High glucose induces formation of tau hyperphosphorylation via Cav-1-mTOR pathway: A potential molecular mechanism for diabetes-induced cognitive dysfunction
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// Jing Wu 1 , Shan-Lei Zhou 1 , Lin-Hua Pi 1 , Xia-Jie Shi 1 , Ling-Ran Ma 2 , Zi Chen 1 , Min-Li Qu 1 , Xin Li 2 , Sheng-Dan Nie 3 , Duan-Fang Liao 4 , Jin-Jing Pei 5, 6, 7 and Shan Wang 1, 2 1 Department of Endocrinology, Xiang-Ya Hospital, Central South University, Changsha, Hunan, China 2 Department of Pharmaceutical Engineering, College of Chemistry and Chemical Engineering, Central South University, Changsha, Hunan, China 3 Institute of Clinical Medicine, People’s Hospital of Hunan Province, The First Affiliated Hospital of Hunan Normal University, Changsha, Hunan, China 4 Division of Stem Cell Regulation and Application, School of Pharmacy, Hunan University of Traditional Chinese Medicine, Changsha, Hunan, China 5 KI-Alzheimer’s Disease Research Center, Karolinska Institutet, Novum, Stockholm, Sweden 6 Department of Neurology, Xuan Wu Hospital, Capital Medical University, Xicheng, Beijing, China 7 Center of Alzheimer’s Disease, Beijing Institute for Brain Disorders, Beijing, China Correspondence to: Shan Wang, email: wangshancsu0717@163.com Jing Wu, email: wujing0731@163.com Keywords: diabetes mellitus, cognitive dysfunction, caveolin-1, tau hyperphosphorylation, mTOR Received: February 20, 2017 Accepted: April 07, 2017 Published: April 19, 2017 ABSTRACT The abnormally hyperphosphorylated tau is thought to be implicated in diabetes-associated cognitive deficits. The role of mammalian target of rapamycin (mTOR) / S6 kinase (S6K) signalling in the formation of tau hyperphosphorylation has been previously studied. Caveolin-1 (Cav-1), the essential structure protein of caveolae, promotes neuronal survival and growth, and inhibits glucose metabolism. In this study, we aimed to investigate the role of Cav-1 in the formation of tau hyperphosphorylation under chronic hyperglycemic condition (HGC). Diabetic rats were induced by streptozotocin (STZ). Primary hippocampal neurons with or without molecular intervention such as the transient over-expression or knock-down were subjected to HGC. The obtained experimental samples were analyzed by real time quantitative RT-PCR, Western blot, immunofluorescence or immunohistochemisty. We found: 1) that a chronic HGC directly decreases Cav-1 expression, increases tau phosphorylation and activates mTOR/S6K signalling in the brain neurons of diabetic rats, 2) that overexpression of Cav-1 attenuates tau hyperphosphorylation induced by chronic HGC in primary hippocampal neurons, whereas down-regulation of Cav-1 using Cav-1 siRNA dramatically worsens tau hyperphosphorylation via mTOR/S6K signalling pathway, and 3) that the down-regulation of Cav-1 induced by HGC is independent of mTOR signalling. Our results suggest that tau hyperphosphorylation and the sustained over-activated mTOR signalling under hyperglycemia may be due to the suppression of Cav-1. Therefore, Cav-1 is a potential therapeutic target for diabetes-induced cognitive dysfunction.
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Hyperphosphorylation of tau protein and sustained hyperactivation of mTOR signalling in hyperglycaemia may be associated with inhibition of caveolin-1.
“the hyperphosphorylation of tau protein and sustained hyperactivation of mTOR signalling in hyperglycaemia may be associated with the inhibition of caveolin-1 (Cav-1) [37].”
From Role of Tau Protein in Neurodegenerative Diseases and Development of Its Targeted Drugs: A Literature Review (2024) · cites this paper as [37]
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“High glucose regulates tau hyperphosphorylation and neuronal apoptosis through the TLR9-P38MAPK signalling pathway [36], and the hyperphosphorylation of tau protein and sustained hyperactivation of mTOR signalling in hyperglycaemia may be associated with the inhibition of caveolin-1 (Cav-1) [37].”
Background
- Authors
- Wu, J., Zhou, S.-L., Pi, L.-H., Shi, X.-J., Ma, L.-R., Chen, Z., Qu, M.-L., Li, X., Nie, S.-D., Liao, D.-F., Pei, J.-J., & Wang, S.
- Affiliations
- Central South University (CN)
- Department of Endocrinology, Xiang-Ya Hospital, Central South University, Changsha, Hunan, China
- Institute of Clinical Medicine, People's Hospital of Hunan Province, The First Affiliated Hospital of Hunan Normal University, Changsha, Hunan, China
- Hunan University of Traditional Chinese Medicine (CN)
- Capital Medical University (CN)
- Venue
- Oncotarget
- Publisher
- Impact Journals, LLC
- Published
- 2017-04-19
- Volume
- 8
- Issue
- 25
- Pages
- 40843-40856
- ISSN
- 1949-2553 (ISSN-L)
- PMC
- PMC5522306
- OpenAlex
- W2607382890
- Cited by
- 50
- References
- 86
- Citations by year
- 2026: 4 · 2025: 7 · 2024: 6 · 2023: 7 · 2022: 8 · 2021: 5 · 2020: 7 · 2019: 2 · 2018: 3 · 2017: 1
- FWCI
- 2.63
- Type
- journal article
- Language
- en
- Open access
- diamond
- doi.org
- Licence
- cc-by
- Locations
- Oncotarget (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Caveolin-1 and cellular processes
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- tau hyperphosphorylation, caveolin-1, mTOR signaling, S6 kinase, high glucose, hyperglycemia, hippocampal neurons, streptozotocin-induced diabetes, Alzheimer's disease, neurodegeneration, caveolae, neuroprotection, neuroinflammation, oxidative stress, autophagy
- MeSH terms
- Animals, Diabetes Mellitus, Experimental, Glucose, Hyperglycemia, Male, Phosphorylation, Transfection, tau Proteins, Rats, Sprague-Dawley, Caveolin 1, Rats, TOR Serine-Threonine Kinases, Cognitive Dysfunction
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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