https://scholars.lib.ntu.edu.tw/handle/123456789/468496
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.author | Pu C.-M. | en_US |
dc.contributor.author | Liu C.-W. | en_US |
dc.contributor.author | Liang C.-J. | en_US |
dc.contributor.author | Yen Y.-H. | en_US |
dc.contributor.author | Chen S.-H. | en_US |
dc.contributor.author | Jiang-Shieh Y.-F. | en_US |
dc.contributor.author | CHUNG-LIANG CHIEN | en_US |
dc.contributor.author | Chen Y.-C. | en_US |
dc.contributor.author | YUH-LIEN CHEN | en_US |
dc.creator | Pu C.-M.;Liu C.-W.;Liang C.-J.;Yen Y.-H.;Chen S.-H.;Jiang-Shieh Y.-F.;Chien C.-L.;Chen Y.-C.;Yuh-Lien Chen | - |
dc.date.accessioned | 2020-03-03T02:28:33Z | - |
dc.date.available | 2020-03-03T02:28:33Z | - |
dc.date.issued | 2017 | - |
dc.identifier.issn | 0022-202X | - |
dc.identifier.uri | https://www.scopus.com/inward/record.uri?eid=2-s2.0-85019897244&doi=10.1016%2fj.jid.2016.12.030&partnerID=40&md5=62a846cc512e61691b5a99042d98096b | - |
dc.identifier.uri | https://scholars.lib.ntu.edu.tw/handle/123456789/468496 | - |
dc.description.abstract | Flap necrosis is the most frequent postoperative complication encountered in reconstructive surgery. We elucidated whether adipose-derived stem cells (ADSCs) and their derivatives might induce neovascularization and protect skin flaps during ischemia/reperfusion (I/R) injury. Flaps were subjected to 3 hours of ischemia by ligating long thoracic vessels and then to blood reperfusion. Qtracker-labeled ADSCs, ADSCs in conditioned medium (ADSC-CM), or ADSC exosomes (ADSC-Exo) were injected into the flaps. These treatments led to significantly increased flap survival and capillary density compared with I/R on postoperative day 5. IL-6 levels in the cell lysates or in conditioned medium were significantly higher in ADSCs than in Hs68 fibroblasts. ADSC-CM and ADSC-Exo increased tube formation. This result was corroborated by a strong decrease in skin repair after adding IL-6–neutralizing antibodies or small interfering RNA for IL-6 ADSCs. ADSC transplantation also increased flap recovery in I/R injury of IL-6–knockout mice. IL-6 was secreted from ADSCs through signal transducer and activator of transcription phosphorylation, and then IL-6 stimulated angiogenesis and enhanced recovery after I/R injury by the classic signaling pathway. The mechanism of skin recovery includes the direct differentiation of ADSCs into endothelial cells and the indirect effect of IL-6 released from ADSCs. ADSC-CM and ADSC-Exo could be used as off-the-shelf products for this therapy. ? 2017 The Authors | - |
dc.publisher | Elsevier B.V. | - |
dc.relation.ispartof | Journal of Investigative Dermatology | - |
dc.subject.classification | [SDGs]SDG3 | - |
dc.subject.other | interleukin 6; mitogen activated protein kinase; small interfering RNA; STAT3 protein; interleukin 6; STAT3 protein; STAT3 protein, human; adipose derived stem cell; adult; angiogenesis; animal experiment; Article; capillary density; cell differentiation; cell lysate; conditioned medium; controlled study; cytokine release; endothelium cell; human; male; mouse; neovascularization (pathology); nonhuman; postoperative period; priority journal; protein expression; protein phosphorylation; reperfusion injury; skin fibroblast; skin flap; skin flap survival; stem cell transplantation; upregulation; adipose tissue; angiogenesis; animal; C57BL mouse; cell culture; cytology; disease model; fibroblast; genetics; graft survival; immunohistochemistry; immunology; metabolism; pathology; phosphorylation; procedures; randomization; reperfusion injury; stem cell; stem cell transplantation; surgical flaps; Adipose Tissue; Animals; Cells, Cultured; Disease Models, Animal; Fibroblasts; Graft Survival; Immunohistochemistry; Interleukin-6; Male; Mice; Mice, Inbred C57BL; Neovascularization, Physiologic; Phosphorylation; Random Allocation; Reperfusion Injury; STAT3 Transcription Factor; Stem Cell Transplantation; Stem Cells; Surgical Flaps | - |
dc.title | Adipose-Derived Stem Cells Protect Skin Flaps against Ischemia/Reperfusion Injury via IL-6 Expression | en_US |
dc.type | journal article | en |
dc.identifier.doi | 10.1016/j.jid.2016.12.030 | - |
dc.identifier.pmid | 28163069 | - |
dc.identifier.scopus | 2-s2.0-85019897244 | - |
dc.relation.pages | 1353-1362 | - |
dc.relation.journalvolume | 137 | - |
dc.relation.journalissue | 6 | - |
item.cerifentitytype | Publications | - |
item.grantfulltext | none | - |
item.fulltext | no fulltext | - |
item.openairecristype | http://purl.org/coar/resource_type/c_6501 | - |
item.openairetype | journal article | - |
crisitem.author.dept | Anatomy and Cell Biology | - |
crisitem.author.dept | Medical Genomics and Proteomics | - |
crisitem.author.dept | Anatomy and Cell Biology | - |
crisitem.author.orcid | 0000-0001-9806-486X | - |
crisitem.author.orcid | 0000-0002-6498-4008 | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | College of Medicine | - |
顯示於: | 解剖學暨細胞生物學科所 |
在 IR 系統中的文件,除了特別指名其著作權條款之外,均受到著作權保護,並且保留所有的權利。