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GalR3 activation promotes adult neural stem cell survival in response to a diabetic milieu
Shiva Mansouri1, Swapnali Barde, Henrik Ortsäter
1Karolinska Institutet, Department of Clinical Science and Education, Södersjukhuset, Stockholm, Sweden.
Abstract:
Type 2 diabetes impairs adult neurogenesis which could play a role in the CNS complications of this serious disease. The goal of this study was to determine the potential role of galanin in protecting adult neural stem cells (NSCs) from glucolipotoxicity and to analyze whether apoptosis and the unfolded protein response were involved in the galanin-mediated effect. We also studied the regulation of galanin and its receptor subtypes under diabetes in NSCs in vitro and in the subventricular zone (SVZ) in vivo. The viability of mouse SVZ-derived NSCs and the involvement of apoptosis (Bcl-2, cleaved caspase-3) and unfolded protein response [C/EBP homologous protein (CHOP) Glucose-regulated protein 78/immunoglobulin heavy-chain binding protein (GRP78/BiP), spliced X-box binding protein 1 (XBP1), c-Jun N-terminal kinases (JNK) phosphorylation] were assessed in the presence of glucolipotoxic conditions after 24 h. The effect of diabetes on the regulation of galanin and its receptor subtypes was assessed on NSCs in vitro and in SVZ tissues isolated from normal and type 2 diabetes ob/ob mice. We show increased NSC viability following galanin receptor (GalR)3 activation. This protective effect correlated with decreased apoptosis and CHOP levels. We also report how galanin and its receptors are regulated by diabetes in vitro and in vivo. This study shows GalR3-mediated neuroprotection, supporting a potential future therapeutic development, based on GalR3 activation, for the treatment of brain disorders.
Insights
Type 2 diabetes harms brain stem cells. Galanin receptor 3 activation protects these cells by reducing apoptosis and the unfolded protein response, offering potential therapeutic strategies for brain disorders.
Area of Science:
- Neuroscience
- Endocrinology
- Cell Biology
Background:
- Type 2 diabetes is linked to central nervous system complications.
- Adult neurogenesis impairment is a potential contributor to these complications.
- Galanin's role in protecting neural stem cells (NSCs) from glucolipotoxicity is unexplored.
Purpose of the Study:
- To investigate galanin's protective role in adult neural stem cells (NSCs) against glucolipotoxicity.
- To determine the involvement of apoptosis and the unfolded protein response in galanin's effects.
- To analyze the regulation of galanin and its receptor subtypes in diabetes.
Main Methods:
- Assessed viability of mouse subventricular zone (SVZ)-derived NSCs under glucolipotoxic conditions.
- Evaluated apoptosis markers (Bcl-2, cleaved caspase-3) and unfolded protein response pathways (CHOP, GRP78/BiP, XBP1, JNK phosphorylation).
- Examined galanin and receptor subtype regulation in NSCs in vitro and SVZ tissues from normal and type 2 diabetic mice.
Main Results:
- Galanin receptor (GalR)3 activation significantly increased NSC viability.
- This neuroprotection was associated with reduced apoptosis and C/EBP homologous protein (CHOP) levels.
- Diabetes differentially regulated galanin and its receptor subtypes in NSCs both in vitro and in vivo.
Conclusions:
- Galanin receptor 3 activation mediates neuroprotection against glucolipotoxicity.
- This pathway offers a potential therapeutic target for treating brain disorders associated with diabetes.
- Understanding galanin's role provides insights into managing CNS complications of type 2 diabetes.
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