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Endoplasmic reticulum stress responses in mouse models of Alzheimer's disease: Overexpression paradigm versus knockin paradigm

Hashimoto, Shoko, Ishii, Ayano, Kamano, Naoko, Watamura, Naoto, Saito, Takashi, Ohshima, Toshio, Yokosuka, Makoto, Saido, Takaomi C.·2018·Journal of Biological Chemistry
DOI 10.1074/jbc.m117.811315
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Abstract

Endoplasmic reticulum (ER) stress is believed to play an important role in the etiology of Alzheimer's disease (AD). The accumulation of misfolded proteins and perturbation of intracellular calcium homeostasis are thought to underlie the induction of ER stress, resulting in neuronal dysfunction and cell death. Several reports have shown an increased ER stress response in amyloid precursor protein (APP) and presenilin1 (PS1) double-transgenic (Tg) AD mouse models. However, whether the ER stress observed in these mouse models is actually caused by AD pathology remains unclear. APP and PS1 contain one and nine transmembrane domains, respectively, for which it has been postulated that overexpressed membrane proteins can become wedged in a misfolded configuration in ER membranes, thereby inducing nonspecific ER stress. Here, we used an App-knockin (KI) AD mouse model that accumulates amyloid-β (Aβ) peptide without overexpressing APP to investigate whether the ER stress response is heightened because of Aβ pathology. Thorough examinations indicated that no ER stress responses arose in App-KI or single APP-Tg mice. These results suggest that PS1 overexpression or mutation induced a nonspecific ER stress response that was independent of Aβ pathology in the double-Tg mice. Moreover, we observed no ER stress in a mouse model of tauopathy (P301S-Tau-Tg mice) at various ages, suggesting that ER stress is also not essential in tau pathology–induced neurodegeneration. We conclude that the…

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Figure 2 Expression of ER stress markers in P301S-Tau-Tg mice. a , expression levels of ER stress markers in the cortices (3-15 months ( M )) and hippocampi (12 months) of WT and P301S-Tau-Tg mice were determined. Arrowheads show bands of CHOP and p-eIF2 𝛂 , and asterisks show nonspecific bands. b , XBP1 mRNAwas detected by semiquantitative reverse transcription-PCR. c and d , mean levels ± S.E. of relative expression of ER stress markers ( n = 3). c , cortex; d , hippocampus. Differences between groups were examined for statistical significance via two-way ANOVA. n.s. , no significant difference. Error bars represent S.E.
Figure 2 Expression of ER stress markers in P301S-Tau-Tg mice. a , expression levels of ER stress markers in the cortices (3-15 months ( M )) and hippocampi (12 months) of WT and P301S-Tau-Tg mice were determined. Arrowheads show bands of CHOP and p-eIF2 𝛂 , and asterisks show nonspecific bands. b , XBP1 mRNAwas detected by semiquantitative reverse transcription-PCR. c and d , mean levels ± S.E. of relative expression of ER stress markers ( n = 3). c , cortex; d , hippocampus. Differences between groups were examined for statistical significance via two-way ANOVA. n.s. , no significant difference. Error bars represent S.E.From the PDF

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Research works printed but not linked: 33

  1. Hardy, 2002, The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics, Science, 297, 353, 10.1126/science.1072994 · DOI · Paper page
  2. Sasaguri, 2017, APP mouse models for Alzheimer's disease preclinical studies, EMBO J, 36, 2473, 10.15252/embj.201797397 · DOI · Paper page
  3. Higuchi, 2012, Mechanistic involvement of the calpain-calpastatin system in Alzheimer neuropathology, FASEB J, 26, 1204, 10.1096/fj.11-187740 · DOI
  4. Hitomi, 2004, Involvement of caspase-4 in endoplasmic reticulum stress-induced apoptosis and Aβ-induced cell death, J. Cell Biol, 165, 347, 10.1083/jcb.200310015 · DOI · Paper page
  5. Kang, 2013, Treadmill exercise represses neuronal cell death and inflammation during Aβ-induced ER stress by regulating unfolded protein response in aged presenilin 2 mutant mice, Apoptosis, 18, 1332, 10.1007/s10495-013-0884-9 · DOI
  6. Costa, 2013, Inhibition of mitochondrial cytochrome c oxidase potentiates Aβ-induced ER stress and cell death in cortical neurons, Mol. Cell. Neurosci, 52, 1, 10.1016/j.mcn.2012.09.005 · DOI
  7. Cornejo, 2013, The unfolded protein response in Alzheimer's disease, Semin. Immunopathol, 35, 277, 10.1007/s00281-013-0373-9 · DOI
  8. Endres, 2013, ER-stress in Alzheimer's disease: turning the scale?, Am. J. Neurodegener. Dis., 2, 247
  9. Barbero-Camps, 2014, Endoplasmic reticulum stress mediates amyloid β neurotoxicity via mitochondrial cholesterol trafficking, Am. J. Pathol, 184, 2066, 10.1016/j.ajpath.2014.03.014 · DOI
  10. Ron, 2007, Signal integration in the endoplasmic reticulum unfolded protein response, Nat. Rev. Mol. Cell Biol, 8, 519, 10.1038/nrm2199 · DOI · Paper page
  11. O'Connor, 2008, Phosphorylation of the translation initiation factor eIF2α increases BACE1 levels and promotes amyloidogenesis, Neuron, 60, 988, 10.1016/j.neuron.2008.10.047 · DOI · Paper page
  12. Reinhardt, 2014, Unfolded protein response signaling by transcription factor XBP-1 regulates ADAM10 and is affected in Alzheimer's disease, FASEB J, 28, 978, 10.1096/fj.13-234864 · DOI
  13. Soejima, 2013, Intracellular accumulation of toxic turn amyloid-β is associated with endoplasmic reticulum stress in Alzheimer's disease, Curr. Alzheimer Res., 10, 11
  14. Lee, 2010, Induction of the unfolded protein response and cell death pathway in Alzheimer's disease, but not in aged Tg2576 mice, Exp. Mol. Med., 42, 386, 10.3858/emm.2010.42.5.040 · DOI
  15. Tomita, 1999, C terminus of presenilin is required for overproduction of amyloidogenic Aβ42 through stabilization and endoproteolysis of presenilin, J. Neurosci, 19, 10627, 10.1523/JNEUROSCI.19-24-10627.1999 · DOI
  16. Sato, 2008, The C-terminal PAL motif and transmembrane domain 9 of presenilin 1 are involved in the formation of the catalytic pore of the γ-secretase, J. Neurosci, 28, 6264, 10.1523/JNEUROSCI.1163-08.2008 · DOI
  17. Annaert, 1999, Presenilin 1 controls γ-secretase processing of amyloid precursor protein in pre-Golgi compartments of hippocampal neurons, J. Cell Biol, 147, 277, 10.1083/jcb.147.2.277 · DOI · Paper page
  18. Area-Gomez, 2009, Presenilins are enriched in endoplasmic reticulum membranes associated with mitochondria, Am. J. Pathol, 175, 1810, 10.2353/ajpath.2009.090219 · DOI · Paper page
  19. Honarnejad, 2012, Presenilins: role in calcium homeostasis, Int. J. Biochem. Cell Biol, 44, 1983, 10.1016/j.biocel.2012.07.019 · DOI
  20. Zhang, 2010, Role of presenilins in neuronal calcium homeostasis, J. Neurosci, 30, 8566, 10.1523/JNEUROSCI.1554-10.2010 · DOI
  21. Green, 2008, SERCA pump activity is physiologically regulated by presenilin and regulates amyloid β production, J. Cell Biol, 181, 1107, 10.1083/jcb.200706171 · DOI · Paper page
  22. Guo, 1996, Alzheimer's PS-1 mutation perturbs calcium homeostasis and sensitizes PC12 cells to death induced by amyloid β-peptide, Neuroreport, 8, 379, 10.1097/00001756-199612200-00074 · DOI · Paper page
  23. Stutzmann, 2004, Dysregulated IP3 signaling in cortical neurons of knock-in mice expressing an Alzheimer's-linked mutation in presenilin1 results in exaggerated Ca2+ signals and altered membrane excitability, J. Neurosci, 24, 508, 10.1523/JNEUROSCI.4386-03.2004 · DOI · Paper page
  24. Chan, 2000, Presenilin-1 mutations increase levels of ryanodine receptors and calcium release in PC12 cells and cortical neurons, J. Biol. Chem., 275, 18195, 10.1074/jbc.M000040200 · DOI · Paper page
  25. Stutzmann, 2006, Enhanced ryanodine receptor recruitment contributes to Ca2+ disruptions in young, adult, and aged Alzheimer's disease mice, J. Neurosci, 26, 5180, 10.1523/JNEUROSCI.0739-06.2006 · DOI · Paper page
  26. Rogers, 1995, Use of thapsigargin to study Ca2+ homeostasis in cardiac cells, Biosci. Rep., 15, 341, 10.1007/BF01788366 · DOI · Paper page
  27. Katayama, 1999, Presenilin-1 mutations downregulate the signalling pathway of the unfolded-protein response, Nat. Cell Biol, 1, 479, 10.1038/70265 · DOI · Paper page
  28. Katayama, 2001, Disturbed activation of endoplasmic reticulum stress transducers by familial Alzheimer's disease-linked presenilin-1 mutations, J. Biol. Chem., 276, 43446, 10.1074/jbc.M104096200 · DOI
  29. Sato, 2000, Upregulation of BiP and CHOP by the unfolded-protein response is independent of presenilin expression, Nat. Cell Biol, 2, 863, 10.1038/35046500 · DOI
  30. Terro, 2002, Neurons overexpressing mutant presenilin-1 are more sensitive to apoptosis induced by endoplasmic reticulum-Golgi stress, J. Neurosci. Res., 69, 530, 10.1002/jnr.10312 · DOI
  31. Nijholt, 2011, Endoplasmic reticulum stress activates autophagy but not the proteasome in neuronal cells: implications for Alzheimer's disease, Cell Death Differ, 18, 1071, 10.1038/cdd.2010.176 · DOI
  32. Hsiao, 1996, Correlative memory deficits, Aβ elevation, and amyloid plaques in transgenic mice, Science, 274, 99, 10.1126/science.274.5284.99 · DOI · Paper page
  33. Hiroi, 2006, Bisphenol A binds to protein disulfide isomerase and inhibits its enzymatic and hormone-binding activities, Endocrinology, 147, 2773, 10.1210/en.2005-1235 · DOI

Cited by

Metadata

Authors
Hashimoto, S., Ishii, A., Kamano, N., Watamura, N., Saito, T., Ohshima, T., Yokosuka, M., & Saido, T. C.
ORCID
Venue
Journal of Biological Chemistry
Publisher
Elsevier BV
Published
2018-03
Volume
293
Issue
9
Pages
3118-3125
ISSN
0021-9258
DOI
10.1074/jbc.m117.811315
Cited by
76
References
8
Language
en
Licence
Funders
  • Ministry of Education, Culture, Sports, Science and Technology (Grant-in-aid for young scientists (B) 15K19036, Grant-in-aid for scientific research (B) 26290019)
  • Japan Agency for Medical Research and Development (JP15km0908001)

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