Adipose-derived stem cells promote proliferation, migration, and tube formation of lymphatic endothelial cells in vitro by secreting lymphangiogenic factors.
Identifieur interne : 002177 ( Main/Curation ); précédent : 002176; suivant : 002178Adipose-derived stem cells promote proliferation, migration, and tube formation of lymphatic endothelial cells in vitro by secreting lymphangiogenic factors.
Auteurs : Kohsuke Takeda [Japon] ; Yoshihiro Sowa ; Kenichi Nishino ; Kyoko Itoh ; Shinji FushikiSource :
- Annals of plastic surgery [ 1536-3708 ] ; 2015.
Descripteurs français
- KwdFr :
- Animaux, Cellules endothéliales (physiologie), Cellules stromales mésenchymateuses (métabolisme), Cellules stromales mésenchymateuses (physiologie), Graisse sous-cutanée (cytologie), Humains, Lymphangiogenèse (physiologie), Marqueurs biologiques (métabolisme), Milieux de culture conditionnés, Mouvement cellulaire, Mâle, Prolifération cellulaire, RT-PCR, Régulation positive, Souris, Souris de lignée C57BL, Test ELISA.
- MESH :
- cytologie : Graisse sous-cutanée.
- métabolisme : Cellules stromales mésenchymateuses, Marqueurs biologiques.
- physiologie : Cellules endothéliales, Cellules stromales mésenchymateuses, Lymphangiogenèse.
- Animaux, Humains, Milieux de culture conditionnés, Mouvement cellulaire, Mâle, Prolifération cellulaire, RT-PCR, Régulation positive, Souris, Souris de lignée C57BL, Test ELISA.
English descriptors
- KwdEn :
- Animals, Biomarkers (metabolism), Cell Movement, Cell Proliferation, Culture Media, Conditioned, Endothelial Cells (physiology), Enzyme-Linked Immunosorbent Assay, Humans, Lymphangiogenesis (physiology), Male, Mesenchymal Stromal Cells (metabolism), Mesenchymal Stromal Cells (physiology), Mice, Mice, Inbred C57BL, Reverse Transcriptase Polymerase Chain Reaction, Subcutaneous Fat (cytology), Up-Regulation.
- MESH :
- chemical , metabolism : Biomarkers.
- cytology : Subcutaneous Fat.
- metabolism : Mesenchymal Stromal Cells.
- physiology : Endothelial Cells, Lymphangiogenesis, Mesenchymal Stromal Cells.
- Animals, Cell Movement, Cell Proliferation, Culture Media, Conditioned, Enzyme-Linked Immunosorbent Assay, Humans, Male, Mice, Mice, Inbred C57BL, Reverse Transcriptase Polymerase Chain Reaction, Up-Regulation.
Abstract
Adipose-derived stem cells (ADSCs) are a promising new therapeutic modality for several diseases and have been applied to various clinical fields because of their multidifferentiation potential and capacity for growth-factor secretion. Recently, 2 in vivo studies showed ADSCs to have potential applications in lymphedema therapy. However, it remains unclear whether ADSCs have direct effects on lymphatic endothelial cells (LECs). In this study, human LECs were treated with murine ADSC-derived conditioned media. Changes in LEC proliferation, migration, and tube formation were assessed by WST-8 assay, transwell chamber assay, and Matrigel-based tube formation assay, respectively, with recombinant human vascular endothelial growth factor-C used as a positive control. Additionally, the expression of several lymphangiogenic factors in ADSCs was examined by quantitative reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay. Factors secreted by ADSCs induced LEC proliferation, migration, and tube formation more potently than recombinant human vascular endothelial growth factor-C. We confirmed by quantitative reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay that some of the lymphangiogenic factors of ADSCs were dramatically up-regulated under serum-starved conditions. These data indicate that ADSCs could directly contribute to lymphangiogenesis via secretory factors in vitro and may thus provide a therapeutic modality for patients with lymphedema.
DOI: 10.1097/SAP.0000000000000084
PubMed: 24401810
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sortKey="Sowa, Yoshihiro" sort="Sowa, Yoshihiro" uniqKey="Sowa Y" first="Yoshihiro" last="Sowa">Yoshihiro Sowa</name></author><author><name sortKey="Nishino, Kenichi" sort="Nishino, Kenichi" uniqKey="Nishino K" first="Kenichi" last="Nishino">Kenichi Nishino</name></author><author><name sortKey="Itoh, Kyoko" sort="Itoh, Kyoko" uniqKey="Itoh K" first="Kyoko" last="Itoh">Kyoko Itoh</name></author><author><name sortKey="Fushiki, Shinji" sort="Fushiki, Shinji" uniqKey="Fushiki S" first="Shinji" last="Fushiki">Shinji Fushiki</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2015">2015</date><idno type="RBID">pubmed:24401810</idno><idno type="pmid">24401810</idno><idno type="doi">10.1097/SAP.0000000000000084</idno><idno type="wicri:Area/PubMed/Corpus">001735</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001735</idno><idno type="wicri:Area/PubMed/Curation">001735</idno><idno type="wicri:explorRef" 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Recently, 2 in vivo studies showed ADSCs to have potential applications in lymphedema therapy. However, it remains unclear whether ADSCs have direct effects on lymphatic endothelial cells (LECs). In this study, human LECs were treated with murine ADSC-derived conditioned media. Changes in LEC proliferation, migration, and tube formation were assessed by WST-8 assay, transwell chamber assay, and Matrigel-based tube formation assay, respectively, with recombinant human vascular endothelial growth factor-C used as a positive control. Additionally, the expression of several lymphangiogenic factors in ADSCs was examined by quantitative reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay. Factors secreted by ADSCs induced LEC proliferation, migration, and tube formation more potently than recombinant human vascular endothelial growth factor-C. We confirmed by quantitative reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay that some of the lymphangiogenic factors of ADSCs were dramatically up-regulated under serum-starved conditions. These data indicate that ADSCs could directly contribute to lymphangiogenesis via secretory factors in vitro and may thus provide a therapeutic modality for patients with lymphedema.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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