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Article

Upregulation of the Sarco-Endoplasmic Reticulum Calcium ATPase 1 Truncated Isoform Plays a Pathogenic Role in Alzheimer’s Disease

1
Université Côte d’Azur, INSERM, CNRS, IPMC, France, Laboratory of excellence DistALZ, 660 route des Lucioles, 06560 Sophia-Antipolis, Valbonne, France
2
Present address: UK Dementia Research Institute, Imperial College London, Department of Medicine, Burlington Danes Building, Hammersmith Hospital Campus, Du Cane Road, London W12 0NN, UK
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Institut Cochin, Team Cutaneous Biology, INSERM U1016, CNRS UMR8104, Université Paris Descartes, 24 rue du Faubourg Saint-Jacques, 75014 Paris, France
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Université Côte d’Azur, INSERM, U1065, C3M, 06200 Nice, France
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Unité INSERM U1151 (Eq. 13), Faculté de Médecine Paris Descartes, 75993 Paris CEDEX 14, France
*
Author to whom correspondence should be addressed.
Cells 2019, 8(12), 1539; https://doi.org/10.3390/cells8121539
Received: 12 November 2019 / Revised: 25 November 2019 / Accepted: 26 November 2019 / Published: 28 November 2019
(This article belongs to the Section Cellular Pathology)
Dysregulation of the Endoplasmic Reticulum (ER) Ca2+ homeostasis and subsequent ER stress activation occur in Alzheimer Disease (AD). We studied the contribution of the human truncated isoform of the sarco-endoplasmic reticulum Ca2+ ATPase 1 (S1T) to AD. We examined S1T expression in human AD-affected brains and its functional consequences in cellular and transgenic mice AD models. S1T expression is increased in sporadic AD brains and correlates with amyloid β (Aβ) and ER stress chaperone protein levels. Increased S1T expression was also observed in human neuroblastoma cells expressing Swedish-mutated β-amyloid precursor protein (βAPP) or treated with Aβ oligomers. Lentiviral overexpression of S1T enhances in return the production of APP C-terminal fragments and Aβ through specific increases of β-secretase expression and activity, and triggers neuroinflammation. We describe a molecular interplay between S1T-dependent ER Ca2+ leak, ER stress and βAPP-derived fragments that could contribute to AD setting and/or progression. View Full-Text
Keywords: Alzheimer disease; amyloid β; amyloid precursor protein; BACE1; C83; C99; endoplasmic reticulum stress; neuroinflammation; truncated isoform of the sarco-endoplasmic reticulum Ca2+ ATPase 1 (S1T) Alzheimer disease; amyloid β; amyloid precursor protein; BACE1; C83; C99; endoplasmic reticulum stress; neuroinflammation; truncated isoform of the sarco-endoplasmic reticulum Ca2+ ATPase 1 (S1T)
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MDPI and ACS Style

Bussiere, R.; Oulès, B.; Mary, A.; Vaillant-Beuchot, L.; Martin, C.; El Manaa, W.; Vallée, D.; Duplan, E.; Paterlini-Bréchot, P.; Alves Da Costa, C.; Checler, F.; Chami, M. Upregulation of the Sarco-Endoplasmic Reticulum Calcium ATPase 1 Truncated Isoform Plays a Pathogenic Role in Alzheimer’s Disease. Cells 2019, 8, 1539. https://doi.org/10.3390/cells8121539

AMA Style

Bussiere R, Oulès B, Mary A, Vaillant-Beuchot L, Martin C, El Manaa W, Vallée D, Duplan E, Paterlini-Bréchot P, Alves Da Costa C, Checler F, Chami M. Upregulation of the Sarco-Endoplasmic Reticulum Calcium ATPase 1 Truncated Isoform Plays a Pathogenic Role in Alzheimer’s Disease. Cells. 2019; 8(12):1539. https://doi.org/10.3390/cells8121539

Chicago/Turabian Style

Bussiere, Renaud; Oulès, Bénédicte; Mary, Arnaud; Vaillant-Beuchot, Loan; Martin, Cécile; El Manaa, Wejdane; Vallée, Déborah; Duplan, Eric; Paterlini-Bréchot, Patrizia; Alves Da Costa, Cristine; Checler, Frédéric; Chami, Mounia. 2019. "Upregulation of the Sarco-Endoplasmic Reticulum Calcium ATPase 1 Truncated Isoform Plays a Pathogenic Role in Alzheimer’s Disease" Cells 8, no. 12: 1539. https://doi.org/10.3390/cells8121539

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