Role of TGF-β and p38 MAPK in TSG-6 Expression in Adipose Tissue-Derived Stem Cells In Vitro and In Vivo
Mesenchymal stem cells (MSCs) regulate immune cell activity by expressing tumor necrosis factor-α (TNF-α)-stimulated gene 6 (TSG-6) in inflammatory environments; however, whether anti-inflammatory responses affect TSG-6 expression in MSCs is not well understood. Therefore, we investigated whether tr...
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| Veröffentlicht in: | International journal of molecular sciences 2023-12, Vol.25 (1), p.477 |
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| creator | Kwon, Hye Youn Yoon, Yongdae Hong, Ju-Eun Rhee, Ki-Jong Sohn, Joon Hyung Jung, Pil Young Kim, Moon Young Baik, Soon Koo Ryu, Hoon Eom, Young Woo |
| description | Mesenchymal stem cells (MSCs) regulate immune cell activity by expressing tumor necrosis factor-α (TNF-α)-stimulated gene 6 (TSG-6) in inflammatory environments; however, whether anti-inflammatory responses affect TSG-6 expression in MSCs is not well understood. Therefore, we investigated whether transforming growth factor-β (TGF-β) regulates TSG-6 expression in adipose tissue-derived stem cells (ASCs) and whether effective immunosuppression can be achieved using ASCs and TGF-β signaling inhibitor A83-01. TGF-β significantly decreased TSG-6 expression in ASCs, but A83-01 and the p38 inhibitor SB202190 significantly increased it. However, in septic C57BL/6 mice, A83-01 further reduced the survival rate of the lipopolysaccharide (LPS)-treated group and ASC transplantation did not improve the severity induced by LPS. ASC transplantation alleviated the severity of sepsis induced by LPS+A83-01. In co-culture of macrophages and ASCs, A83-01 decreased TSG-6 expression whereas A83-01 and SB202190 reduced Cox-2 and IDO-2 expression in ASCs. These results suggest that TSG-6 expression in ASCs can be regulated by high concentrations of pro-inflammatory cytokines in vitro and in vivo, and that A83-01 and SB202190 can reduce the expression of immunomodulators in ASCs. Therefore, our data suggest that co-treatment of ASCs with TGF-β or p38 inhibitors is not adequate to modulate inflammation. |
| doi_str_mv | 10.3390/ijms25010477 |
| format | Article |
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Therefore, we investigated whether transforming growth factor-β (TGF-β) regulates TSG-6 expression in adipose tissue-derived stem cells (ASCs) and whether effective immunosuppression can be achieved using ASCs and TGF-β signaling inhibitor A83-01. TGF-β significantly decreased TSG-6 expression in ASCs, but A83-01 and the p38 inhibitor SB202190 significantly increased it. However, in septic C57BL/6 mice, A83-01 further reduced the survival rate of the lipopolysaccharide (LPS)-treated group and ASC transplantation did not improve the severity induced by LPS. ASC transplantation alleviated the severity of sepsis induced by LPS+A83-01. In co-culture of macrophages and ASCs, A83-01 decreased TSG-6 expression whereas A83-01 and SB202190 reduced Cox-2 and IDO-2 expression in ASCs. These results suggest that TSG-6 expression in ASCs can be regulated by high concentrations of pro-inflammatory cytokines in vitro and in vivo, and that A83-01 and SB202190 can reduce the expression of immunomodulators in ASCs. Therefore, our data suggest that co-treatment of ASCs with TGF-β or p38 inhibitors is not adequate to modulate inflammation.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms25010477</identifier><identifier>PMID: 38203646</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Adipose Tissue ; Adipose tissues ; Animals ; Anti-inflammatory drugs ; Atherosclerosis ; Body fat ; Bone marrow ; Cytokines ; Dendritic cells ; Heart attacks ; Inflammation ; Kinases ; Lipopolysaccharides - pharmacology ; Macrophages ; Mice ; Mice, Inbred C57BL ; Neutrophils ; p38 Mitogen-Activated Protein Kinases ; Phosphorylation ; Pyrazoles ; Scientific equipment and supplies industry ; Sepsis ; Stem Cells ; Thiosemicarbazones ; Transforming Growth Factor beta ; Transforming growth factors ; Tumor necrosis factor ; Tumor necrosis factor-TNF</subject><ispartof>International journal of molecular sciences, 2023-12, Vol.25 (1), p.477</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><cites>FETCH-LOGICAL-c437t-ef12f64d2788ce51f5226b87a70c9ed8e659c3d5495eb583fabc63a69cda3ca83</cites><orcidid>0000-0002-5985-6490 ; 0000-0001-6460-8072 ; 0000-0002-2501-2206 ; 0000-0001-5130-2728 ; 0000-0002-9229-9331 ; 0000-0002-5357-4476</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/PMC10778696/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10778696/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27903,27904,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38203646$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kwon, Hye Youn</creatorcontrib><creatorcontrib>Yoon, Yongdae</creatorcontrib><creatorcontrib>Hong, Ju-Eun</creatorcontrib><creatorcontrib>Rhee, Ki-Jong</creatorcontrib><creatorcontrib>Sohn, Joon Hyung</creatorcontrib><creatorcontrib>Jung, Pil Young</creatorcontrib><creatorcontrib>Kim, Moon Young</creatorcontrib><creatorcontrib>Baik, Soon Koo</creatorcontrib><creatorcontrib>Ryu, Hoon</creatorcontrib><creatorcontrib>Eom, Young Woo</creatorcontrib><title>Role of TGF-β and p38 MAPK in TSG-6 Expression in Adipose Tissue-Derived Stem Cells In Vitro and In Vivo</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>Mesenchymal stem cells (MSCs) regulate immune cell activity by expressing tumor necrosis factor-α (TNF-α)-stimulated gene 6 (TSG-6) in inflammatory environments; however, whether anti-inflammatory responses affect TSG-6 expression in MSCs is not well understood. Therefore, we investigated whether transforming growth factor-β (TGF-β) regulates TSG-6 expression in adipose tissue-derived stem cells (ASCs) and whether effective immunosuppression can be achieved using ASCs and TGF-β signaling inhibitor A83-01. TGF-β significantly decreased TSG-6 expression in ASCs, but A83-01 and the p38 inhibitor SB202190 significantly increased it. However, in septic C57BL/6 mice, A83-01 further reduced the survival rate of the lipopolysaccharide (LPS)-treated group and ASC transplantation did not improve the severity induced by LPS. ASC transplantation alleviated the severity of sepsis induced by LPS+A83-01. In co-culture of macrophages and ASCs, A83-01 decreased TSG-6 expression whereas A83-01 and SB202190 reduced Cox-2 and IDO-2 expression in ASCs. These results suggest that TSG-6 expression in ASCs can be regulated by high concentrations of pro-inflammatory cytokines in vitro and in vivo, and that A83-01 and SB202190 can reduce the expression of immunomodulators in ASCs. Therefore, our data suggest that co-treatment of ASCs with TGF-β or p38 inhibitors is not adequate to modulate inflammation.</description><subject>Adipose Tissue</subject><subject>Adipose tissues</subject><subject>Animals</subject><subject>Anti-inflammatory drugs</subject><subject>Atherosclerosis</subject><subject>Body fat</subject><subject>Bone marrow</subject><subject>Cytokines</subject><subject>Dendritic cells</subject><subject>Heart attacks</subject><subject>Inflammation</subject><subject>Kinases</subject><subject>Lipopolysaccharides - pharmacology</subject><subject>Macrophages</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Neutrophils</subject><subject>p38 Mitogen-Activated Protein Kinases</subject><subject>Phosphorylation</subject><subject>Pyrazoles</subject><subject>Scientific equipment and supplies industry</subject><subject>Sepsis</subject><subject>Stem Cells</subject><subject>Thiosemicarbazones</subject><subject>Transforming Growth Factor beta</subject><subject>Transforming growth factors</subject><subject>Tumor necrosis factor</subject><subject>Tumor necrosis factor-TNF</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNptkstu1DAUhiNERUthxxpZYsOCFN_iywqNhnZatQhEB7aWxzkpHiV2sJMRvBYPwjOR6Y0pQl7Y5_g7v_Vbf1G8IPiIMY3f-nWXaYUJ5lI-Kg4Ip7TEWMjHO-f94mnOa4wpo5V-UuwzRTETXBwU_nNsAcUGLRcn5e9fyIYa9UyhD7NP58gHtLxclAId_-gT5Oxj2PZmte9jBrT0OY9QvofkN1CjywE6NIe2zegsoK9-SPFa7rrYxGfFXmPbDM9v98Piy8nxcn5aXnxcnM1nF6XjTA4lNIQ2gtdUKuWgIk1FqVgpaSV2GmoFotKO1RXXFawqxRq7coJZoV1tmbOKHRbvbnT7cdVB7SAMybamT76z6aeJ1puHN8F_M1dxYwiWUgktJoXXtwopfh8hD6bz2U3GbIA4ZkM1YZwLrPWEvvoHXccxhcnflqIKV5zyv9SVbcH40MTpYbcVNTMpNSUUKzlRR_-hplVD510M0Pip_2Dgzc2ASzHnBM29SYLNNhtmNxsT_nL3Y-7huzCwPyWBsfk</recordid><startdate>20231229</startdate><enddate>20231229</enddate><creator>Kwon, Hye Youn</creator><creator>Yoon, Yongdae</creator><creator>Hong, Ju-Eun</creator><creator>Rhee, Ki-Jong</creator><creator>Sohn, Joon Hyung</creator><creator>Jung, Pil Young</creator><creator>Kim, Moon Young</creator><creator>Baik, Soon Koo</creator><creator>Ryu, Hoon</creator><creator>Eom, Young Woo</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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-5985-6490</orcidid><orcidid>https://orcid.org/0000-0001-6460-8072</orcidid><orcidid>https://orcid.org/0000-0002-2501-2206</orcidid><orcidid>https://orcid.org/0000-0001-5130-2728</orcidid><orcidid>https://orcid.org/0000-0002-9229-9331</orcidid><orcidid>https://orcid.org/0000-0002-5357-4476</orcidid></search><sort><creationdate>20231229</creationdate><title>Role of TGF-β and p38 MAPK in TSG-6 Expression in Adipose Tissue-Derived Stem Cells In Vitro and In Vivo</title><author>Kwon, Hye Youn ; 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however, whether anti-inflammatory responses affect TSG-6 expression in MSCs is not well understood. Therefore, we investigated whether transforming growth factor-β (TGF-β) regulates TSG-6 expression in adipose tissue-derived stem cells (ASCs) and whether effective immunosuppression can be achieved using ASCs and TGF-β signaling inhibitor A83-01. TGF-β significantly decreased TSG-6 expression in ASCs, but A83-01 and the p38 inhibitor SB202190 significantly increased it. However, in septic C57BL/6 mice, A83-01 further reduced the survival rate of the lipopolysaccharide (LPS)-treated group and ASC transplantation did not improve the severity induced by LPS. ASC transplantation alleviated the severity of sepsis induced by LPS+A83-01. In co-culture of macrophages and ASCs, A83-01 decreased TSG-6 expression whereas A83-01 and SB202190 reduced Cox-2 and IDO-2 expression in ASCs. These results suggest that TSG-6 expression in ASCs can be regulated by high concentrations of pro-inflammatory cytokines in vitro and in vivo, and that A83-01 and SB202190 can reduce the expression of immunomodulators in ASCs. Therefore, our data suggest that co-treatment of ASCs with TGF-β or p38 inhibitors is not adequate to modulate inflammation.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>38203646</pmid><doi>10.3390/ijms25010477</doi><orcidid>https://orcid.org/0000-0002-5985-6490</orcidid><orcidid>https://orcid.org/0000-0001-6460-8072</orcidid><orcidid>https://orcid.org/0000-0002-2501-2206</orcidid><orcidid>https://orcid.org/0000-0001-5130-2728</orcidid><orcidid>https://orcid.org/0000-0002-9229-9331</orcidid><orcidid>https://orcid.org/0000-0002-5357-4476</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Adipose Tissue Adipose tissues Animals Anti-inflammatory drugs Atherosclerosis Body fat Bone marrow Cytokines Dendritic cells Heart attacks Inflammation Kinases Lipopolysaccharides - pharmacology Macrophages Mice Mice, Inbred C57BL Neutrophils p38 Mitogen-Activated Protein Kinases Phosphorylation Pyrazoles Scientific equipment and supplies industry Sepsis Stem Cells Thiosemicarbazones Transforming Growth Factor beta Transforming growth factors Tumor necrosis factor Tumor necrosis factor-TNF |
| title | Role of TGF-β and p38 MAPK in TSG-6 Expression in Adipose Tissue-Derived Stem Cells In Vitro and In Vivo |
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