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Published on: July 13, 2014
Ethanol Gestational Exposure Impairs Vascular Development and Endothelial Potential to Control BBB-Associated
Michele Siqueira1, Ana Paula Bérgamo Araujo1, Flávia Carvalho Alcantara Gomes1
1Laboratório de Neurobiologia Celular, Instituto de Ciências Biomédicas, Centro de Ciências da Saúde, Universidade Federal do Rio de Janeiro, Bloco F, Sala F15, Ilha do Fundão, Rio de Janeiro, RJ, 21949-902, Brazil.
Ethanol exposure during pregnancy harms developing brains, causing fetal alcohol spectrum disorders (FASD). This study shows ethanol disrupts brain blood vessel and astrocyte function, impairing blood-brain barrier development.
Area of Science:
- Neuroscience
- Developmental Biology
- Toxicology
Background:
- Ethanol consumption during pregnancy can cause fetal alcohol spectrum disorders (FASD), permanently damaging the central nervous system (CNS).
- Proper CNS development relies on neural cells, blood vessel (BV) formation, and blood-brain barrier (BBB) establishment.
- The specific effects of ethanol on these critical developmental processes are not well understood.
Purpose of the Study:
- To investigate how ethanol exposure impacts endothelial cell (EC) function.
- To examine ethanol's effects on EC interaction with astrocytes during blood-brain barrier (BBB) formation.
- To elucidate the mechanisms underlying ethanol-induced neurovascular dysfunction in fetal alcohol spectrum disorders (FASD).
Main Methods:
- Utilized a mouse model of fetal alcohol spectrum disorders (FASD) involving in utero ethanol exposure.
- Examined cerebral cortex vascularization, tight junction protein distribution, and astrocytic endfeet.
- Conducted in vitro studies on human brain microcapillary endothelial cells (HBMEC) exposed to ethanol.
- Analyzed gene and protein expression, glucose uptake, nitric oxide secretion, and astrocyte activation.
Main Results:
- Ethanol-exposed fetal mice exhibited hypervascularization with increased vessel density and aberrant ZO-1 distribution.
- In vitro ethanol exposure disrupted ECs' tight junctions, reduced glucose transporter (GLUT-1) expression, and increased nitric oxide secretion.
- Ethanol-exposed ECs secreted factors that activated astrocytes, upregulating glial fibrillary acidic protein (GFAP) and pro-inflammatory cytokines.
Conclusions:
- Ethanol exposure induces a dysfunctional phenotype in brain endothelial cells (ECs).
- This dysfunction impairs cortical vascular network formation and astrocyte function, crucial for blood-brain barrier (BBB) establishment.
- Ethanol's impact on ECs and astrocytes contributes to neurodevelopmental deficits seen in fetal alcohol spectrum disorders (FASD).
