity.
- Demonstrated potent, cell-intrinsic neuroprotection by lithium against GC-induced apoptosis.
- Confirmed lithium's efficacy in both in vivo and in vitro experimental settings.
Conclusions:
- Lithium offers significant neuroprotection against glucocorticoid-induced neural progenitor cell toxicity.
- This finding suggests lithium as a potential therapeutic agent to mitigate GC-related neurodevelopmental deficits in vulnerable infants.
Abstract:
Respiratory dysfunction is one of the most common causes of death associated with premature birth (Barton et al., 1999). In the United States, 7-10% of pregnant women receive antenatal glucocorticoid (GC) therapy (Matthews et al., 2004), while approximately 19% of very low birth weight infants receive postnatal GC therapy (Jobe, 2009). Clinical research suggests that GC treatment causes permanent neuromotor and cognitive deficits (Yeh et al., 2004) and stunts cerebellar growth (Parikh et al., 2007; Tam et al., 2011). We previously reported that GC-mediated neural progenitor cell (NPC) apoptosis may be responsible for cerebellar neuropathology (Maloney et al., 2011; Noguchi et al., 2008, 2011). The goal of the current study was to determine whether lithium protects NPCs from GC neuroapoptosis in vivo and in vitro. Given that it protects against a range of brain insults, we hypothesized that lithium would significantly attenuate GC induced NPC toxicity. We report that acute lithium pretreatment provides potent, cell-intrinsic neuroprotection against GC induced NPC toxicity in vivo and in vitro.
