https://scholars.lib.ntu.edu.tw/handle/123456789/569418
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.author | HSIAO-HUA CHANG | en_US |
dc.contributor.author | Chen I.-L. | en_US |
dc.contributor.author | YIN-LIN WANG | en_US |
dc.contributor.author | Chang M.-C. | en_US |
dc.contributor.author | YI-LING TSAI | en_US |
dc.contributor.author | Lan W.-C. | en_US |
dc.contributor.author | TONG-MEI WANG | en_US |
dc.contributor.author | Yeung S.-Y. | en_US |
dc.contributor.author | JIIANG-HUEI JENG | en_US |
dc.date.accessioned | 2021-07-05T07:59:12Z | - |
dc.date.available | 2021-07-05T07:59:12Z | - |
dc.date.issued | 2020 | - |
dc.identifier.issn | 1945-4589 | - |
dc.identifier.uri | https://www.scopus.com/inward/record.uri?eid=2-s2.0-85096814639&doi=10.18632%2faging.103848&partnerID=40&md5=5a9f7f79d6e9d7141f1f1b1a7d9fcc98 | - |
dc.identifier.uri | https://scholars.lib.ntu.edu.tw/handle/123456789/569418 | - |
dc.description.abstract | Transforming growth factor-β1 (TGF-β1) regulates wound healing/regeneration and aging processes. Dental pulp stem cells from human exfoliated deciduous teeth (SHED) are cell sources for treatment of age-related disorders. We studied the effect of TGF-β1 on SHED and related signaling. SHED were treated with TGF-β1 with/without pretreatment/co-incubation by SB431542, U0126, 5Z-7-oxozeaenol or SB203580. Sircol collagen assay, 3-(4,5-Dimethylthiazol-2-yl)-2,5- diphenyl tetrazolium bromide (MTT) assay, alkaline phosphatase (ALP) assay, RT-PCR, western blotting and PathScan phospho-ELISA were used to measure the effects. We found that SHED expressed ALK1, ALK3, ALK5, TGF-RII, betaglycan and endoglin mRNA. TGF-β1 stimulated p-Smad2, p-TAK1, p-ERK, p-p38 and cyclooxygenase-2 (COX-2) protein expression. It enhanced proliferation and collagen content of SHED that were attenuated by SB431542, 5Z-7-oxozeaenol and SB203580, but not U0126. TGF-β1 (0.5-1 ng/ml) stimulated ALP of SHED, whereas 5-10 ng/ml TGF-β1 suppressed ALP. SB431542 reversed the effects of TGF-β1. However, 5Z-7-oxozeaenol, SB203580 and U0126 only reversed the stimulatory effect of TGF-β1 on ALP. Four inhibitors attenuated TGF-β1-induced COX-2 expression. TGF-β1-stimulated TIMP-1 and N-cadherin was inhibited by SB431542 and 5Z-7-oxozeaenol. These results indicate that TGF-β1 affects SHED by differential regulation of ALK5/Smad2/3, TAK1, p38 and MEK/ERK. TGF-β1 and SHED could potentially be used for tissue engineering/regeneration and treatment of age-related diseases. ? 2020. All Rights Reserved. | - |
dc.publisher | Impact Journals LLC | - |
dc.relation.ispartof | Aging | - |
dc.subject.classification | [SDGs]SDG3 | - |
dc.subject.other | MAP kinase kinase kinase 7; mitogen activated protein kinase; mitogen activated protein kinase kinase; mitogen activated protein kinase kinase kinase; mitogen activated protein kinase p38; Smad2 protein; SMAD2 protein, human; Smad3 protein; SMAD3 protein, human; TGFBR1 protein, human; transforming growth factor beta1; cell culture; cell proliferation; cytology; deciduous tooth; drug effect; enzymology; human; metabolism; phosphorylation; regeneration; signal transduction; stem cell; tooth pulp; Cell Proliferation; Cells, Cultured; Dental Pulp; Extracellular Signal-Regulated MAP Kinases; Humans; MAP Kinase Kinase Kinases; Mitogen-Activated Protein Kinase Kinases; p38 Mitogen-Activated Protein Kinases; Phosphorylation; Receptor, Transforming Growth Factor-beta Type I; Regeneration; Signal Transduction; Smad2 Protein; Smad3 Protein; Stem Cells; Tooth, Deciduous; Transforming Growth Factor beta1 | - |
dc.title | Regulation of the regenerative activity of dental pulp stem cells from exfoliated deciduous teeth (SHED) of children by TGF-β1 is associated with ALK5/Smad2, TAK1, p38 and MEK/ERK signaling | en_US |
dc.type | journal article | en |
dc.identifier.doi | 10.18632/aging.103848 | - |
dc.identifier.pmid | 33148869 | - |
dc.identifier.scopus | 2-s2.0-85096814639 | - |
dc.relation.pages | 21253-21272 | - |
dc.relation.journalvolume | 12 | - |
dc.relation.journalissue | 21 | - |
item.openairetype | journal article | - |
item.fulltext | no fulltext | - |
item.openairecristype | http://purl.org/coar/resource_type/c_6501 | - |
item.grantfulltext | none | - |
item.cerifentitytype | Publications | - |
crisitem.author.dept | Clinical Dentistry | - |
crisitem.author.dept | Dentistry-NTUH | - |
crisitem.author.dept | School of Dentistry | - |
crisitem.author.dept | Dentistry | - |
crisitem.author.dept | School of Dentistry | - |
crisitem.author.dept | Dentistry-NTUH | - |
crisitem.author.dept | Dentistry | - |
crisitem.author.dept | School of Dentistry | - |
crisitem.author.dept | Dentistry-NTUH | - |
crisitem.author.dept | Dentistry | - |
crisitem.author.dept | School of Dentistry | - |
crisitem.author.dept | Dentistry-NTUH | - |
crisitem.author.dept | Clinical Dentistry | - |
crisitem.author.dept | Dentistry-NTUH | - |
crisitem.author.dept | School of Dentistry | - |
crisitem.author.orcid | 0000-0002-8417-8847 | - |
crisitem.author.orcid | 0000-0001-6790-1311 | - |
crisitem.author.orcid | 0000-0002-0576-6692 | - |
crisitem.author.orcid | 0000-0002-9885-6899 | - |
crisitem.author.orcid | 0000-0002-2068-5380 | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | College of Medicine | - |
顯示於: | 臨床牙醫學研究所 |
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