Impairment of mitochondrial dynamics involved in iron oxide nanoparticle‐induced dysfunction of dendritic cells was alleviated by autophagy inhibitor 3‐methyladenine

Iron oxide nanoparticles are nanomaterials that are used extensively in the biomedical field, but they are associated with adverse effects, including mitochondrial toxicity. Mitochondrial homeostasis is achieved through dynamic stability based on two sets of antagonistic balanced processes: mitochon...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Journal of applied toxicology 2020-05, Vol.40 (5), p.631-642
Hauptverfasser: Zhang, Tian‐guang, Zhang, Yu‐long, Zhou, Qian‐qian, Wang, Xiao‐hui, Zhan, Lin‐sheng
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 642
container_issue 5
container_start_page 631
container_title Journal of applied toxicology
container_volume 40
creator Zhang, Tian‐guang
Zhang, Yu‐long
Zhou, Qian‐qian
Wang, Xiao‐hui
Zhan, Lin‐sheng
description Iron oxide nanoparticles are nanomaterials that are used extensively in the biomedical field, but they are associated with adverse effects, including mitochondrial toxicity. Mitochondrial homeostasis is achieved through dynamic stability based on two sets of antagonistic balanced processes: mitochondrial biogenesis and degradation as well as mitochondrial fission and fusion. In this study, we showed that PEG‐COOH‐coated Fe3O4 (PEG‐Fe3O4) nanoparticles induced mitochondrial instability in dendritic cells (DCs) by impairing mitochondrial dynamics due to promotion of mitochondrial biogenesis through activation of the peroxisome proliferator‐activated receptor γ coactivator 1α (PGC1α) pathway, inhibiting mitochondrial degradation via decreased autophagy, and facilitating mitochondrial fragmentation involving increased levels of DRP1 and MFN2. The resulting reduced levels of dextran uptake, CD80, CD86 and chemokine receptor 7 (CCR7) suggested that PEG‐Fe3O4 nanoparticles impaired the functionally immature state of DCs. Autophagy inhibitor 3‐methyladenine (3‐MA) alleviated PEG‐Fe3O4 nanoparticle‐induced mitochondrial instability and impairment of the functionally immature state of DCs due to unexpected enhancement of PGC1α/MFN2‐mediated coordination of mitochondrial biogenesis and fusion. Iron oxide nanoparticles are adversely associated with mitochondrial toxicity. The present study showed that PEG‐COOH‐coated Fe3O4 (PEG‐Fe3O4) nanoparticles induced mitochondrial instability in dendritic cells (DCs) by promoting mitochondrial biogenesis, inhibiting mitochondrial degradation and facilitating mitochondrial fragmentation. The resulting reduced levels of dextran uptake, costimulatory molecules and chemokine receptor 7 suggested that PEG‐Fe3O4 nanoparticles impaired DC function. 3‐methyladenine alleviated PEG‐Fe3O4 nanoparticle‐induced mitochondrial instability and impairment of DC function due to enhancing the coordination of mitochondrial biogenesis and fusion.
doi_str_mv 10.1002/jat.3933
format Article
fullrecord <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2336260369</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2336260369</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3493-6571c177dba740e1e37b96bc15137356ea7d04e49a56a9f68408c8066d6288df3</originalsourceid><addsrcrecordid>eNp1kc-K1TAUh4MoznUUfAIJuHHTMWnatFkOg39GBtyM4K6cJqfeXNKkJu0du_MRfA1fyycxdcZZCK5yIB_f-XF-hDzn7IwzVr4-wHwmlBAPyI4zpQpeSvGQ7FgpWVGJ5vMJeZLSgbH8V7aPyYngqixLqXbk5-U4gY0j-pmGgY52DnofvIkWHDWrh9HqRK0_BndEkwdqY_A0fLMGqQcfJoiz1Q5_ff9hvVl0hsyahsXr2W7gQA1uugxRjc4legOJgnN4tDBnul8pLHOY9vBlzf697XOGSEUWjjjvVwdZYD0-JY8GcAmf3b2n5NPbN9cX74urj-8uL86vCi0qJQpZN1zzpjE9NBVDjqLplew1r7loRC0RGsMqrBTUEtQg24q1umVSGlm2rRnEKXl1651i-LpgmrvRpi05eAxL6kohZL6rkCqjL_9BD2GJPqfLlGKirlXeei_UMaQUceimaEeIa8dZt9XX5fq6rb6MvrgTLv2I5h7821cGilvgxjpc_yvqPpxf_xH-BoNeqSk</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2390355951</pqid></control><display><type>article</type><title>Impairment of mitochondrial dynamics involved in iron oxide nanoparticle‐induced dysfunction of dendritic cells was alleviated by autophagy inhibitor 3‐methyladenine</title><source>Access via Wiley Online Library</source><creator>Zhang, Tian‐guang ; Zhang, Yu‐long ; Zhou, Qian‐qian ; Wang, Xiao‐hui ; Zhan, Lin‐sheng</creator><creatorcontrib>Zhang, Tian‐guang ; Zhang, Yu‐long ; Zhou, Qian‐qian ; Wang, Xiao‐hui ; Zhan, Lin‐sheng</creatorcontrib><description>Iron oxide nanoparticles are nanomaterials that are used extensively in the biomedical field, but they are associated with adverse effects, including mitochondrial toxicity. Mitochondrial homeostasis is achieved through dynamic stability based on two sets of antagonistic balanced processes: mitochondrial biogenesis and degradation as well as mitochondrial fission and fusion. In this study, we showed that PEG‐COOH‐coated Fe3O4 (PEG‐Fe3O4) nanoparticles induced mitochondrial instability in dendritic cells (DCs) by impairing mitochondrial dynamics due to promotion of mitochondrial biogenesis through activation of the peroxisome proliferator‐activated receptor γ coactivator 1α (PGC1α) pathway, inhibiting mitochondrial degradation via decreased autophagy, and facilitating mitochondrial fragmentation involving increased levels of DRP1 and MFN2. The resulting reduced levels of dextran uptake, CD80, CD86 and chemokine receptor 7 (CCR7) suggested that PEG‐Fe3O4 nanoparticles impaired the functionally immature state of DCs. Autophagy inhibitor 3‐methyladenine (3‐MA) alleviated PEG‐Fe3O4 nanoparticle‐induced mitochondrial instability and impairment of the functionally immature state of DCs due to unexpected enhancement of PGC1α/MFN2‐mediated coordination of mitochondrial biogenesis and fusion. Iron oxide nanoparticles are adversely associated with mitochondrial toxicity. The present study showed that PEG‐COOH‐coated Fe3O4 (PEG‐Fe3O4) nanoparticles induced mitochondrial instability in dendritic cells (DCs) by promoting mitochondrial biogenesis, inhibiting mitochondrial degradation and facilitating mitochondrial fragmentation. The resulting reduced levels of dextran uptake, costimulatory molecules and chemokine receptor 7 suggested that PEG‐Fe3O4 nanoparticles impaired DC function. 3‐methyladenine alleviated PEG‐Fe3O4 nanoparticle‐induced mitochondrial instability and impairment of DC function due to enhancing the coordination of mitochondrial biogenesis and fusion.</description><identifier>ISSN: 0260-437X</identifier><identifier>EISSN: 1099-1263</identifier><identifier>DOI: 10.1002/jat.3933</identifier><identifier>PMID: 31922269</identifier><language>eng</language><publisher>England: Wiley Subscription Services, Inc</publisher><subject>3‐methyladenine ; Autophagy ; Biocompatibility ; Biosynthesis ; CC chemokine receptors ; CCR7 protein ; CD80 antigen ; CD86 antigen ; Degradation ; Dendritic cells ; Dextran ; Dynamic stability ; Homeostasis ; Impairment ; Inhibitors ; iron oxide nanoparticles ; Iron oxides ; Mitochondria ; mitochondrial dynamics ; mitochondrial homeostasis ; Nanomaterials ; Nanoparticles ; Nanotechnology ; Phagocytosis ; Polyethylene glycol ; Receptors ; Toxicity</subject><ispartof>Journal of applied toxicology, 2020-05, Vol.40 (5), p.631-642</ispartof><rights>2020 John Wiley &amp; Sons, Ltd.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3493-6571c177dba740e1e37b96bc15137356ea7d04e49a56a9f68408c8066d6288df3</citedby><cites>FETCH-LOGICAL-c3493-6571c177dba740e1e37b96bc15137356ea7d04e49a56a9f68408c8066d6288df3</cites><orcidid>0000-0001-5753-1804</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjat.3933$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjat.3933$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31922269$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Tian‐guang</creatorcontrib><creatorcontrib>Zhang, Yu‐long</creatorcontrib><creatorcontrib>Zhou, Qian‐qian</creatorcontrib><creatorcontrib>Wang, Xiao‐hui</creatorcontrib><creatorcontrib>Zhan, Lin‐sheng</creatorcontrib><title>Impairment of mitochondrial dynamics involved in iron oxide nanoparticle‐induced dysfunction of dendritic cells was alleviated by autophagy inhibitor 3‐methyladenine</title><title>Journal of applied toxicology</title><addtitle>J Appl Toxicol</addtitle><description>Iron oxide nanoparticles are nanomaterials that are used extensively in the biomedical field, but they are associated with adverse effects, including mitochondrial toxicity. Mitochondrial homeostasis is achieved through dynamic stability based on two sets of antagonistic balanced processes: mitochondrial biogenesis and degradation as well as mitochondrial fission and fusion. In this study, we showed that PEG‐COOH‐coated Fe3O4 (PEG‐Fe3O4) nanoparticles induced mitochondrial instability in dendritic cells (DCs) by impairing mitochondrial dynamics due to promotion of mitochondrial biogenesis through activation of the peroxisome proliferator‐activated receptor γ coactivator 1α (PGC1α) pathway, inhibiting mitochondrial degradation via decreased autophagy, and facilitating mitochondrial fragmentation involving increased levels of DRP1 and MFN2. The resulting reduced levels of dextran uptake, CD80, CD86 and chemokine receptor 7 (CCR7) suggested that PEG‐Fe3O4 nanoparticles impaired the functionally immature state of DCs. Autophagy inhibitor 3‐methyladenine (3‐MA) alleviated PEG‐Fe3O4 nanoparticle‐induced mitochondrial instability and impairment of the functionally immature state of DCs due to unexpected enhancement of PGC1α/MFN2‐mediated coordination of mitochondrial biogenesis and fusion. Iron oxide nanoparticles are adversely associated with mitochondrial toxicity. The present study showed that PEG‐COOH‐coated Fe3O4 (PEG‐Fe3O4) nanoparticles induced mitochondrial instability in dendritic cells (DCs) by promoting mitochondrial biogenesis, inhibiting mitochondrial degradation and facilitating mitochondrial fragmentation. The resulting reduced levels of dextran uptake, costimulatory molecules and chemokine receptor 7 suggested that PEG‐Fe3O4 nanoparticles impaired DC function. 3‐methyladenine alleviated PEG‐Fe3O4 nanoparticle‐induced mitochondrial instability and impairment of DC function due to enhancing the coordination of mitochondrial biogenesis and fusion.</description><subject>3‐methyladenine</subject><subject>Autophagy</subject><subject>Biocompatibility</subject><subject>Biosynthesis</subject><subject>CC chemokine receptors</subject><subject>CCR7 protein</subject><subject>CD80 antigen</subject><subject>CD86 antigen</subject><subject>Degradation</subject><subject>Dendritic cells</subject><subject>Dextran</subject><subject>Dynamic stability</subject><subject>Homeostasis</subject><subject>Impairment</subject><subject>Inhibitors</subject><subject>iron oxide nanoparticles</subject><subject>Iron oxides</subject><subject>Mitochondria</subject><subject>mitochondrial dynamics</subject><subject>mitochondrial homeostasis</subject><subject>Nanomaterials</subject><subject>Nanoparticles</subject><subject>Nanotechnology</subject><subject>Phagocytosis</subject><subject>Polyethylene glycol</subject><subject>Receptors</subject><subject>Toxicity</subject><issn>0260-437X</issn><issn>1099-1263</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><recordid>eNp1kc-K1TAUh4MoznUUfAIJuHHTMWnatFkOg39GBtyM4K6cJqfeXNKkJu0du_MRfA1fyycxdcZZCK5yIB_f-XF-hDzn7IwzVr4-wHwmlBAPyI4zpQpeSvGQ7FgpWVGJ5vMJeZLSgbH8V7aPyYngqixLqXbk5-U4gY0j-pmGgY52DnofvIkWHDWrh9HqRK0_BndEkwdqY_A0fLMGqQcfJoiz1Q5_ff9hvVl0hsyahsXr2W7gQA1uugxRjc4legOJgnN4tDBnul8pLHOY9vBlzf697XOGSEUWjjjvVwdZYD0-JY8GcAmf3b2n5NPbN9cX74urj-8uL86vCi0qJQpZN1zzpjE9NBVDjqLplew1r7loRC0RGsMqrBTUEtQg24q1umVSGlm2rRnEKXl1651i-LpgmrvRpi05eAxL6kohZL6rkCqjL_9BD2GJPqfLlGKirlXeei_UMaQUceimaEeIa8dZt9XX5fq6rb6MvrgTLv2I5h7821cGilvgxjpc_yvqPpxf_xH-BoNeqSk</recordid><startdate>202005</startdate><enddate>202005</enddate><creator>Zhang, Tian‐guang</creator><creator>Zhang, Yu‐long</creator><creator>Zhou, Qian‐qian</creator><creator>Wang, Xiao‐hui</creator><creator>Zhan, Lin‐sheng</creator><general>Wiley Subscription Services, Inc</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7ST</scope><scope>7TK</scope><scope>7U7</scope><scope>C1K</scope><scope>K9.</scope><scope>SOI</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-5753-1804</orcidid></search><sort><creationdate>202005</creationdate><title>Impairment of mitochondrial dynamics involved in iron oxide nanoparticle‐induced dysfunction of dendritic cells was alleviated by autophagy inhibitor 3‐methyladenine</title><author>Zhang, Tian‐guang ; Zhang, Yu‐long ; Zhou, Qian‐qian ; Wang, Xiao‐hui ; Zhan, Lin‐sheng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3493-6571c177dba740e1e37b96bc15137356ea7d04e49a56a9f68408c8066d6288df3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>3‐methyladenine</topic><topic>Autophagy</topic><topic>Biocompatibility</topic><topic>Biosynthesis</topic><topic>CC chemokine receptors</topic><topic>CCR7 protein</topic><topic>CD80 antigen</topic><topic>CD86 antigen</topic><topic>Degradation</topic><topic>Dendritic cells</topic><topic>Dextran</topic><topic>Dynamic stability</topic><topic>Homeostasis</topic><topic>Impairment</topic><topic>Inhibitors</topic><topic>iron oxide nanoparticles</topic><topic>Iron oxides</topic><topic>Mitochondria</topic><topic>mitochondrial dynamics</topic><topic>mitochondrial homeostasis</topic><topic>Nanomaterials</topic><topic>Nanoparticles</topic><topic>Nanotechnology</topic><topic>Phagocytosis</topic><topic>Polyethylene glycol</topic><topic>Receptors</topic><topic>Toxicity</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Tian‐guang</creatorcontrib><creatorcontrib>Zhang, Yu‐long</creatorcontrib><creatorcontrib>Zhou, Qian‐qian</creatorcontrib><creatorcontrib>Wang, Xiao‐hui</creatorcontrib><creatorcontrib>Zhan, Lin‐sheng</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Environment Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>Environment Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of applied toxicology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Tian‐guang</au><au>Zhang, Yu‐long</au><au>Zhou, Qian‐qian</au><au>Wang, Xiao‐hui</au><au>Zhan, Lin‐sheng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Impairment of mitochondrial dynamics involved in iron oxide nanoparticle‐induced dysfunction of dendritic cells was alleviated by autophagy inhibitor 3‐methyladenine</atitle><jtitle>Journal of applied toxicology</jtitle><addtitle>J Appl Toxicol</addtitle><date>2020-05</date><risdate>2020</risdate><volume>40</volume><issue>5</issue><spage>631</spage><epage>642</epage><pages>631-642</pages><issn>0260-437X</issn><eissn>1099-1263</eissn><abstract>Iron oxide nanoparticles are nanomaterials that are used extensively in the biomedical field, but they are associated with adverse effects, including mitochondrial toxicity. Mitochondrial homeostasis is achieved through dynamic stability based on two sets of antagonistic balanced processes: mitochondrial biogenesis and degradation as well as mitochondrial fission and fusion. In this study, we showed that PEG‐COOH‐coated Fe3O4 (PEG‐Fe3O4) nanoparticles induced mitochondrial instability in dendritic cells (DCs) by impairing mitochondrial dynamics due to promotion of mitochondrial biogenesis through activation of the peroxisome proliferator‐activated receptor γ coactivator 1α (PGC1α) pathway, inhibiting mitochondrial degradation via decreased autophagy, and facilitating mitochondrial fragmentation involving increased levels of DRP1 and MFN2. The resulting reduced levels of dextran uptake, CD80, CD86 and chemokine receptor 7 (CCR7) suggested that PEG‐Fe3O4 nanoparticles impaired the functionally immature state of DCs. Autophagy inhibitor 3‐methyladenine (3‐MA) alleviated PEG‐Fe3O4 nanoparticle‐induced mitochondrial instability and impairment of the functionally immature state of DCs due to unexpected enhancement of PGC1α/MFN2‐mediated coordination of mitochondrial biogenesis and fusion. Iron oxide nanoparticles are adversely associated with mitochondrial toxicity. The present study showed that PEG‐COOH‐coated Fe3O4 (PEG‐Fe3O4) nanoparticles induced mitochondrial instability in dendritic cells (DCs) by promoting mitochondrial biogenesis, inhibiting mitochondrial degradation and facilitating mitochondrial fragmentation. The resulting reduced levels of dextran uptake, costimulatory molecules and chemokine receptor 7 suggested that PEG‐Fe3O4 nanoparticles impaired DC function. 3‐methyladenine alleviated PEG‐Fe3O4 nanoparticle‐induced mitochondrial instability and impairment of DC function due to enhancing the coordination of mitochondrial biogenesis and fusion.</abstract><cop>England</cop><pub>Wiley Subscription Services, Inc</pub><pmid>31922269</pmid><doi>10.1002/jat.3933</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0001-5753-1804</orcidid></addata></record>
fulltext fulltext
identifier ISSN: 0260-437X
ispartof Journal of applied toxicology, 2020-05, Vol.40 (5), p.631-642
issn 0260-437X
1099-1263
language eng
recordid cdi_proquest_miscellaneous_2336260369
source Access via Wiley Online Library
subjects 3‐methyladenine
Autophagy
Biocompatibility
Biosynthesis
CC chemokine receptors
CCR7 protein
CD80 antigen
CD86 antigen
Degradation
Dendritic cells
Dextran
Dynamic stability
Homeostasis
Impairment
Inhibitors
iron oxide nanoparticles
Iron oxides
Mitochondria
mitochondrial dynamics
mitochondrial homeostasis
Nanomaterials
Nanoparticles
Nanotechnology
Phagocytosis
Polyethylene glycol
Receptors
Toxicity
title Impairment of mitochondrial dynamics involved in iron oxide nanoparticle‐induced dysfunction of dendritic cells was alleviated by autophagy inhibitor 3‐methyladenine
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-25T23%3A45%3A21IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Impairment%20of%20mitochondrial%20dynamics%20involved%20in%20iron%20oxide%20nanoparticle%E2%80%90induced%20dysfunction%20of%20dendritic%20cells%20was%20alleviated%20by%20autophagy%20inhibitor%203%E2%80%90methyladenine&rft.jtitle=Journal%20of%20applied%20toxicology&rft.au=Zhang,%20Tian%E2%80%90guang&rft.date=2020-05&rft.volume=40&rft.issue=5&rft.spage=631&rft.epage=642&rft.pages=631-642&rft.issn=0260-437X&rft.eissn=1099-1263&rft_id=info:doi/10.1002/jat.3933&rft_dat=%3Cproquest_cross%3E2336260369%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2390355951&rft_id=info:pmid/31922269&rfr_iscdi=true