Expression of Glutamate Transporters in Mouse Liver, Kidney, and Intestine
| Autor: | Sigrid Ottestad-Hansen, Qiu Xiang Hu, Bjørnar Hassel, Yun Zhou, Niels C. Danbolt, Silvia Holmseth |
|---|---|
| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
medicine.medical_specialty Histology Immunoblotting Central nervous system Biology Kidney Mice 03 medical and health sciences 0302 clinical medicine Internal medicine Glutamine synthetase medicine Animals Staining and Labeling Fatty liver Glutamate receptor Transporter Articles medicine.disease Immunohistochemistry Small intestine Excitatory Amino Acid Transporter 1 Intestines Excitatory Amino Acid Transporter 3 030104 developmental biology medicine.anatomical_structure Endocrinology Excitatory Amino Acid Transporter 2 Liver Hepatocyte Anatomy 030217 neurology & neurosurgery |
| Zdroj: | Journal of Histochemistry & Cytochemistry. 66:189-202 |
| ISSN: | 1551-5044 0022-1554 |
| Popis: | Glutamate transport activities have been identified not only in the brain, but also in the liver, kidney, and intestine. Although glutamate transporter distributions in the central nervous system are fairly well known, there are still uncertainties with respect to the distribution of these transporters in peripheral organs. Quantitative information is mostly lacking, and few of the studies have included genetically modified animals as specificity controls. The present study provides validated qualitative and semi-quantitative data on the excitatory amino acid transporter (EAAT)1–3 subtypes in the mouse liver, kidney, and intestine. In agreement with the current view, we found high EAAT3 protein levels in the brush borders of both the distal small intestine and the renal proximal tubules. Neither EAAT1 nor EAAT2 was detected at significant levels in murine kidney or intestine. In contrast, the liver only expressed EAAT2 (but 2 C-terminal splice variants). EAAT2 was detected in the plasma membranes of perivenous hepatocytes. These cells also expressed glutamine synthetase. Conditional deletion of hepatic EAAT2 did neither lead to overt neurological disturbances nor development of fatty liver. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|