Differential expression of glycogen synthase kinase 3α and 3β isomers in brain cortex of mice following high doses of glucose
| Autor: | Tarek Hussein, Bahaa Al-Trad, Ammar Almaaytah, Mohamed J. Saadh, Ashfaque Hossain, Mohd Alaraj, Irena Kosińska |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
medicine.medical_specialty
Chemistry Neurodegeneration Mitochondrion medicine.disease medicine.anatomical_structure Endocrinology Real-time polymerase chain reaction Cerebral cortex GSK-3 Cortex (anatomy) Internal medicine Gene expression medicine General Pharmacology Toxicology and Pharmaceutics Protein kinase A |
| Zdroj: | International Journal of Research in Pharmaceutical Sciences. 11:993-999 |
| ISSN: | 0975-7538 |
| DOI: | 10.26452/ijrps.v11i1.1926 |
| Popis: | Glycogen synthase kinase 3 (GSK3) encodes a serine/threonine protein kinase. We investigated the effects of Subcutaneous (SC) glucose administration on the expression of glycogen synthase kinase 3 (GKS-3) isomers (α and β) genes in the cerebral cortex of mice with the aim of determining the possible mechanism(s) involved in mitochondrial dysfunction induced by hyperglycemia. Adult male BALB/c mice were treated with 12 gm/kg glucose solution SC once daily for 3 days. Ultrastructure study, histopathological analysis, and Real-time PCR investigations were carried out on the cerebral cortex from glucose treated mice and from vehicle-treated control animals. We observed significant ultrastructural damage of mitochondria in the cerebral cortex of mice received high doses of glucose. Histopathological alterations in the cortex of these animals were also detected. A significant increased of GSK-3α gene expression and decreased expressions of GKS-3β gene in high glucose treated animals were noticed. The hyperglycemia-induced ultrastructural changes may occur via modulation of gene expression of GSK-3 isomers, and we hypothesize this as an early etiopathological factor in hyperglycemia-related neurodegenerative diseases (NDD). It considered the first study describing "modulation of expression of GSK-3 isomer genes" as a possible mechanism of hyperglycemia-induced mitochondrial dysfunction. |
| Databáze: | OpenAIRE |
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