Abstract
Glutamine transporter protein SLC1A5 and glutamate transporter protein EAAT2 responsible for cell-cell communication and energetic coupling were studied using in vitro model of multicellular neurovascular unit consisting of astrocytes, neurons, and endotheliocytes under standard conditions and during chemical hypoxia in vitro. Hypoxic damage to the neurovascular unit cells increased the number of SLC1A5-expressing cells and reduced the number of EAAT2-expressing astrocytes. Metabolic uncoupling in the neurovascular unit cells under hypoxic conditions resulted from abnormal expression of glutamine and glutamate transporter proteins, which is indicative of impaired glutamine and glutamate transport.
Keywords:
cell–cell interactions; hypoxia; neurovascular unit; transport proteins.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Amino Acid Transport System ASC / genetics*
-
Amino Acid Transport System ASC / metabolism
-
Animals
-
Astrocytes / cytology
-
Astrocytes / drug effects*
-
Astrocytes / metabolism
-
Biological Transport
-
Brain
-
Cell Communication
-
Cell Differentiation
-
Cell Hypoxia
-
Embryo, Mammalian
-
Endothelial Cells / cytology
-
Endothelial Cells / drug effects*
-
Endothelial Cells / metabolism
-
Excitatory Amino Acid Transporter 2 / genetics*
-
Excitatory Amino Acid Transporter 2 / metabolism
-
Gene Expression / drug effects*
-
Glutamic Acid / metabolism
-
Glutamine / metabolism
-
Iodoacetic Acid / pharmacology
-
Minor Histocompatibility Antigens
-
Models, Biological
-
Neural Stem Cells / cytology
-
Neural Stem Cells / drug effects
-
Neural Stem Cells / metabolism
-
Neurons / cytology
-
Neurons / drug effects*
-
Neurons / metabolism
-
Primary Cell Culture
-
Rats
Substances
-
Amino Acid Transport System ASC
-
Excitatory Amino Acid Transporter 2
-
Minor Histocompatibility Antigens
-
Slc1a2 protein, rat
-
Slc1a5 protein, rat
-
Glutamine
-
Glutamic Acid
-
Iodoacetic Acid