Expression of CD24 in Human Bone Marrow-Derived Mesenchymal Stromal Cells Is Regulated by TGFβ3 and Induces a Myofibroblast-Like Genotype
Human bone marrow-derived stromal cells (hBMSCs) derived from the adult organism hold great promise for diverse settings in regenerative medicine. Therefore a more complete understanding of hBMSC biology to fully exploit the cells’ potential for clinical settings is important. The protein CD24 has b...
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| Format: | Article |
| Language: | English |
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Wiley
2016-01-01
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| Series: | Stem Cells International |
| Online Access: | http://dx.doi.org/10.1155/2016/1319578 |
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| _version_ | 1832568438324723712 |
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| author | Luisa Marilena Schäck Manuela Buettner Alexander Wirth Claudia Neunaber Christian Krettek Andrea Hoffmann Sandra Noack |
| author_facet | Luisa Marilena Schäck Manuela Buettner Alexander Wirth Claudia Neunaber Christian Krettek Andrea Hoffmann Sandra Noack |
| author_sort | Luisa Marilena Schäck |
| collection | DOAJ |
| description | Human bone marrow-derived stromal cells (hBMSCs) derived from the adult organism hold great promise for diverse settings in regenerative medicine. Therefore a more complete understanding of hBMSC biology to fully exploit the cells’ potential for clinical settings is important. The protein CD24 has been reported to be involved in a diverse range of processes such as cancer, adaptive immunity, inflammation, and autoimmune diseases in other cell types. Its expression in hBMSCs, which has not yet been analyzed, may add an important aspect in the understanding of hBMSC biology. The present study therefore analyzes the expression, regulation, and functional implication of the surface protein CD24 in hBMSCs. Methods used are stimulation studies with TGF beta as well as shRNA-mediated knockdown and overexpression of CD24 followed by microarray, immunocytochemistry, and flow cytometric analyses. To our knowledge, we demonstrate for the first time that the expression of CD24 is an inherent property of hBMSCs. Importantly, the data links the upregulation of CD24 to the adoption of a myofibroblast-like gene expression pattern in hBMSCs. We demonstrate that CD24 is an important modulator in transforming growth factor beta 3 (TGFβ3) signaling with a reciprocal regulatory relationship between these two proteins. |
| format | Article |
| id | doaj-art-763ac66fbfce4bad8f30147f0b3024cf |
| institution | Kabale University |
| issn | 1687-966X 1687-9678 |
| language | English |
| publishDate | 2016-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Stem Cells International |
| spelling | doaj-art-763ac66fbfce4bad8f30147f0b3024cf2025-02-03T00:59:08ZengWileyStem Cells International1687-966X1687-96782016-01-01201610.1155/2016/13195781319578Expression of CD24 in Human Bone Marrow-Derived Mesenchymal Stromal Cells Is Regulated by TGFβ3 and Induces a Myofibroblast-Like GenotypeLuisa Marilena Schäck0Manuela Buettner1Alexander Wirth2Claudia Neunaber3Christian Krettek4Andrea Hoffmann5Sandra Noack6Trauma Department, Hannover Medical School, 30625 Hannover, GermanyInstitute of Laboratory Animal Science, Hannover Medical School, 30625 Hannover, GermanyCellular Neurophysiology, Hannover Medical School, 30625 Hannover, GermanyTrauma Department, Hannover Medical School, 30625 Hannover, GermanyTrauma Department, Hannover Medical School, 30625 Hannover, GermanyTrauma Department, Hannover Medical School, 30625 Hannover, GermanyTrauma Department, Hannover Medical School, 30625 Hannover, GermanyHuman bone marrow-derived stromal cells (hBMSCs) derived from the adult organism hold great promise for diverse settings in regenerative medicine. Therefore a more complete understanding of hBMSC biology to fully exploit the cells’ potential for clinical settings is important. The protein CD24 has been reported to be involved in a diverse range of processes such as cancer, adaptive immunity, inflammation, and autoimmune diseases in other cell types. Its expression in hBMSCs, which has not yet been analyzed, may add an important aspect in the understanding of hBMSC biology. The present study therefore analyzes the expression, regulation, and functional implication of the surface protein CD24 in hBMSCs. Methods used are stimulation studies with TGF beta as well as shRNA-mediated knockdown and overexpression of CD24 followed by microarray, immunocytochemistry, and flow cytometric analyses. To our knowledge, we demonstrate for the first time that the expression of CD24 is an inherent property of hBMSCs. Importantly, the data links the upregulation of CD24 to the adoption of a myofibroblast-like gene expression pattern in hBMSCs. We demonstrate that CD24 is an important modulator in transforming growth factor beta 3 (TGFβ3) signaling with a reciprocal regulatory relationship between these two proteins.http://dx.doi.org/10.1155/2016/1319578 |
| spellingShingle | Luisa Marilena Schäck Manuela Buettner Alexander Wirth Claudia Neunaber Christian Krettek Andrea Hoffmann Sandra Noack Expression of CD24 in Human Bone Marrow-Derived Mesenchymal Stromal Cells Is Regulated by TGFβ3 and Induces a Myofibroblast-Like Genotype Stem Cells International |
| title | Expression of CD24 in Human Bone Marrow-Derived Mesenchymal Stromal Cells Is Regulated by TGFβ3 and Induces a Myofibroblast-Like Genotype |
| title_full | Expression of CD24 in Human Bone Marrow-Derived Mesenchymal Stromal Cells Is Regulated by TGFβ3 and Induces a Myofibroblast-Like Genotype |
| title_fullStr | Expression of CD24 in Human Bone Marrow-Derived Mesenchymal Stromal Cells Is Regulated by TGFβ3 and Induces a Myofibroblast-Like Genotype |
| title_full_unstemmed | Expression of CD24 in Human Bone Marrow-Derived Mesenchymal Stromal Cells Is Regulated by TGFβ3 and Induces a Myofibroblast-Like Genotype |
| title_short | Expression of CD24 in Human Bone Marrow-Derived Mesenchymal Stromal Cells Is Regulated by TGFβ3 and Induces a Myofibroblast-Like Genotype |
| title_sort | expression of cd24 in human bone marrow derived mesenchymal stromal cells is regulated by tgfβ3 and induces a myofibroblast like genotype |
| url | http://dx.doi.org/10.1155/2016/1319578 |
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