Neuroprotective effects of human bone marrow mesenchymal stem cells against cerebral ischemia are mediated in part by an anti-apoptotic mechanism
Transplantation of human bone marrow mesenchymal stem cells (hMSCs) stands as a potent stroke therapy, but its exact mechanism remains unknown. This study investigated the anti-apoptotic mechanisms by which hMSCs exert neuroprotective effects on cerebral ischemia. Primary mixed cultures of rat neuro...
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| Published in | Neural regeneration research Vol. 14; no. 4; pp. 597 - 604 |
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| Main Authors | , , , , , , , , |
| Format | Journal Article |
| Language | English |
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India
Wolters Kluwer India Pvt. Ltd
01.04.2019
Medknow Publications and Media Pvt. Ltd Medknow Publications & Media Pvt. Ltd Department of Neurosurgery and Brain Repair, Center of Excellence for Aging and Brain Repair, University of South Florida, Tampa, FL, USA Department of Pharmacology / School of Life Science and Biopharmaceutical Science, Shenyang Pharmaceutical University, Shenyang, Liaoning Province, China%Department of Neurosurgery and Brain Repair, Center of Excellence for Aging and Brain Repair, University of South Florida, Tampa, FL, USA Medknow Publications & Media Pvt Ltd Wolters Kluwer Medknow Publications |
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| Abstract | Transplantation of human bone marrow mesenchymal stem cells (hMSCs) stands as a potent stroke therapy, but its exact mechanism remains unknown. This study investigated the anti-apoptotic mechanisms by which hMSCs exert neuroprotective effects on cerebral ischemia. Primary mixed cultures of rat neurons and astrocytes were cultured and exposed to oxygen-glucose deprivation. A two-hour period of "reperfusion" in standard medium and normoxic conditions was allowed and immediately followed by hMSCs and/or Bcl-2 antibody treatment. Cell viability of primary rat neurons and astrocytes was determined by 3-(4,5-dimethylthianol-2-yl)-2,5 diphenyl tetrazolium bromide and trypan blue exclusion methods. hMSC survival and differentiation were characterized by immunocytochemistry, while the concentration of Bcl-2 in the supernatant was measured by enzyme-linked immunosorbent assay to reveal the secretory anti-apoptotic function of hMSCs. Cultured hMSCs expressed embryonic-like stem cell phenotypic markers CXCR4, Oct4, SSEA4, and Nanog, as well as immature neural phenotypic marker Nestin. Primary rat neurons and astrocytes were protected from oxygen-glucose deprivation by hMSCs, which was antagonized by the Bcl-2 antibody. However, Bcl-2 levels in the supernatants did not differ between hMSC- and non-treated cells exposed to oxygen-glucose deprivation. Neuroprotective effects of hMSCs against cerebral ischemia were partially mediated by the anti-apoptotic mechanisms. However, further studies are warranted to fully elucidate this pathway. |
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| AbstractList | Transplantation of human bone marrow mesenchymal stem cells (hMSCs) stands as a potent stroke ther-apy, but its exact mechanism remains unknown. This study investigated the anti-apoptotic mechanisms by which hMSCs exert neuroprotective effects on cerebral ischemia. Primary mixed cultures of rat neurons and astrocytes were cultured and exposed to oxygen-glucose deprivation. A two-hour period of "reper-fusion" in standard medium and normoxic conditions was allowed and immediately followed by hMSCs and/or Bcl-2 antibody treatment. Cell viability of primary rat neurons and astrocytes was determined by 3-(4,5-dimethylthianol-2-yl)-2,5 diphenyl tetrazolium bromide and trypan blue exclusion methods. hMSC survival and differentiation were characterized by immunocytochemistry, while the concentration of Bcl-2 in the supernatant was measured by enzyme-linked immunosorbent assay to reveal the secreto-ry anti-apoptotic function of hMSCs. Cultured hMSCs expressed embryonic-like stem cell phenotypic markers CXCR4, Oct4, SSEA4, and Nanog, as well as immature neural phenotypic marker Nestin. Primary rat neurons and astrocytes were protected from oxygen-glucose deprivation by hMSCs, which was an-tagonized by the Bcl-2 antibody. However, Bcl-2 levels in the supernatants did not differ between hMSC-and non-treated cells exposed to oxygen-glucose deprivation. Neuroprotective effects of hMSCs against cerebral ischemia were partially mediated by the anti-apoptotic mechanisms. However, further studies are warranted to fully elucidate this pathway. Transplantation of human bone marrow mesenchymal stem cells (hMSCs) stands as a potent stroke therapy, but its exact mechanism remains unknown. This study investigated the anti-apoptotic mechanisms by which hMSCs exert neuroprotective effects on cerebral ischemia. Primary mixed cultures of rat neurons and astrocytes were cultured and exposed to oxygen-glucose deprivation. A two-hour period of “reperfusion” in standard medium and normoxic conditions was allowed and immediately followed by hMSCs and/or Bcl-2 antibody treatment. Cell viability of primary rat neurons and astrocytes was determined by 3-(4,5-dimethylthianol-2-yl)-2,5 diphenyl tetrazolium bromide and trypan blue exclusion methods. hMSC survival and differentiation were characterized by immunocytochemistry, while the concentration of Bcl-2 in the supernatant was measured by enzyme-linked immunosorbent assay to reveal the secretory anti-apoptotic function of hMSCs. Cultured hMSCs expressed embryonic-like stem cell phenotypic markers CXCR4, Oct4, SSEA4, and Nanog, as well as immature neural phenotypic marker Nestin. Primary rat neurons and astrocytes were protected from oxygen-glucose deprivation by hMSCs, which was antagonized by the Bcl-2 antibody. However, Bcl-2 levels in the supernatants did not differ between hMSC- and non-treated cells exposed to oxygen-glucose deprivation. Neuroprotective effects of hMSCs against cerebral ischemia were partially mediated by the anti-apoptotic mechanisms. However, further studies are warranted to fully elucidate this pathway. |
| Audience | Academic |
| Author | Corey, Sydney Kvederis, Lauren Zhang, Yuyang Kaneko, Yuji Tuazon, Julian Kingsbury, Chase Yu, Seongjin Lee, Jea-Young Borlongan, Cesar |
| AuthorAffiliation | Department of Neurosurgery and Brain Repair, Center of Excellence for Aging and Brain Repair, University of South Florida, Tampa, FL, USA;Department of Pharmacology / School of Life Science and Biopharmaceutical Science, Shenyang Pharmaceutical University, Shenyang, Liaoning Province, China%Department of Neurosurgery and Brain Repair, Center of Excellence for Aging and Brain Repair, University of South Florida, Tampa, FL, USA |
| AuthorAffiliation_xml | – name: Department of Neurosurgery and Brain Repair, Center of Excellence for Aging and Brain Repair, University of South Florida, Tampa, FL, USA;Department of Pharmacology / School of Life Science and Biopharmaceutical Science, Shenyang Pharmaceutical University, Shenyang, Liaoning Province, China%Department of Neurosurgery and Brain Repair, Center of Excellence for Aging and Brain Repair, University of South Florida, Tampa, FL, USA – name: 1 Department of Neurosurgery and Brain Repair, Center of Excellence for Aging and Brain Repair, University of South Florida, Tampa, FL, USA – name: 2 Department of Pharmacology / School of Life Science and Biopharmaceutical Science, Shenyang Pharmaceutical University, Shenyang, Liaoning Province, China |
| Author_xml | – sequence: 1 givenname: Yuyang surname: Zhang fullname: Zhang, Yuyang organization: Department of Neurosurgery and Brain Repair, Center of Excellence for Aging and Brain Repair, University of South Florida, Tampa, FL, USA; Department of Pharmacology / School of Life Science and Biopharmaceutical Science, Shenyang Pharmaceutical University, Shenyang, Liaoning Province, China – sequence: 2 givenname: Seongjin surname: Yu fullname: Yu, Seongjin organization: Department of Neurosurgery and Brain Repair, Center of Excellence for Aging and Brain Repair, University of South Florida, Tampa, FL – sequence: 3 givenname: Julian surname: Tuazon fullname: Tuazon, Julian organization: Department of Neurosurgery and Brain Repair, Center of Excellence for Aging and Brain Repair, University of South Florida, Tampa, FL – sequence: 4 givenname: Jea-Young surname: Lee fullname: Lee, Jea-Young organization: Department of Neurosurgery and Brain Repair, Center of Excellence for Aging and Brain Repair, University of South Florida, Tampa, FL – sequence: 5 givenname: Sydney surname: Corey fullname: Corey, Sydney organization: Department of Neurosurgery and Brain Repair, Center of Excellence for Aging and Brain Repair, University of South Florida, Tampa, FL – sequence: 6 givenname: Lauren surname: Kvederis fullname: Kvederis, Lauren organization: Department of Neurosurgery and Brain Repair, Center of Excellence for Aging and Brain Repair, University of South Florida, Tampa, FL – sequence: 7 givenname: Chase surname: Kingsbury fullname: Kingsbury, Chase organization: Department of Neurosurgery and Brain Repair, Center of Excellence for Aging and Brain Repair, University of South Florida, Tampa, FL – sequence: 8 givenname: Yuji surname: Kaneko fullname: Kaneko, Yuji organization: Department of Neurosurgery and Brain Repair, Center of Excellence for Aging and Brain Repair, University of South Florida, Tampa, FL – sequence: 9 givenname: Cesar surname: Borlongan fullname: Borlongan, Cesar organization: Department of Neurosurgery and Brain Repair, Center of Excellence for Aging and Brain Repair, University of South Florida, Tampa, FL |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/30632499$$D View this record in MEDLINE/PubMed |
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| Keywords | oxygen glucose deprivation Bcl-2 antibody apoptosis human mesenchymal stem cells neuroprotection ischemia |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Author contributions: Experiment implementation, collection and analysis of the data, drafting of the manuscript: YZ; experiment implementation, data interpretation, drafting of the manuscript: SY; data interpretation and drafting of the manuscript: JPT, JYL, SC, LK, and CK; study concept, data interpretation and manuscript preparation: YK and CV. All authors approved the final version of the manuscript. |
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| Publisher | Wolters Kluwer India Pvt. Ltd Medknow Publications and Media Pvt. Ltd Medknow Publications & Media Pvt. Ltd Department of Neurosurgery and Brain Repair, Center of Excellence for Aging and Brain Repair, University of South Florida, Tampa, FL, USA Department of Pharmacology / School of Life Science and Biopharmaceutical Science, Shenyang Pharmaceutical University, Shenyang, Liaoning Province, China%Department of Neurosurgery and Brain Repair, Center of Excellence for Aging and Brain Repair, University of South Florida, Tampa, FL, USA Medknow Publications & Media Pvt Ltd Wolters Kluwer Medknow Publications |
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| Snippet | Transplantation of human bone marrow mesenchymal stem cells (hMSCs) stands as a potent stroke therapy, but its exact mechanism remains unknown. This study... Transplantation of human bone marrow mesenchymal stem cells (hMSCs) stands as a potent stroke ther-apy, but its exact mechanism remains unknown. This study... |
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| SubjectTerms | Apoptosis apoptosis; Bcl-2 antibody; human mesenchymal stem cells; ischemia; neuroprotection; oxygen glucose deprivation Bone marrow Bone marrow cells Care and treatment Cellular signal transduction Gene expression Health aspects Ischemia Neurogenesis Stem cells Stroke |
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| Title | Neuroprotective effects of human bone marrow mesenchymal stem cells against cerebral ischemia are mediated in part by an anti-apoptotic mechanism |
| URI | http://www.nrronline.org/article.asp?issn=1673-5374;year=2019;volume=14;issue=4;spage=597;epage=604;aulast=Zhang;type=0 https://www.ncbi.nlm.nih.gov/pubmed/30632499 https://www.proquest.com/docview/2382127063 https://search.proquest.com/docview/2179365144 https://d.wanfangdata.com.cn/periodical/zgsjzsyj-e201904011 https://pubmed.ncbi.nlm.nih.gov/PMC6352592 https://doaj.org/article/1d3eedd8cbff4d82848a51f0b1d41516 |
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