Arrestin domain-containing protein 1-mediated microvesicles (ARMMs) protect against cadmium-induced neurotoxicity

Exposure to environmental heavy metals such as cadmium (Cd) is often linked to neurotoxicity but the underlying mechanisms remain poorly understood. Here we show that Arrestin domain-containing protein 1 (ARRDC1)-mediated microvesicles (ARMMs)–an important class of extracellular vesicles (EVs) whose...

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Main Authors: Zunwei Chen, Zhi Qiao, Charlotte R. Wirth, Hae-Ryung Park, Quan Lu
Format: Article
Language:English
Published: Elsevier 2023-12-01
Series:Extracellular Vesicle
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Online Access:http://www.sciencedirect.com/science/article/pii/S2773041723000069
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author Zunwei Chen
Zhi Qiao
Charlotte R. Wirth
Hae-Ryung Park
Quan Lu
author_facet Zunwei Chen
Zhi Qiao
Charlotte R. Wirth
Hae-Ryung Park
Quan Lu
author_sort Zunwei Chen
collection DOAJ
description Exposure to environmental heavy metals such as cadmium (Cd) is often linked to neurotoxicity but the underlying mechanisms remain poorly understood. Here we show that Arrestin domain-containing protein 1 (ARRDC1)-mediated microvesicles (ARMMs)–an important class of extracellular vesicles (EVs) whose biogenesis occurs at the plasma membrane–protect against Cd-induced neurotoxicity. Cd increased the production of EVs, including ARMMs, in a human neural progenitor cell line, ReNcell CX (ReN) cells. ReN cells that lack ARMMs production as a result of CRISPR-mediated ARRDC1 knockout were more susceptible to Cd toxicity as evidenced by increased LDH production as well as elevated level of oxidative stress markers. Importantly, adding ARMMs back to the ARRDC1-knockout ReN cells significantly reduced Cd-induced toxicity. Consistent with this finding, proteomics data showed that anti-oxidative stress proteins are enriched in ARMMs secreted from ReN cells. Together our study reveals a novel protective role of ARMMs in Cd neurotoxicity and suggests that ARMMs may be used therapeutically to reduce neurotoxicity caused by exposure to Cd and potentially other metal toxicants.
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spelling doaj-art-dfbef20b59734c6f82083a76ba22fd0f2025-08-20T02:50:23ZengElsevierExtracellular Vesicle2773-04172023-12-01210002710.1016/j.vesic.2023.100027Arrestin domain-containing protein 1-mediated microvesicles (ARMMs) protect against cadmium-induced neurotoxicityZunwei Chen0Zhi Qiao1Charlotte R. Wirth2Hae-Ryung Park3Quan Lu4Program in Molecular and Integrative Physiological Sciences, Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA, United States of AmericaProgram in Molecular and Integrative Physiological Sciences, Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA, United States of AmericaProgram in Molecular and Integrative Physiological Sciences, Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA, United States of AmericaDepartment of Environmental Medicine, School of Medicine and Dentistry, University of Rochester, Rochester, NY, United States of AmericaProgram in Molecular and Integrative Physiological Sciences, Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA, United States of America; Correspondence to: Program in Molecular and Integrative Physiological Sciences, Department of Environmental Health, Harvard T.H. Chan School of Public Health, 665 Huntington Avenue, Boston, MA 02115, United States of AmericaExposure to environmental heavy metals such as cadmium (Cd) is often linked to neurotoxicity but the underlying mechanisms remain poorly understood. Here we show that Arrestin domain-containing protein 1 (ARRDC1)-mediated microvesicles (ARMMs)–an important class of extracellular vesicles (EVs) whose biogenesis occurs at the plasma membrane–protect against Cd-induced neurotoxicity. Cd increased the production of EVs, including ARMMs, in a human neural progenitor cell line, ReNcell CX (ReN) cells. ReN cells that lack ARMMs production as a result of CRISPR-mediated ARRDC1 knockout were more susceptible to Cd toxicity as evidenced by increased LDH production as well as elevated level of oxidative stress markers. Importantly, adding ARMMs back to the ARRDC1-knockout ReN cells significantly reduced Cd-induced toxicity. Consistent with this finding, proteomics data showed that anti-oxidative stress proteins are enriched in ARMMs secreted from ReN cells. Together our study reveals a novel protective role of ARMMs in Cd neurotoxicity and suggests that ARMMs may be used therapeutically to reduce neurotoxicity caused by exposure to Cd and potentially other metal toxicants.http://www.sciencedirect.com/science/article/pii/S2773041723000069Heavy metalsNeurotoxicityExtracellular vesiclesARRDC1Proteomics
spellingShingle Zunwei Chen
Zhi Qiao
Charlotte R. Wirth
Hae-Ryung Park
Quan Lu
Arrestin domain-containing protein 1-mediated microvesicles (ARMMs) protect against cadmium-induced neurotoxicity
Extracellular Vesicle
Heavy metals
Neurotoxicity
Extracellular vesicles
ARRDC1
Proteomics
title Arrestin domain-containing protein 1-mediated microvesicles (ARMMs) protect against cadmium-induced neurotoxicity
title_full Arrestin domain-containing protein 1-mediated microvesicles (ARMMs) protect against cadmium-induced neurotoxicity
title_fullStr Arrestin domain-containing protein 1-mediated microvesicles (ARMMs) protect against cadmium-induced neurotoxicity
title_full_unstemmed Arrestin domain-containing protein 1-mediated microvesicles (ARMMs) protect against cadmium-induced neurotoxicity
title_short Arrestin domain-containing protein 1-mediated microvesicles (ARMMs) protect against cadmium-induced neurotoxicity
title_sort arrestin domain containing protein 1 mediated microvesicles armms protect against cadmium induced neurotoxicity
topic Heavy metals
Neurotoxicity
Extracellular vesicles
ARRDC1
Proteomics
url http://www.sciencedirect.com/science/article/pii/S2773041723000069
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