Epstein-Barr virus-induced gene 3 commits human mesenchymal stem cells to differentiate into chondrocytes via endoplasmic reticulum stress sensor
Mesenchymal stem cells (MSC) can differentiate into chondrocytes. Epstein-Barr virus-induced gene 3 (EBI3) is differentially expressed during chondrogenic differentiation and can be produced by MSC. EBI3 is also a subunit of interleukin (IL)-27 and IL-35, and it accumulates in the endoplasmic reticu...
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| Veröffentlicht in: | PloS one 2022-12, Vol.17 (12), p.e0279584 |
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| creator | Zhang, Tong Yamagata, Kaoru Iwata, Shigeru Sonomoto, Koshiro Trimova, Gulzhan Nguyen, Anh Phuong Hao, He Shan, Yu Nguyen, Mai-Phuong Nakayamada, Shingo Tanaka, Yoshiya |
| description | Mesenchymal stem cells (MSC) can differentiate into chondrocytes. Epstein-Barr virus-induced gene 3 (EBI3) is differentially expressed during chondrogenic differentiation and can be produced by MSC. EBI3 is also a subunit of interleukin (IL)-27 and IL-35, and it accumulates in the endoplasmic reticulum (ER) when its partners, such as IL-27 p28 and IL-35 p35, are insufficient. ER stress induced by protein accumulation is responsible for chondrogenic differentiation. However, the role of EBI3 and its relevance to the ER stress in chondrogenic differentiation of MSC have never been addressed. Here, we demonstrate that EBI3 protein is expressed in the early stage of chondrogenic differentiation of MSC. Additionally, knockdown, overexpression, or induction of EBI3 through IL-1β inhibits chondrogenesis. We show that EBI3 localizes and accumulates in the ER of MSC after overexpression or induction by IL-1β and TNF-α, whereas ER stress inhibitor 4-phenylbutyric acid decreases its accumulation in MSC. Moreover, EBI3 modulates ER stress sensor inositol-requiring enzyme 1 α (IRE1α) after induced by IL-1β, and MSC-like cells coexpress EBI3 and IRE1α in rheumatoid arthritis (RA) synovial tissue. Altogether, these data demonstrate that intracellular EBI3 commits to chondrogenic differentiation by regulating ER stress sensor IRE1α. |
| doi_str_mv | 10.1371/journal.pone.0279584 |
| format | Article |
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Epstein-Barr virus-induced gene 3 (EBI3) is differentially expressed during chondrogenic differentiation and can be produced by MSC. EBI3 is also a subunit of interleukin (IL)-27 and IL-35, and it accumulates in the endoplasmic reticulum (ER) when its partners, such as IL-27 p28 and IL-35 p35, are insufficient. ER stress induced by protein accumulation is responsible for chondrogenic differentiation. However, the role of EBI3 and its relevance to the ER stress in chondrogenic differentiation of MSC have never been addressed. Here, we demonstrate that EBI3 protein is expressed in the early stage of chondrogenic differentiation of MSC. Additionally, knockdown, overexpression, or induction of EBI3 through IL-1β inhibits chondrogenesis. We show that EBI3 localizes and accumulates in the ER of MSC after overexpression or induction by IL-1β and TNF-α, whereas ER stress inhibitor 4-phenylbutyric acid decreases its accumulation in MSC. Moreover, EBI3 modulates ER stress sensor inositol-requiring enzyme 1 α (IRE1α) after induced by IL-1β, and MSC-like cells coexpress EBI3 and IRE1α in rheumatoid arthritis (RA) synovial tissue. Altogether, these data demonstrate that intracellular EBI3 commits to chondrogenic differentiation by regulating ER stress sensor IRE1α.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0279584</identifier><identifier>PMID: 36548354</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Accumulation ; Analysis ; Antibodies ; Arthritis ; Biology and Life Sciences ; Bone marrow ; Cartilage ; Cell cycle ; Cell differentiation ; Cell Differentiation - genetics ; Chondrocytes ; Chondrocytes - cytology ; Chondrogenesis ; Chondrogenesis - genetics ; Control ; Cytokines ; Differentiation ; EBI3 protein ; Endoplasmic reticulum ; Endoplasmic Reticulum Stress - genetics ; Endoribonucleases - genetics ; Endoribonucleases - metabolism ; Epstein-Barr virus ; Health aspects ; Humans ; Identification and classification ; IL-1β ; Inositol ; Inositols ; Interleukin 27 ; Interleukins ; Interleukins - genetics ; Interleukins - physiology ; Kinases ; Medicine and Health Sciences ; Mesenchymal stem cells ; Mesenchymal Stem Cells - cytology ; Minor Histocompatibility Antigens - genetics ; Minor Histocompatibility Antigens - physiology ; Phenylbutyric acid ; Prevention ; Protein Serine-Threonine Kinases - genetics ; Protein Serine-Threonine Kinases - metabolism ; Proteins ; Research and Analysis Methods ; Rheumatoid arthritis ; Risk factors ; Sensors ; Stem cells ; Stress ; Stress (Physiology) ; Tumor necrosis factor-α ; Viruses</subject><ispartof>PloS one, 2022-12, Vol.17 (12), p.e0279584</ispartof><rights>Copyright: © 2022 Zhang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.</rights><rights>COPYRIGHT 2022 Public Library of Science</rights><rights>2022 Zhang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2022 Zhang et al 2022 Zhang et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-49a32752fae5b26e6b79683e30616549e8c3f557643a0f01273f1199a0fe877e3</citedby><cites>FETCH-LOGICAL-c692t-49a32752fae5b26e6b79683e30616549e8c3f557643a0f01273f1199a0fe877e3</cites><orcidid>0000-0001-9419-5766 ; 0000-0002-0807-7139 ; 0000-0003-3483-2668 ; 0000-0003-4029-443X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9778607/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9778607/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2095,2914,23846,27903,27904,53769,53771,79346,79347</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36548354$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Trajkovic, Vladimir</contributor><creatorcontrib>Zhang, Tong</creatorcontrib><creatorcontrib>Yamagata, Kaoru</creatorcontrib><creatorcontrib>Iwata, Shigeru</creatorcontrib><creatorcontrib>Sonomoto, Koshiro</creatorcontrib><creatorcontrib>Trimova, Gulzhan</creatorcontrib><creatorcontrib>Nguyen, Anh Phuong</creatorcontrib><creatorcontrib>Hao, He</creatorcontrib><creatorcontrib>Shan, Yu</creatorcontrib><creatorcontrib>Nguyen, Mai-Phuong</creatorcontrib><creatorcontrib>Nakayamada, Shingo</creatorcontrib><creatorcontrib>Tanaka, Yoshiya</creatorcontrib><title>Epstein-Barr virus-induced gene 3 commits human mesenchymal stem cells to differentiate into chondrocytes via endoplasmic reticulum stress sensor</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Mesenchymal stem cells (MSC) can differentiate into chondrocytes. Epstein-Barr virus-induced gene 3 (EBI3) is differentially expressed during chondrogenic differentiation and can be produced by MSC. EBI3 is also a subunit of interleukin (IL)-27 and IL-35, and it accumulates in the endoplasmic reticulum (ER) when its partners, such as IL-27 p28 and IL-35 p35, are insufficient. ER stress induced by protein accumulation is responsible for chondrogenic differentiation. However, the role of EBI3 and its relevance to the ER stress in chondrogenic differentiation of MSC have never been addressed. Here, we demonstrate that EBI3 protein is expressed in the early stage of chondrogenic differentiation of MSC. Additionally, knockdown, overexpression, or induction of EBI3 through IL-1β inhibits chondrogenesis. We show that EBI3 localizes and accumulates in the ER of MSC after overexpression or induction by IL-1β and TNF-α, whereas ER stress inhibitor 4-phenylbutyric acid decreases its accumulation in MSC. Moreover, EBI3 modulates ER stress sensor inositol-requiring enzyme 1 α (IRE1α) after induced by IL-1β, and MSC-like cells coexpress EBI3 and IRE1α in rheumatoid arthritis (RA) synovial tissue. Altogether, these data demonstrate that intracellular EBI3 commits to chondrogenic differentiation by regulating ER stress sensor IRE1α.</description><subject>Accumulation</subject><subject>Analysis</subject><subject>Antibodies</subject><subject>Arthritis</subject><subject>Biology and Life Sciences</subject><subject>Bone marrow</subject><subject>Cartilage</subject><subject>Cell cycle</subject><subject>Cell differentiation</subject><subject>Cell Differentiation - genetics</subject><subject>Chondrocytes</subject><subject>Chondrocytes - cytology</subject><subject>Chondrogenesis</subject><subject>Chondrogenesis - genetics</subject><subject>Control</subject><subject>Cytokines</subject><subject>Differentiation</subject><subject>EBI3 protein</subject><subject>Endoplasmic reticulum</subject><subject>Endoplasmic Reticulum Stress - genetics</subject><subject>Endoribonucleases - genetics</subject><subject>Endoribonucleases - metabolism</subject><subject>Epstein-Barr virus</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Identification and classification</subject><subject>IL-1β</subject><subject>Inositol</subject><subject>Inositols</subject><subject>Interleukin 27</subject><subject>Interleukins</subject><subject>Interleukins - genetics</subject><subject>Interleukins - physiology</subject><subject>Kinases</subject><subject>Medicine and Health Sciences</subject><subject>Mesenchymal stem cells</subject><subject>Mesenchymal Stem Cells - cytology</subject><subject>Minor Histocompatibility Antigens - genetics</subject><subject>Minor Histocompatibility Antigens - physiology</subject><subject>Phenylbutyric acid</subject><subject>Prevention</subject><subject>Protein Serine-Threonine Kinases - genetics</subject><subject>Protein Serine-Threonine Kinases - metabolism</subject><subject>Proteins</subject><subject>Research and Analysis Methods</subject><subject>Rheumatoid arthritis</subject><subject>Risk factors</subject><subject>Sensors</subject><subject>Stem 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virus-induced gene 3 commits human mesenchymal stem cells to differentiate into chondrocytes via endoplasmic reticulum stress sensor</title><author>Zhang, Tong ; Yamagata, Kaoru ; Iwata, Shigeru ; Sonomoto, Koshiro ; Trimova, Gulzhan ; Nguyen, Anh Phuong ; Hao, He ; Shan, Yu ; Nguyen, Mai-Phuong ; Nakayamada, Shingo ; Tanaka, Yoshiya</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-49a32752fae5b26e6b79683e30616549e8c3f557643a0f01273f1199a0fe877e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Accumulation</topic><topic>Analysis</topic><topic>Antibodies</topic><topic>Arthritis</topic><topic>Biology and Life Sciences</topic><topic>Bone marrow</topic><topic>Cartilage</topic><topic>Cell cycle</topic><topic>Cell differentiation</topic><topic>Cell Differentiation - genetics</topic><topic>Chondrocytes</topic><topic>Chondrocytes - cytology</topic><topic>Chondrogenesis</topic><topic>Chondrogenesis - genetics</topic><topic>Control</topic><topic>Cytokines</topic><topic>Differentiation</topic><topic>EBI3 protein</topic><topic>Endoplasmic reticulum</topic><topic>Endoplasmic Reticulum Stress - genetics</topic><topic>Endoribonucleases - genetics</topic><topic>Endoribonucleases - metabolism</topic><topic>Epstein-Barr virus</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Identification and classification</topic><topic>IL-1β</topic><topic>Inositol</topic><topic>Inositols</topic><topic>Interleukin 27</topic><topic>Interleukins</topic><topic>Interleukins - genetics</topic><topic>Interleukins - physiology</topic><topic>Kinases</topic><topic>Medicine and Health Sciences</topic><topic>Mesenchymal stem cells</topic><topic>Mesenchymal Stem Cells - cytology</topic><topic>Minor Histocompatibility Antigens - genetics</topic><topic>Minor Histocompatibility Antigens - physiology</topic><topic>Phenylbutyric 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Mai-Phuong</au><au>Nakayamada, Shingo</au><au>Tanaka, Yoshiya</au><au>Trajkovic, Vladimir</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Epstein-Barr virus-induced gene 3 commits human mesenchymal stem cells to differentiate into chondrocytes via endoplasmic reticulum stress sensor</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2022-12-22</date><risdate>2022</risdate><volume>17</volume><issue>12</issue><spage>e0279584</spage><pages>e0279584-</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Mesenchymal stem cells (MSC) can differentiate into chondrocytes. Epstein-Barr virus-induced gene 3 (EBI3) is differentially expressed during chondrogenic differentiation and can be produced by MSC. EBI3 is also a subunit of interleukin (IL)-27 and IL-35, and it accumulates in the endoplasmic reticulum (ER) when its partners, such as IL-27 p28 and IL-35 p35, are insufficient. ER stress induced by protein accumulation is responsible for chondrogenic differentiation. However, the role of EBI3 and its relevance to the ER stress in chondrogenic differentiation of MSC have never been addressed. Here, we demonstrate that EBI3 protein is expressed in the early stage of chondrogenic differentiation of MSC. Additionally, knockdown, overexpression, or induction of EBI3 through IL-1β inhibits chondrogenesis. We show that EBI3 localizes and accumulates in the ER of MSC after overexpression or induction by IL-1β and TNF-α, whereas ER stress inhibitor 4-phenylbutyric acid decreases its accumulation in MSC. Moreover, EBI3 modulates ER stress sensor inositol-requiring enzyme 1 α (IRE1α) after induced by IL-1β, and MSC-like cells coexpress EBI3 and IRE1α in rheumatoid arthritis (RA) synovial tissue. Altogether, these data demonstrate that intracellular EBI3 commits to chondrogenic differentiation by regulating ER stress sensor IRE1α.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>36548354</pmid><doi>10.1371/journal.pone.0279584</doi><tpages>e0279584</tpages><orcidid>https://orcid.org/0000-0001-9419-5766</orcidid><orcidid>https://orcid.org/0000-0002-0807-7139</orcidid><orcidid>https://orcid.org/0000-0003-3483-2668</orcidid><orcidid>https://orcid.org/0000-0003-4029-443X</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2022-12, Vol.17 (12), p.e0279584 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_2757027714 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS) Journals Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Accumulation Analysis Antibodies Arthritis Biology and Life Sciences Bone marrow Cartilage Cell cycle Cell differentiation Cell Differentiation - genetics Chondrocytes Chondrocytes - cytology Chondrogenesis Chondrogenesis - genetics Control Cytokines Differentiation EBI3 protein Endoplasmic reticulum Endoplasmic Reticulum Stress - genetics Endoribonucleases - genetics Endoribonucleases - metabolism Epstein-Barr virus Health aspects Humans Identification and classification IL-1β Inositol Inositols Interleukin 27 Interleukins Interleukins - genetics Interleukins - physiology Kinases Medicine and Health Sciences Mesenchymal stem cells Mesenchymal Stem Cells - cytology Minor Histocompatibility Antigens - genetics Minor Histocompatibility Antigens - physiology Phenylbutyric acid Prevention Protein Serine-Threonine Kinases - genetics Protein Serine-Threonine Kinases - metabolism Proteins Research and Analysis Methods Rheumatoid arthritis Risk factors Sensors Stem cells Stress Stress (Physiology) Tumor necrosis factor-α Viruses |
| title | Epstein-Barr virus-induced gene 3 commits human mesenchymal stem cells to differentiate into chondrocytes via endoplasmic reticulum stress sensor |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-26T08%3A09%3A55IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Epstein-Barr%20virus-induced%20gene%203%20commits%20human%20mesenchymal%20stem%20cells%20to%20differentiate%20into%20chondrocytes%20via%20endoplasmic%20reticulum%20stress%20sensor&rft.jtitle=PloS%20one&rft.au=Zhang,%20Tong&rft.date=2022-12-22&rft.volume=17&rft.issue=12&rft.spage=e0279584&rft.pages=e0279584-&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0279584&rft_dat=%3Cgale_plos_%3EA730926275%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2757027714&rft_id=info:pmid/36548354&rft_galeid=A730926275&rft_doaj_id=oai_doaj_org_article_dc26cdf01e0a4c9991ed11ad66e6f1a5&rfr_iscdi=true |