The Anemonia Sulcata Toxin BDS-I Protects Astrocytes Exposed to Aβ1-42 Oligomers by Restoring [Ca2+]i Transients and ER Ca2+ Signaling
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Intracellular calcium concentration ([Ca2+]i) transients in astrocytes represent a highly plastic signaling pathway underlying the communication between neurons and glial cells. However, how this important phenomenon may be compromised in Alzheimer’s disease (AD) remains unexplored. Moreover, the involvement of several K+ channels, including KV3.4 underlying the fast-inactivating currents, has been demonstrated in several AD models. Here, the effect of KV3.4 modulation by the marine toxin blood depressing substance-I (BDS-I) extracted from Anemonia sulcata has been studied on [Ca2+]i transients in rat primary cortical astrocytes exposed to Aβ1–42 oligomers. We showed that: (1) primary cortical astrocytes expressing KV3.4 channels displayed [Ca2+]i transients depending on the occurrence of membrane potential spikes, (2) BDS-I restored, in a dose-dependent way, [Ca2+]i transients in astrocytes exposed to Aβ1–42 oligomers (5 µM/48 h) by inhibiting hyperfunctional KV3.4 channels, (3) BDS-I counteracted Ca2+ overload into the endoplasmic reticulum (ER) induced by Aβ1–42 oligomers, (4) BDS-I prevented the expression of the ER stress markers including active caspase 12 and GRP78/BiP in astrocytes treated with Aβ1–42 oligomers, and (5) BDS-I prevented Aβ1–42-induced reactive oxygen species (ROS) production and cell suffering measured as mitochondrial activity and lactate dehydrogenase (LDH) release. Collectively, we proposed that the marine toxin BDS-I, by inhibiting the hyperfunctional KV3.4 channels and restoring [Ca2+]i oscillation frequency, prevented Aβ1–42-induced ER stress and cell suffering in astrocytes.
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Aβ exerts oxidative stress in astrocytes by altering astrocytic Ca2+ homeostasis and mitochondrial function.
“Moreover, Aβ has been recognized to exert oxidative stress in astrocytes by altering astrocytic Ca2+ homeostasis and mitochondrial function (Abramov et al., 2004; Verkhratsky et al., 2017; Piccialli et al., 2020).”
From Exploring the Therapeutic Potential of Phytochemicals in Alzheimer’s Disease: Focus on Polyphenols and Monoterpenes (2022) · cites this paper as Piccialli et al., 2020
Aβ-induced dysregulation of ionic homeostasis in astroglial cells may crucially contribute to their pathological remodelling.
“In turn, the Aβ-induced dysregulation of ionic homeostasis in astroglial cells may crucially contribute to their pathological remodelling (Boscia et al., 2017; Verkhratsky et al., 2017; Piccialli et al., 2020).”
From Exploring the Therapeutic Potential of Phytochemicals in Alzheimer’s Disease: Focus on Polyphenols and Monoterpenes (2022) · cites this paper as Piccialli et al., 2020
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Seasonal and Interannual Metal Bioaccumulation in the Sea Anemone Anemonia viridis
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Cytotoxic Effects of Cnidarian Venoms: One Cancer, Two Cell Lines
Azaiez, K., Killi, N., Türk, K. E., Demir, H. K., Babayeva, A., & Çetin, E. S. (2026) · Marine Biotechnology · doi:10.1007/s10126-026-10625-2
- Authors
- Piccialli, I., Tedeschi, V., Boscia, F., Ciccone, R., Casamassa, A., de Rosa, V., Grieco, P., Secondo, A., & Pannaccione, A.
- Affiliations
- University of Naples Federico II (IT)
- Division of Pharmacology, Department of Neuroscience, Reproductive and Dentistry Sciences, School of Medicine, Federico II University of Naples, 80131 Napoli, Italy
- Corresponding author
- Secondo, Agnese
- Pannaccione, Anna
- ORCID
- Venue
- Toxins
- Publisher
- MDPI AG
- Published
- 2020-12-31
- Volume
- 13
- Issue
- 1
- Pages
- 20
- ISSN
- 2072-6651 (ISSN-L)
- PMC
- PMC7823622
- OpenAlex
- W3117807164
- Cited by
- 14
- References
- 77
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 3 · 2023: 3 · 2022: 2 · 2021: 2
- FWCI
- 1.05
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Toxins (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, other-oa)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Università Politecnica delle Marche (Università Politecnica delle Marche) (submittedVersion)
- Funders
- University Of Naples Federico II (CA.04_CDA_n_103 27.03.2019, Progetto Ateneo Federico II)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- Anemonia sulcata, marine toxins, astrocytes, Alzheimer's disease, calcium transients, endoplasmic reticulum calcium signaling, endoplasmic reticulum stress, caspase-12, GRP78, reactive oxygen species, cell death, neuroprotection
- MeSH terms
- Animals, Astrocytes, Calcium, Cells, Cultured, Cnidarian Venoms, Endoplasmic Reticulum, Peptide Fragments, Amyloid beta-Peptides, Calcium Signaling, Rats
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