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Akt and MAPK/ERK signaling regulate neurite extension in adult neural progenitor cells but do not directly mediate disruption of cytoskeletal structure and neurite dynamics by low-level silver nanoparticles.
Toxicol In Vitro. 2021 Aug; 74:105151.TV

Abstract

Silver nanoparticles (AgNPs) are an environmental contaminant of emerging concern. Ionic and colloidal silver has long been used for its antimicrobial properties, but with the development of engineered AgNPs, these are increasingly incorporated in the manufacture of nano-enhanced products. AgNPs are released into the environment from manufacturing plants and they can be shed from products during use and after disposal. This can lead to chronic low-level environmental exposure in animals. Unlike traditional forms of silver, the unique physical properties of AgNPs allow them to bypass biological barriers and enter tissues, like the brain, where they can bioaccumulate. Thus, it is important to understand if low-level AgNPs induce physiological changes in brain cells. Previously we found that 1.0 μg/mL AgNP exposure resulted in disruption of f-actin organization and neurite collapse in cultured differentiating adult neural stem cells, and that interaction with β-catenin signaling was involved. Here, we report that AgNP exposure may interact with pAkt signaling irreversibly or indirectly to disrupt cytoskeleton and inhibit neurite extension. Furthermore, the MAPK/ERK signaling pathway is not a target for AgNP-mediated dysregulation. Environmental exposure to low-level AgNPs therefore appears to target specific cellular mechanisms to alter brain cell physiology. Understanding these underlying mechanisms is important for decisions regulating the use and disposal of manufactured AgNPs.

Authors+Show Affiliations

Department of Biological Sciences, Marshall University, One John Marshall Dr., Huntington, WV, 25755, United States of America. Electronic address: spitzern@marshall.edu.Department of Biological Sciences, Marshall University, One John Marshall Dr., Huntington, WV, 25755, United States of America.Department of Biological Sciences, Marshall University, One John Marshall Dr., Huntington, WV, 25755, United States of America.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

33753175

Citation

Spitzer, Nadja, et al. "Akt and MAPK/ERK Signaling Regulate Neurite Extension in Adult Neural Progenitor Cells but Do Not Directly Mediate Disruption of Cytoskeletal Structure and Neurite Dynamics By Low-level Silver Nanoparticles." Toxicology in Vitro : an International Journal Published in Association With BIBRA, vol. 74, 2021, p. 105151.
Spitzer N, Patterson KK, Kipps DW. Akt and MAPK/ERK signaling regulate neurite extension in adult neural progenitor cells but do not directly mediate disruption of cytoskeletal structure and neurite dynamics by low-level silver nanoparticles. Toxicol In Vitro. 2021;74:105151.
Spitzer, N., Patterson, K. K., & Kipps, D. W. (2021). Akt and MAPK/ERK signaling regulate neurite extension in adult neural progenitor cells but do not directly mediate disruption of cytoskeletal structure and neurite dynamics by low-level silver nanoparticles. Toxicology in Vitro : an International Journal Published in Association With BIBRA, 74, 105151. https://doi.org/10.1016/j.tiv.2021.105151
Spitzer N, Patterson KK, Kipps DW. Akt and MAPK/ERK Signaling Regulate Neurite Extension in Adult Neural Progenitor Cells but Do Not Directly Mediate Disruption of Cytoskeletal Structure and Neurite Dynamics By Low-level Silver Nanoparticles. Toxicol In Vitro. 2021;74:105151. PubMed PMID: 33753175.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Akt and MAPK/ERK signaling regulate neurite extension in adult neural progenitor cells but do not directly mediate disruption of cytoskeletal structure and neurite dynamics by low-level silver nanoparticles. AU - Spitzer,Nadja, AU - Patterson,Kay-Cee K, AU - Kipps,Daniel W, Y1 - 2021/03/19/ PY - 2020/11/30/received PY - 2021/02/23/revised PY - 2021/03/18/accepted PY - 2021/3/24/pubmed PY - 2021/3/24/medline PY - 2021/3/23/entrez KW - F-actin KW - Neural stem cells KW - Subventricular zone SP - 105151 EP - 105151 JF - Toxicology in vitro : an international journal published in association with BIBRA JO - Toxicol In Vitro VL - 74 N2 - Silver nanoparticles (AgNPs) are an environmental contaminant of emerging concern. Ionic and colloidal silver has long been used for its antimicrobial properties, but with the development of engineered AgNPs, these are increasingly incorporated in the manufacture of nano-enhanced products. AgNPs are released into the environment from manufacturing plants and they can be shed from products during use and after disposal. This can lead to chronic low-level environmental exposure in animals. Unlike traditional forms of silver, the unique physical properties of AgNPs allow them to bypass biological barriers and enter tissues, like the brain, where they can bioaccumulate. Thus, it is important to understand if low-level AgNPs induce physiological changes in brain cells. Previously we found that 1.0 μg/mL AgNP exposure resulted in disruption of f-actin organization and neurite collapse in cultured differentiating adult neural stem cells, and that interaction with β-catenin signaling was involved. Here, we report that AgNP exposure may interact with pAkt signaling irreversibly or indirectly to disrupt cytoskeleton and inhibit neurite extension. Furthermore, the MAPK/ERK signaling pathway is not a target for AgNP-mediated dysregulation. Environmental exposure to low-level AgNPs therefore appears to target specific cellular mechanisms to alter brain cell physiology. Understanding these underlying mechanisms is important for decisions regulating the use and disposal of manufactured AgNPs. SN - 1879-3177 UR - https://www.unboundmedicine.com/medline/citation/33753175/Akt_and_MAPK/ERK_signaling_regulate_neurite_extension_in_adult_neural_progenitor_cells_but_do_not_directly_mediate_disruption_of_cytoskeletal_structure_and_neurite_dynamics_by_low-level_silver_nanoparticles. L2 - https://linkinghub.elsevier.com/retrieve/pii/S0887-2333(21)00076-X DB - PRIME DP - Unbound Medicine ER -
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