TUDCA-treated chronic kidney disease-derived hMSCs improve therapeutic efficacy in ischemic disease via PrP C
Although autologous human mesenchymal stem cells (hMSCs) are a promising source for regenerative stem cell therapy in chronic kidney disease (CKD), the barriers associated with pathophysiological conditions limit therapeutic applicability to patients. We confirmed that level of cellular prion protei...
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| Veröffentlicht in: | Redox biology 2019-04, Vol.22, p.101144 |
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| creator | Yoon, Yeo Min Kim, SangMin Han, Yong-Seok Yun, Chul Won Lee, Jun Hee Noh, Hyunjin Lee, Sang Hun |
| description | Although autologous human mesenchymal stem cells (hMSCs) are a promising source for regenerative stem cell therapy in chronic kidney disease (CKD), the barriers associated with pathophysiological conditions limit therapeutic applicability to patients. We confirmed that level of cellular prion protein (PrP
) in serum was decreased and mitochondria function of CKD-derived hMSCs (CKD-hMSCs) was impaired in patients with CKD. We proved that treatment of CKD-hMSCs with tauroursodeoxycholic acid (TUDCA), a bile acid, enhanced the mitochondrial function of these cells through regulation of PINK1-PrP
-dependent pathway. In a murine hindlimb ischemia model with CKD, tail vein injection of TUDCA-treated CKD-hMSCs improved the functional recovery, including kidney recovery, limb salvage, blood perfusion ratio, and vessel formation along with restored expression of PrP
in the blood serum of the mice. These data suggest that TUDCA-treated CKD-hMSCs are a promising new autologous stem cell therapeutic intervention that dually treats cardiovascular problems and CKD in patients. |
| doi_str_mv | 10.1016/j.redox.2019.101144 |
| format | Article |
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) in serum was decreased and mitochondria function of CKD-derived hMSCs (CKD-hMSCs) was impaired in patients with CKD. We proved that treatment of CKD-hMSCs with tauroursodeoxycholic acid (TUDCA), a bile acid, enhanced the mitochondrial function of these cells through regulation of PINK1-PrP
-dependent pathway. In a murine hindlimb ischemia model with CKD, tail vein injection of TUDCA-treated CKD-hMSCs improved the functional recovery, including kidney recovery, limb salvage, blood perfusion ratio, and vessel formation along with restored expression of PrP
in the blood serum of the mice. These data suggest that TUDCA-treated CKD-hMSCs are a promising new autologous stem cell therapeutic intervention that dually treats cardiovascular problems and CKD in patients.</description><identifier>EISSN: 2213-2317</identifier><identifier>DOI: 10.1016/j.redox.2019.101144</identifier><identifier>PMID: 30785084</identifier><language>eng</language><publisher>Netherlands</publisher><subject>Animals ; Biomarkers ; Cell Proliferation ; Cytokines - metabolism ; Disease Models, Animal ; Humans ; Inflammation Mediators - metabolism ; Ischemia - metabolism ; Ischemia - pathology ; Ischemia - therapy ; Membrane Potential, Mitochondrial - drug effects ; Mesenchymal Stem Cell Transplantation ; Mesenchymal Stem Cells - drug effects ; Mesenchymal Stem Cells - metabolism ; Mesenchymal Stem Cells - ultrastructure ; Mice ; Mitochondria - drug effects ; Mitochondria - metabolism ; Mitophagy - drug effects ; PrPC Proteins - metabolism ; Renal Insufficiency, Chronic - metabolism ; Renal Insufficiency, Chronic - pathology ; Taurochenodeoxycholic Acid - pharmacology</subject><ispartof>Redox biology, 2019-04, Vol.22, p.101144</ispartof><rights>Copyright © 2019. Published by Elsevier B.V.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,860,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30785084$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yoon, Yeo Min</creatorcontrib><creatorcontrib>Kim, SangMin</creatorcontrib><creatorcontrib>Han, Yong-Seok</creatorcontrib><creatorcontrib>Yun, Chul Won</creatorcontrib><creatorcontrib>Lee, Jun Hee</creatorcontrib><creatorcontrib>Noh, Hyunjin</creatorcontrib><creatorcontrib>Lee, Sang Hun</creatorcontrib><title>TUDCA-treated chronic kidney disease-derived hMSCs improve therapeutic efficacy in ischemic disease via PrP C</title><title>Redox biology</title><addtitle>Redox Biol</addtitle><description>Although autologous human mesenchymal stem cells (hMSCs) are a promising source for regenerative stem cell therapy in chronic kidney disease (CKD), the barriers associated with pathophysiological conditions limit therapeutic applicability to patients. We confirmed that level of cellular prion protein (PrP
) in serum was decreased and mitochondria function of CKD-derived hMSCs (CKD-hMSCs) was impaired in patients with CKD. We proved that treatment of CKD-hMSCs with tauroursodeoxycholic acid (TUDCA), a bile acid, enhanced the mitochondrial function of these cells through regulation of PINK1-PrP
-dependent pathway. In a murine hindlimb ischemia model with CKD, tail vein injection of TUDCA-treated CKD-hMSCs improved the functional recovery, including kidney recovery, limb salvage, blood perfusion ratio, and vessel formation along with restored expression of PrP
in the blood serum of the mice. These data suggest that TUDCA-treated CKD-hMSCs are a promising new autologous stem cell therapeutic intervention that dually treats cardiovascular problems and CKD in patients.</description><subject>Animals</subject><subject>Biomarkers</subject><subject>Cell Proliferation</subject><subject>Cytokines - metabolism</subject><subject>Disease Models, Animal</subject><subject>Humans</subject><subject>Inflammation Mediators - metabolism</subject><subject>Ischemia - metabolism</subject><subject>Ischemia - pathology</subject><subject>Ischemia - therapy</subject><subject>Membrane Potential, Mitochondrial - drug effects</subject><subject>Mesenchymal Stem Cell Transplantation</subject><subject>Mesenchymal Stem Cells - drug effects</subject><subject>Mesenchymal Stem Cells - metabolism</subject><subject>Mesenchymal Stem Cells - ultrastructure</subject><subject>Mice</subject><subject>Mitochondria - drug effects</subject><subject>Mitochondria - metabolism</subject><subject>Mitophagy - drug effects</subject><subject>PrPC Proteins - metabolism</subject><subject>Renal Insufficiency, Chronic - metabolism</subject><subject>Renal Insufficiency, Chronic - pathology</subject><subject>Taurochenodeoxycholic Acid - pharmacology</subject><issn>2213-2317</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFjkFrwkAUhBehVGn9BYK8P5B0dxM1Hktq6UUQtGfZ7r6Qp24S3sZg_n1TsGfnMjAzH4wQMyVjJdXy7RQzuvoWa6nWf4lK05GYaK2SSCdqNRbTEE5yUJalWslnMU7kKlvILJ0If_j-yN-jltG06MCWXFdk4Uyuwh4cBTQBI4dM3VCX230egHzDdYfQlsimwWs7AFgUZI3tgSqgYEv0Q3jHoSMDO95B_iqeCnMJOL37i5h_bg75V9Rcfzy6Y8PkDffH_3_Jw8EvimVNiQ</recordid><startdate>201904</startdate><enddate>201904</enddate><creator>Yoon, Yeo Min</creator><creator>Kim, SangMin</creator><creator>Han, Yong-Seok</creator><creator>Yun, Chul Won</creator><creator>Lee, Jun Hee</creator><creator>Noh, Hyunjin</creator><creator>Lee, Sang Hun</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope></search><sort><creationdate>201904</creationdate><title>TUDCA-treated chronic kidney disease-derived hMSCs improve therapeutic efficacy in ischemic disease via PrP C</title><author>Yoon, Yeo Min ; Kim, SangMin ; Han, Yong-Seok ; Yun, Chul Won ; Lee, Jun Hee ; Noh, Hyunjin ; Lee, Sang Hun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-pubmed_primary_307850843</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Animals</topic><topic>Biomarkers</topic><topic>Cell Proliferation</topic><topic>Cytokines - metabolism</topic><topic>Disease Models, Animal</topic><topic>Humans</topic><topic>Inflammation Mediators - metabolism</topic><topic>Ischemia - metabolism</topic><topic>Ischemia - pathology</topic><topic>Ischemia - therapy</topic><topic>Membrane Potential, Mitochondrial - drug effects</topic><topic>Mesenchymal Stem Cell Transplantation</topic><topic>Mesenchymal Stem Cells - drug effects</topic><topic>Mesenchymal Stem Cells - metabolism</topic><topic>Mesenchymal Stem Cells - ultrastructure</topic><topic>Mice</topic><topic>Mitochondria - drug effects</topic><topic>Mitochondria - metabolism</topic><topic>Mitophagy - drug effects</topic><topic>PrPC Proteins - metabolism</topic><topic>Renal Insufficiency, Chronic - metabolism</topic><topic>Renal Insufficiency, Chronic - pathology</topic><topic>Taurochenodeoxycholic Acid - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yoon, Yeo Min</creatorcontrib><creatorcontrib>Kim, SangMin</creatorcontrib><creatorcontrib>Han, Yong-Seok</creatorcontrib><creatorcontrib>Yun, Chul Won</creatorcontrib><creatorcontrib>Lee, Jun Hee</creatorcontrib><creatorcontrib>Noh, Hyunjin</creatorcontrib><creatorcontrib>Lee, Sang Hun</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><jtitle>Redox biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yoon, Yeo Min</au><au>Kim, SangMin</au><au>Han, Yong-Seok</au><au>Yun, Chul Won</au><au>Lee, Jun Hee</au><au>Noh, Hyunjin</au><au>Lee, Sang Hun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>TUDCA-treated chronic kidney disease-derived hMSCs improve therapeutic efficacy in ischemic disease via PrP C</atitle><jtitle>Redox biology</jtitle><addtitle>Redox Biol</addtitle><date>2019-04</date><risdate>2019</risdate><volume>22</volume><spage>101144</spage><pages>101144-</pages><eissn>2213-2317</eissn><abstract>Although autologous human mesenchymal stem cells (hMSCs) are a promising source for regenerative stem cell therapy in chronic kidney disease (CKD), the barriers associated with pathophysiological conditions limit therapeutic applicability to patients. We confirmed that level of cellular prion protein (PrP
) in serum was decreased and mitochondria function of CKD-derived hMSCs (CKD-hMSCs) was impaired in patients with CKD. We proved that treatment of CKD-hMSCs with tauroursodeoxycholic acid (TUDCA), a bile acid, enhanced the mitochondrial function of these cells through regulation of PINK1-PrP
-dependent pathway. In a murine hindlimb ischemia model with CKD, tail vein injection of TUDCA-treated CKD-hMSCs improved the functional recovery, including kidney recovery, limb salvage, blood perfusion ratio, and vessel formation along with restored expression of PrP
in the blood serum of the mice. These data suggest that TUDCA-treated CKD-hMSCs are a promising new autologous stem cell therapeutic intervention that dually treats cardiovascular problems and CKD in patients.</abstract><cop>Netherlands</cop><pmid>30785084</pmid><doi>10.1016/j.redox.2019.101144</doi></addata></record> |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| subjects | Animals Biomarkers Cell Proliferation Cytokines - metabolism Disease Models, Animal Humans Inflammation Mediators - metabolism Ischemia - metabolism Ischemia - pathology Ischemia - therapy Membrane Potential, Mitochondrial - drug effects Mesenchymal Stem Cell Transplantation Mesenchymal Stem Cells - drug effects Mesenchymal Stem Cells - metabolism Mesenchymal Stem Cells - ultrastructure Mice Mitochondria - drug effects Mitochondria - metabolism Mitophagy - drug effects PrPC Proteins - metabolism Renal Insufficiency, Chronic - metabolism Renal Insufficiency, Chronic - pathology Taurochenodeoxycholic Acid - pharmacology |
| title | TUDCA-treated chronic kidney disease-derived hMSCs improve therapeutic efficacy in ischemic disease via PrP C |
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