Sodium Chloride Increases Aβ Levels by Suppressing Aβ Clearance in Cultured Cells
| Autor: | Yuan Gao, Xiao-Juan Cheng, Yuwu Zhao, Xiao-Dong Cheng |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2015 |
| Předmět: |
Apolipoprotein E
medicine.medical_specialty Cell Survival lcsh:Medicine Sodium Chloride Biology Cell Line Mice Apolipoproteins E Alzheimer Disease Internal medicine medicine Amyloid precursor protein Animals Humans Cognitive decline lcsh:Science Gamma secretase Neurons Amyloid beta-Peptides Multidisciplinary HEK 293 cells lcsh:R medicine.disease Coculture Techniques Diet Rats HEK293 Cells Endocrinology Biochemistry Cell culture biology.protein lcsh:Q Amyloid Precursor Protein Secretases Alzheimer's disease Amyloid precursor protein secretase Research Article |
| Zdroj: | PLoS ONE, Vol 10, Iss 6, p e0130432 (2015) PLoS ONE |
| ISSN: | 1932-6203 |
| Popis: | Recent studies suggest that high-salt diet is associated with cognitive decline in human and mouse. The fact that genetic factors account for less than 50% cases of sporadic Alzheimer’s disease (AD) highlights the important contribution of environmental factors, such as high-salt diet, in AD pathogenesis. However, whether and how high-salt diet fits the “amyloid cascade” hypothesis remains unexplored. Here, we show sodium chloride (NaCl) could increase Aβ levels in the medium of HEK293 cells overexpressing amyloid precursor protein (APP) or C99 fragment. NaCl treatment dose not affect APP level, gamma secretase level or activity. Instead, NaCl treatment suppresses the capacity of cells to clear Aβ and reduces Apolipoprotein E (ApoE) level. Finally, NaCl treated THP-1 or BV2 cells are inefficient in clearing Aβ when co-cultured with rat primary neurons. Our study suggests that high-salt diet may increase AD risk by directly modulating Aβ levels. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|