The Effect of Glyceraldehyde-Derived Advanced Glycation End Products on β-Tubulin-Inhibited Neurite Outgrowth in SH-SY5Y Human Neuroblastoma Cells
Nutritional factors can affect the risk of developing neurological disorders and their rate of progression. In particular, abnormalities of carbohydrate metabolism in diabetes mellitus patients lead to an increased risk of neurological disorders such as Alzheimer’s disease (AD). In this study, we in...
| Main Authors: | , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
MDPI AG
2020-09-01
|
| Series: | Nutrients |
| Subjects: | |
| Online Access: | https://www.mdpi.com/2072-6643/12/10/2958 |
| _version_ | 1797552399840182272 |
|---|---|
| author | Ryuto Nasu Ayako Furukawa Keita Suzuki Masayoshi Takeuchi Yoshiki Koriyama |
| author_facet | Ryuto Nasu Ayako Furukawa Keita Suzuki Masayoshi Takeuchi Yoshiki Koriyama |
| author_sort | Ryuto Nasu |
| collection | DOAJ |
| description | Nutritional factors can affect the risk of developing neurological disorders and their rate of progression. In particular, abnormalities of carbohydrate metabolism in diabetes mellitus patients lead to an increased risk of neurological disorders such as Alzheimer’s disease (AD). In this study, we investigated the relationship between nervous system disorder and the pathogenesis of AD by exposing SH-SY5Y neuroblastoma cells to glyceraldehyde (GA). We previously reported that GA-derived toxic advanced glycation end products (toxic AGEs, TAGE) induce AD-like alterations including intracellular tau phosphorylation. However, the role of TAGE and their target molecules in the pathogenesis of AD remains unclear. In this study, we investigated the target protein for TAGE by performing two-dimensional immunoblot analysis with anti-TAGE antibody and mass spectrometry and identified β-tubulin as one of the targets. GA treatment induced TAGE-β-tubulin formation and abnormal aggregation of β-tubulin, and inhibited neurite outgrowth in SH-SY5Y cells. On the other hand, glucose-derived AGEs were also involved in developing AD. However, glucose did not make abnormal aggregation of β-tubulin and did not inhibit neurite outgrowth. Understanding the underlying mechanism of TAGE-β-tubulin formation by GA and its role in neurodegeneration may aid in the development of novel therapeutics and neuroprotection strategies. |
| first_indexed | 2024-03-10T16:00:28Z |
| format | Article |
| id | doaj.art-1cc1acd8d47f4ad3b271334a3393e481 |
| institution | Directory Open Access Journal |
| issn | 2072-6643 |
| language | English |
| last_indexed | 2024-03-10T16:00:28Z |
| publishDate | 2020-09-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Nutrients |
| spelling | doaj.art-1cc1acd8d47f4ad3b271334a3393e4812023-11-20T15:17:52ZengMDPI AGNutrients2072-66432020-09-011210295810.3390/nu12102958The Effect of Glyceraldehyde-Derived Advanced Glycation End Products on β-Tubulin-Inhibited Neurite Outgrowth in SH-SY5Y Human Neuroblastoma CellsRyuto Nasu0Ayako Furukawa1Keita Suzuki2Masayoshi Takeuchi3Yoshiki Koriyama4Graduate School and Faculty of Pharmaceutical Sciences, Suzuka University of Medical Science, 3500-3 Minamitamagaki, Suzuka 513-8670, JapanGraduate School and Faculty of Pharmaceutical Sciences, Suzuka University of Medical Science, 3500-3 Minamitamagaki, Suzuka 513-8670, JapanGraduate School and Faculty of Pharmaceutical Sciences, Suzuka University of Medical Science, 3500-3 Minamitamagaki, Suzuka 513-8670, JapanDepartment of Advanced Medicine, Medical Research Institute, Kanazawa Medical University, Uchinada-machi, Ishikawa 920-0293, JapanGraduate School and Faculty of Pharmaceutical Sciences, Suzuka University of Medical Science, 3500-3 Minamitamagaki, Suzuka 513-8670, JapanNutritional factors can affect the risk of developing neurological disorders and their rate of progression. In particular, abnormalities of carbohydrate metabolism in diabetes mellitus patients lead to an increased risk of neurological disorders such as Alzheimer’s disease (AD). In this study, we investigated the relationship between nervous system disorder and the pathogenesis of AD by exposing SH-SY5Y neuroblastoma cells to glyceraldehyde (GA). We previously reported that GA-derived toxic advanced glycation end products (toxic AGEs, TAGE) induce AD-like alterations including intracellular tau phosphorylation. However, the role of TAGE and their target molecules in the pathogenesis of AD remains unclear. In this study, we investigated the target protein for TAGE by performing two-dimensional immunoblot analysis with anti-TAGE antibody and mass spectrometry and identified β-tubulin as one of the targets. GA treatment induced TAGE-β-tubulin formation and abnormal aggregation of β-tubulin, and inhibited neurite outgrowth in SH-SY5Y cells. On the other hand, glucose-derived AGEs were also involved in developing AD. However, glucose did not make abnormal aggregation of β-tubulin and did not inhibit neurite outgrowth. Understanding the underlying mechanism of TAGE-β-tubulin formation by GA and its role in neurodegeneration may aid in the development of novel therapeutics and neuroprotection strategies.https://www.mdpi.com/2072-6643/12/10/2958toxic advanced glycation-end products (TAGE)glyceraldehyde (GA)Alzheimer’s disease (AD)diabetes mellitus (DM)β-tubulinneurite outgrowth |
| spellingShingle | Ryuto Nasu Ayako Furukawa Keita Suzuki Masayoshi Takeuchi Yoshiki Koriyama The Effect of Glyceraldehyde-Derived Advanced Glycation End Products on β-Tubulin-Inhibited Neurite Outgrowth in SH-SY5Y Human Neuroblastoma Cells Nutrients toxic advanced glycation-end products (TAGE) glyceraldehyde (GA) Alzheimer’s disease (AD) diabetes mellitus (DM) β-tubulin neurite outgrowth |
| title | The Effect of Glyceraldehyde-Derived Advanced Glycation End Products on β-Tubulin-Inhibited Neurite Outgrowth in SH-SY5Y Human Neuroblastoma Cells |
| title_full | The Effect of Glyceraldehyde-Derived Advanced Glycation End Products on β-Tubulin-Inhibited Neurite Outgrowth in SH-SY5Y Human Neuroblastoma Cells |
| title_fullStr | The Effect of Glyceraldehyde-Derived Advanced Glycation End Products on β-Tubulin-Inhibited Neurite Outgrowth in SH-SY5Y Human Neuroblastoma Cells |
| title_full_unstemmed | The Effect of Glyceraldehyde-Derived Advanced Glycation End Products on β-Tubulin-Inhibited Neurite Outgrowth in SH-SY5Y Human Neuroblastoma Cells |
| title_short | The Effect of Glyceraldehyde-Derived Advanced Glycation End Products on β-Tubulin-Inhibited Neurite Outgrowth in SH-SY5Y Human Neuroblastoma Cells |
| title_sort | effect of glyceraldehyde derived advanced glycation end products on β tubulin inhibited neurite outgrowth in sh sy5y human neuroblastoma cells |
| topic | toxic advanced glycation-end products (TAGE) glyceraldehyde (GA) Alzheimer’s disease (AD) diabetes mellitus (DM) β-tubulin neurite outgrowth |
| url | https://www.mdpi.com/2072-6643/12/10/2958 |
| work_keys_str_mv | AT ryutonasu theeffectofglyceraldehydederivedadvancedglycationendproductsonbtubulininhibitedneuriteoutgrowthinshsy5yhumanneuroblastomacells AT ayakofurukawa theeffectofglyceraldehydederivedadvancedglycationendproductsonbtubulininhibitedneuriteoutgrowthinshsy5yhumanneuroblastomacells AT keitasuzuki theeffectofglyceraldehydederivedadvancedglycationendproductsonbtubulininhibitedneuriteoutgrowthinshsy5yhumanneuroblastomacells AT masayoshitakeuchi theeffectofglyceraldehydederivedadvancedglycationendproductsonbtubulininhibitedneuriteoutgrowthinshsy5yhumanneuroblastomacells AT yoshikikoriyama theeffectofglyceraldehydederivedadvancedglycationendproductsonbtubulininhibitedneuriteoutgrowthinshsy5yhumanneuroblastomacells AT ryutonasu effectofglyceraldehydederivedadvancedglycationendproductsonbtubulininhibitedneuriteoutgrowthinshsy5yhumanneuroblastomacells AT ayakofurukawa effectofglyceraldehydederivedadvancedglycationendproductsonbtubulininhibitedneuriteoutgrowthinshsy5yhumanneuroblastomacells AT keitasuzuki effectofglyceraldehydederivedadvancedglycationendproductsonbtubulininhibitedneuriteoutgrowthinshsy5yhumanneuroblastomacells AT masayoshitakeuchi effectofglyceraldehydederivedadvancedglycationendproductsonbtubulininhibitedneuriteoutgrowthinshsy5yhumanneuroblastomacells AT yoshikikoriyama effectofglyceraldehydederivedadvancedglycationendproductsonbtubulininhibitedneuriteoutgrowthinshsy5yhumanneuroblastomacells |