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Inhibition of Mitochondrial Fission Alleviates Zearalenone-Induced Mitochondria-Associated Endoplasmic Reticulum Membrane Dysfunction in Piglet Sertoli Cells
This study aimed to investigate the effects of zearalenone (ZEA) on piglet Sertoli cell (SC)-mitochondria-associated endoplasmic reticulum (ER) membranes (MAMs) based on mitochondrial fission, and to explore the molecular mechanism of ZEA-induced cell damage. After the SCs were exposed to the ZEA, t...
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| Published in: | Toxins 2023-03, Vol.15 (4), p.253 |
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| creator | Ma, Li Chen, Chuangjiang Hai, Sirao Wang, Chenlong Rahman, Sajid Ur Huang, Wanyue Zhao, Chang Feng, Shibin Wang, Xichun |
| description | This study aimed to investigate the effects of zearalenone (ZEA) on piglet Sertoli cell (SC)-mitochondria-associated endoplasmic reticulum (ER) membranes (MAMs) based on mitochondrial fission, and to explore the molecular mechanism of ZEA-induced cell damage. After the SCs were exposed to the ZEA, the cell viability decreased, the Ca
levels increased, and the MAM showed structural damage. Moreover, glucose-regulated protein 75 (Grp75) and mitochondrial Rho-GTPase 1 (Miro1) were upregulated at the mRNA and protein levels. However, phosphofurin acidic cluster protein 2 (PACS2), mitofusin2 (Mfn2), voltage-dependent anion channel 1 (VDAC1), and inositol 1,4,5-trisphosphate receptor (IP3R) were downregulated at the mRNA and protein levels. A pretreatment with mitochondrial division inhibitor 1 (Mdivi-1) decreased the ZEA-induced cytotoxicity toward the SCs. In the ZEA + Mdivi-1 group, the cell viability increased, the Ca
levels decreased, the MAM damage was repaired, and the expression levels of Grp75 and Miro1 decreased, while those of PACS2, Mfn2, VDAC1, and IP3R increased compared with those in the ZEA-only group. Thus, ZEA causes MAM dysfunction in piglet SCs through mitochondrial fission, and mitochondria can regulate the ER via MAM. |
| doi_str_mv | 10.3390/toxins15040253 |
| format | article |
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levels increased, and the MAM showed structural damage. Moreover, glucose-regulated protein 75 (Grp75) and mitochondrial Rho-GTPase 1 (Miro1) were upregulated at the mRNA and protein levels. However, phosphofurin acidic cluster protein 2 (PACS2), mitofusin2 (Mfn2), voltage-dependent anion channel 1 (VDAC1), and inositol 1,4,5-trisphosphate receptor (IP3R) were downregulated at the mRNA and protein levels. A pretreatment with mitochondrial division inhibitor 1 (Mdivi-1) decreased the ZEA-induced cytotoxicity toward the SCs. In the ZEA + Mdivi-1 group, the cell viability increased, the Ca
levels decreased, the MAM damage was repaired, and the expression levels of Grp75 and Miro1 decreased, while those of PACS2, Mfn2, VDAC1, and IP3R increased compared with those in the ZEA-only group. Thus, ZEA causes MAM dysfunction in piglet SCs through mitochondrial fission, and mitochondria can regulate the ER via MAM.</description><identifier>ISSN: 2072-6651</identifier><identifier>EISSN: 2072-6651</identifier><identifier>DOI: 10.3390/toxins15040253</identifier><identifier>PMID: 37104191</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Animals ; Apoptosis ; Calcium - metabolism ; Calcium ions ; Cell division ; Cell growth ; Cell viability ; Cytotoxicity ; Endoplasmic reticulum ; Endoplasmic Reticulum - metabolism ; Fission ; Guanine nucleotide-binding protein ; Health aspects ; Homeostasis ; Inositol trisphosphate ; Inositols ; Ion channels ; Male ; Membrane Proteins - metabolism ; Membranes ; Mitochondria ; mitochondria-associated endoplasmic-reticulum membrane ; Mitochondrial Dynamics ; mitochondrial fission ; Molecular modelling ; Morphology ; mRNA ; Mycotoxins ; Oxidative stress ; Physiological aspects ; piglet Sertoli cells ; Proteins ; RNA, Messenger - metabolism ; Sertoli cells ; Sertoli Cells - metabolism ; Sperm ; Structural damage ; Swine ; Toxicity ; Zearalenone ; Zearalenone - metabolism</subject><ispartof>Toxins, 2023-03, Vol.15 (4), p.253</ispartof><rights>COPYRIGHT 2023 MDPI AG</rights><rights>2023 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2023 by the authors. 2023</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c552t-4479648c40444301d62974aa0ecddd28170f5ba652ac19ae88f1d43cef7938ae3</citedby><cites>FETCH-LOGICAL-c552t-4479648c40444301d62974aa0ecddd28170f5ba652ac19ae88f1d43cef7938ae3</cites><orcidid>0000-0002-5969-5463 ; 0000-0001-8668-0171 ; 0000-0001-5096-3970</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2806633210/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2806633210?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793,75126</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37104191$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ma, Li</creatorcontrib><creatorcontrib>Chen, Chuangjiang</creatorcontrib><creatorcontrib>Hai, Sirao</creatorcontrib><creatorcontrib>Wang, Chenlong</creatorcontrib><creatorcontrib>Rahman, Sajid Ur</creatorcontrib><creatorcontrib>Huang, Wanyue</creatorcontrib><creatorcontrib>Zhao, Chang</creatorcontrib><creatorcontrib>Feng, Shibin</creatorcontrib><creatorcontrib>Wang, Xichun</creatorcontrib><title>Inhibition of Mitochondrial Fission Alleviates Zearalenone-Induced Mitochondria-Associated Endoplasmic Reticulum Membrane Dysfunction in Piglet Sertoli Cells</title><title>Toxins</title><addtitle>Toxins (Basel)</addtitle><description>This study aimed to investigate the effects of zearalenone (ZEA) on piglet Sertoli cell (SC)-mitochondria-associated endoplasmic reticulum (ER) membranes (MAMs) based on mitochondrial fission, and to explore the molecular mechanism of ZEA-induced cell damage. After the SCs were exposed to the ZEA, the cell viability decreased, the Ca
levels increased, and the MAM showed structural damage. Moreover, glucose-regulated protein 75 (Grp75) and mitochondrial Rho-GTPase 1 (Miro1) were upregulated at the mRNA and protein levels. However, phosphofurin acidic cluster protein 2 (PACS2), mitofusin2 (Mfn2), voltage-dependent anion channel 1 (VDAC1), and inositol 1,4,5-trisphosphate receptor (IP3R) were downregulated at the mRNA and protein levels. A pretreatment with mitochondrial division inhibitor 1 (Mdivi-1) decreased the ZEA-induced cytotoxicity toward the SCs. In the ZEA + Mdivi-1 group, the cell viability increased, the Ca
levels decreased, the MAM damage was repaired, and the expression levels of Grp75 and Miro1 decreased, while those of PACS2, Mfn2, VDAC1, and IP3R increased compared with those in the ZEA-only group. Thus, ZEA causes MAM dysfunction in piglet SCs through mitochondrial fission, and mitochondria can regulate the ER via MAM.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Calcium - metabolism</subject><subject>Calcium ions</subject><subject>Cell division</subject><subject>Cell growth</subject><subject>Cell viability</subject><subject>Cytotoxicity</subject><subject>Endoplasmic reticulum</subject><subject>Endoplasmic Reticulum - metabolism</subject><subject>Fission</subject><subject>Guanine nucleotide-binding protein</subject><subject>Health aspects</subject><subject>Homeostasis</subject><subject>Inositol trisphosphate</subject><subject>Inositols</subject><subject>Ion channels</subject><subject>Male</subject><subject>Membrane Proteins - metabolism</subject><subject>Membranes</subject><subject>Mitochondria</subject><subject>mitochondria-associated endoplasmic-reticulum membrane</subject><subject>Mitochondrial Dynamics</subject><subject>mitochondrial fission</subject><subject>Molecular modelling</subject><subject>Morphology</subject><subject>mRNA</subject><subject>Mycotoxins</subject><subject>Oxidative stress</subject><subject>Physiological aspects</subject><subject>piglet Sertoli cells</subject><subject>Proteins</subject><subject>RNA, Messenger - metabolism</subject><subject>Sertoli cells</subject><subject>Sertoli Cells - metabolism</subject><subject>Sperm</subject><subject>Structural damage</subject><subject>Swine</subject><subject>Toxicity</subject><subject>Zearalenone</subject><subject>Zearalenone - metabolism</subject><issn>2072-6651</issn><issn>2072-6651</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNptUk1vEzEQXSEQrUqvHNFKXLhssdf2en1CUT8gUisQHxcultceJ44cO9i7Ff0x_FectFQJqufg0cybN5o3U1WvMTojRKD3Y_ztQsYMUdQy8qw6bhFvm65j-Pmef1Sd5rxC5RGCBeYvqyPCMaLFP67-zMPSDW50MdTR1jdujHoZg0lO-frK5bxNzLyHW6dGyPVPUEl5CDFAMw9m0mAOippZzlFvsaa-DCZuvMprp-uvMDo9-Wld38B6SCpAfXGX7RT0rrUL9Re38DDW3yCN0bv6HLzPr6oXVvkMpw__SfXj6vL7-afm-vPH-fnsutGMtWNDKRcd7TVFlFKCsOlawalSCLQxpu0xR5YNqmOt0lgo6HuLDSUaLBekV0BOqvk9r4lqJTfJrVW6k1E5uQvEtJAqlQE8SMEZ9KLl1pqBUoaHTg-D0L3gPSPa6sL14Z5rMw1rMBrCWBQ7ID3MBLeUi3grMcK0o5gVhncPDCn-miCPcu2yLnoU1eKUZdujTghGO1Sgb_-DruKUQtFqh-oIafEealFWJ12wsTTWW1I545QzijjZtj17AlXMQNlgWbh1Jf5UgU4x5wT2cUiM5PZA5eGBloI3-9I8wv-dI_kLIHjkPw</recordid><startdate>20230330</startdate><enddate>20230330</enddate><creator>Ma, Li</creator><creator>Chen, Chuangjiang</creator><creator>Hai, Sirao</creator><creator>Wang, Chenlong</creator><creator>Rahman, Sajid Ur</creator><creator>Huang, Wanyue</creator><creator>Zhao, Chang</creator><creator>Feng, Shibin</creator><creator>Wang, Xichun</creator><general>MDPI AG</general><general>MDPI</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T7</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PATMY</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PYCSY</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0002-5969-5463</orcidid><orcidid>https://orcid.org/0000-0001-8668-0171</orcidid><orcidid>https://orcid.org/0000-0001-5096-3970</orcidid></search><sort><creationdate>20230330</creationdate><title>Inhibition of Mitochondrial Fission Alleviates Zearalenone-Induced Mitochondria-Associated Endoplasmic Reticulum Membrane Dysfunction in Piglet Sertoli Cells</title><author>Ma, Li ; Chen, Chuangjiang ; Hai, Sirao ; Wang, Chenlong ; Rahman, Sajid Ur ; Huang, Wanyue ; Zhao, Chang ; Feng, Shibin ; Wang, Xichun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c552t-4479648c40444301d62974aa0ecddd28170f5ba652ac19ae88f1d43cef7938ae3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Calcium - metabolism</topic><topic>Calcium ions</topic><topic>Cell division</topic><topic>Cell growth</topic><topic>Cell viability</topic><topic>Cytotoxicity</topic><topic>Endoplasmic reticulum</topic><topic>Endoplasmic Reticulum - metabolism</topic><topic>Fission</topic><topic>Guanine nucleotide-binding protein</topic><topic>Health aspects</topic><topic>Homeostasis</topic><topic>Inositol trisphosphate</topic><topic>Inositols</topic><topic>Ion channels</topic><topic>Male</topic><topic>Membrane Proteins - metabolism</topic><topic>Membranes</topic><topic>Mitochondria</topic><topic>mitochondria-associated endoplasmic-reticulum membrane</topic><topic>Mitochondrial Dynamics</topic><topic>mitochondrial fission</topic><topic>Molecular modelling</topic><topic>Morphology</topic><topic>mRNA</topic><topic>Mycotoxins</topic><topic>Oxidative stress</topic><topic>Physiological aspects</topic><topic>piglet Sertoli cells</topic><topic>Proteins</topic><topic>RNA, Messenger - metabolism</topic><topic>Sertoli cells</topic><topic>Sertoli Cells - metabolism</topic><topic>Sperm</topic><topic>Structural damage</topic><topic>Swine</topic><topic>Toxicity</topic><topic>Zearalenone</topic><topic>Zearalenone - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ma, Li</creatorcontrib><creatorcontrib>Chen, Chuangjiang</creatorcontrib><creatorcontrib>Hai, Sirao</creatorcontrib><creatorcontrib>Wang, Chenlong</creatorcontrib><creatorcontrib>Rahman, Sajid Ur</creatorcontrib><creatorcontrib>Huang, Wanyue</creatorcontrib><creatorcontrib>Zhao, Chang</creatorcontrib><creatorcontrib>Feng, Shibin</creatorcontrib><creatorcontrib>Wang, Xichun</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Toxicology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>Environmental Science Collection</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>Directory of Open Access Journals (Open Access)</collection><jtitle>Toxins</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ma, Li</au><au>Chen, Chuangjiang</au><au>Hai, Sirao</au><au>Wang, Chenlong</au><au>Rahman, Sajid Ur</au><au>Huang, Wanyue</au><au>Zhao, Chang</au><au>Feng, Shibin</au><au>Wang, Xichun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibition of Mitochondrial Fission Alleviates Zearalenone-Induced Mitochondria-Associated Endoplasmic Reticulum Membrane Dysfunction in Piglet Sertoli Cells</atitle><jtitle>Toxins</jtitle><addtitle>Toxins (Basel)</addtitle><date>2023-03-30</date><risdate>2023</risdate><volume>15</volume><issue>4</issue><spage>253</spage><pages>253-</pages><issn>2072-6651</issn><eissn>2072-6651</eissn><abstract>This study aimed to investigate the effects of zearalenone (ZEA) on piglet Sertoli cell (SC)-mitochondria-associated endoplasmic reticulum (ER) membranes (MAMs) based on mitochondrial fission, and to explore the molecular mechanism of ZEA-induced cell damage. After the SCs were exposed to the ZEA, the cell viability decreased, the Ca
levels increased, and the MAM showed structural damage. Moreover, glucose-regulated protein 75 (Grp75) and mitochondrial Rho-GTPase 1 (Miro1) were upregulated at the mRNA and protein levels. However, phosphofurin acidic cluster protein 2 (PACS2), mitofusin2 (Mfn2), voltage-dependent anion channel 1 (VDAC1), and inositol 1,4,5-trisphosphate receptor (IP3R) were downregulated at the mRNA and protein levels. A pretreatment with mitochondrial division inhibitor 1 (Mdivi-1) decreased the ZEA-induced cytotoxicity toward the SCs. In the ZEA + Mdivi-1 group, the cell viability increased, the Ca
levels decreased, the MAM damage was repaired, and the expression levels of Grp75 and Miro1 decreased, while those of PACS2, Mfn2, VDAC1, and IP3R increased compared with those in the ZEA-only group. Thus, ZEA causes MAM dysfunction in piglet SCs through mitochondrial fission, and mitochondria can regulate the ER via MAM.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>37104191</pmid><doi>10.3390/toxins15040253</doi><orcidid>https://orcid.org/0000-0002-5969-5463</orcidid><orcidid>https://orcid.org/0000-0001-8668-0171</orcidid><orcidid>https://orcid.org/0000-0001-5096-3970</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
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| ispartof | Toxins, 2023-03, Vol.15 (4), p.253 |
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| source | Publicly Available Content Database; PubMed Central |
| subjects | Animals Apoptosis Calcium - metabolism Calcium ions Cell division Cell growth Cell viability Cytotoxicity Endoplasmic reticulum Endoplasmic Reticulum - metabolism Fission Guanine nucleotide-binding protein Health aspects Homeostasis Inositol trisphosphate Inositols Ion channels Male Membrane Proteins - metabolism Membranes Mitochondria mitochondria-associated endoplasmic-reticulum membrane Mitochondrial Dynamics mitochondrial fission Molecular modelling Morphology mRNA Mycotoxins Oxidative stress Physiological aspects piglet Sertoli cells Proteins RNA, Messenger - metabolism Sertoli cells Sertoli Cells - metabolism Sperm Structural damage Swine Toxicity Zearalenone Zearalenone - metabolism |
| title | Inhibition of Mitochondrial Fission Alleviates Zearalenone-Induced Mitochondria-Associated Endoplasmic Reticulum Membrane Dysfunction in Piglet Sertoli Cells |
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