ArticleAmerican journal of physiology. Cell physiology2011
Dysregulation of Ca2+ signaling in astrocytes from mice lacking amyloid precursor protein.
Article in American journal of physiology. Cell physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.
- Cell adhesion and intracellular calcium signaling in neurons.Cell communication and signaling : CCS · 2013Pooled it
- Calcium signaling hypothesis: A non-negligible pathogenesis in Alzheimer's disease.Journal of advanced research · 2025Review
- Dysregulation of Ion Channels and Transporters and Blood-Brain Barrier Dysfunction in Alzheimer's Disease and Vascular Dementia.Aging and disease · 2024Review
- Transient Receptor Potential Channels in the Healthy and Diseased Blood-Brain Barrier.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2024Review
- SOCE as a regulator of neuronal activity.The Journal of physiology · 2024Review
- Knockdown of Amyloid Precursor Protein Increases Ion Channel Expression and Alters CaInternational journal of molecular sciences · 2023Article
- Ammonia induces amyloidogenesis in astrocytes by promoting amyloid precursor protein translocation into the endoplasmic reticulum.The Journal of biological chemistry · 2022Article
- Ion Channel Dysfunction in Astrocytes in Neurodegenerative Diseases.Frontiers in physiology · 2022Review
- Review
- APPsα rescues impaired CaProceedings of the National Academy of Sciences of the United States of America · 2021Article
- Functional Importance of Transient Receptor Potential (TRP) Channels in Neurological Disorders.Frontiers in cell and developmental biology · 2021Review
- Molecular Mechanisms of Metal Toxicity in the Pathogenesis of Alzheimer's Disease.Molecular neurobiology · 2021Review
- Alterations of the Endoplasmic Reticulum (ER) Calcium Signaling Molecular Components in Alzheimer's Disease.Cells · 2020Review
- Reversal of Calcium Dysregulation as Potential Approach for Treating Alzheimer's Disease.Current Alzheimer research · 2020Review
- TRP Channels as Emerging Therapeutic Targets for Neurodegenerative Diseases.Frontiers in physiology · 2020Review
- Astroglial Calcium Signaling in Aging and Alzheimer's Disease.Cold Spring Harbor perspectives in biology · 2019Review
- Astroglia in Alzheimer's Disease.Advances in experimental medicine and biology · 2019Review
- Role of STIM1 in neurodegeneration.World journal of biological chemistry · 2018Review
- On the Role of Store-Operated Calcium Entry in Acute and Chronic Neurodegenerative Diseases.Frontiers in molecular neuroscience · 2018Review
- Knockdown of amyloid precursor protein increases calcium levels in the endoplasmic reticulum.Scientific reports · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The relationship between altered metabolism of the amyloid-β precursor protein (APP) and Alzheimer's disease is well established but the physiological roles of APP still remain unclear. Here, we studied Ca(2+) signaling in primary cultured and freshly dissociated cortical astrocytes from APP knockout (KO) mice and from Tg5469 mice overproducing by five- to sixfold wild-type APP. Resting cytosolic Ca(2+) (measured with fura-2) was not altered in cultured astrocytes from APP KO mice. The stored Ca(2+) evaluated by measuring peak amplitude of cyclopiazonic acid [CPA, endoplasmic reticulum (ER) Ca(2+) ATPase inhibitor]-induced Ca(2+) transients in Ca(2+)-free medium was significantly smaller in APP KO astrocytes than in wild-type cells. Store-operated Ca(2+) entry (SOCE) activated by ER Ca(2+) store depletion with CPA was also greatly reduced in APP KO astrocytes. This reflected a downregulated expression in APP KO astrocytes of TRPC1 (C-type transient receptor potential) and Orai1 proteins, essential components of store-operated channels (SOCs). Indeed, silencer RNA (siRNA) knockdown of Orai1 protein expression in wild-type astrocytes significantly attenuated SOCE. SOCE was also essentially reduced in freshly dissociated APP KO astrocytes. Importantly, knockdown of APP with siRNA in cultured wild-type astrocytes markedly attenuated ATP- and CPA-induced ER Ca(2+) release and extracellular Ca(2+) influx. The latter correlated with downregulation of TRPC1. Overproduction of APP in Tg5469 mice did not alter, however, the stored Ca(2+) level, SOCE, and expression of TRPC1/4/5 in cultured astrocytes from these mice. The data demonstrate that the functional role of APP in astrocytes involves the regulation of TRPC1/Orai1-encoded SOCs critical for Ca(2+) signaling.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.