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Expression of Parac...
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Berg von Linde, MariaDepartment of Cardiology, Faculty of Health, Örebro University, Örebro, Sweden
(författare)
Expression of Paracrine Effectors in Human Adipose-Derived Mesenchymal Stem Cells Treated With Plasma From Brown Bears (Ursus arctos)
- Artikel/kapitelEngelska2021
Förlag, utgivningsår, omfång ...
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2020-09-19
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Wiley-Blackwell Publishing Inc.2021
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printrdacarrier
Nummerbeteckningar
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LIBRIS-ID:oai:DiVA.org:oru-85881
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https://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-85881URI
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https://doi.org/10.1111/cts.12872DOI
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Språk:engelska
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Sammanfattning på:engelska
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Ämneskategori:ref swepub-contenttype
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Ämneskategori:art swepub-publicationtype
Anmärkningar
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Funding Agencies:Scandinavian Brown Bear Research Project Norwegian Institute for Nature Research Swedish University of Agricultural Sciences Uppsala Genome Center, Sweden National Bioinformatics Infrastructure Sweden
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Adipose-derived mesenchymal stem cells (ADSCs) are promising candidates for novel cell therapeutic applications. Hibernating brown bears sustain tissue integrity and function via unknown mechanisms, which might be plasma borne. We hypothesized that plasma from hibernating bears may increase the expression of favorable factors from human ADSCs. In an experimental study, ADSCs from patients with ischemic heart disease were treated with interventional media containing plasma from hibernating and active bears, respectively, and with control medium. Extracted RNA from the ADSCs was sequenced using next generation sequencing. Statistical analyses of differentially expressed genes were performed using fold change analysis, pathway analysis, and gene ontology. As a result, we found that genes associated with inflammation, such as IGF1, PGF, IL11, and TGFA, were downregulated by > 10-fold in ADSCs treated with winter plasma compared with control. Genes important for cardiovascular development, ADM, ANGPTL4, and APOL3, were upregulated in ADSCs when treated with winter plasma compared with summer plasma. ADSCs treated with bear plasma, regardless if it was from hibernating or active bears, showed downregulation of IGF1, PGF, IL11, INHBA, IER3, and HMOX1 compared with control, suggesting reduced cell growth and differentiation. This can be summarized in the conclusion that plasma from hibernating bears suppresses inflammatory genes and activates genes associated with cardiovascular development in human ADSCs. Identifying the involved regulator(s) holds therapeutic potential.
Ämnesord och genrebeteckningar
Biuppslag (personer, institutioner, konferenser, titlar ...)
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Johansson, Karin,1970-Region Örebro län,Örebro universitet, Institutionen för medicinska vetenskaper,Department of Clinical Research Laboratory(Swepub:oru)kcjn
(författare)
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Kruse, Robert,1972-Örebro universitet, Institutionen för medicinska vetenskaper,Department of Cardiothoracic and Vascular Surgery, Faculty of Medicine and Health, Örebro University, Örebro, Sweden; University Health Care Research Center, Örebro University, Örebro, Sweden,iRiSC - Inflammatory Response and Infection Susceptibility Centre(Swepub:oru)rke
(författare)
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Helenius, Gisela,1973-Örebro universitet, Institutionen för medicinska vetenskaper,Department of Laboratory Medicine(Swepub:oru)ghs
(författare)
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Samano, Ninos,1972-Region Örebro län,Örebro universitet, Institutionen för medicinska vetenskaper,Department of Cardiothoracic and Vascular Surgery(Swepub:oru)nso
(författare)
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Friberg, ÖrjanDepartment of Cardiothoracic and Vascular Surgery, Faculty of Medicine and Health, Örebro University, Örebro, Sweden
(författare)
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Frøbert, Anne MetteDepartment of Chemistry and Bioscience, Faculty of Engineering and Science, Aalborg University, Aalborg, Denmar
(författare)
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Fröbert, Ole,1964-Örebro universitet, Institutionen för medicinska vetenskaper,Department of Cardiology(Swepub:oru)oft
(författare)
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Region Örebro länDepartment of Cardiology, Faculty of Health, Örebro University, Örebro, Sweden
(creator_code:org_t)
Sammanhörande titlar
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Ingår i:Clinical and Translational Science: Wiley-Blackwell Publishing Inc.14:1, s. 317-3251752-80541752-8062
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