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| 1 | Pirfenidone inhibits epithelial–mesenchymal transition in keloid keratinocytes显示文摘Background:Keloids are benign fibroproliferative skin lesions that are difficult to treat and become a lifetime predicament for patients.Several treatment modalities have been put forth,but as yet no satisfactory approach to the prevention or treatment of keloids has been identified.The process of epithelial-to-mesenchymal transition(EMT)has been implicated in keloid scarring,as keloid keratinocytes display an EMT-like phenotype.This study investigated the potential of pirfenidone,an antifibrotic agent,to counteract EMT-like alterations in keloid keratinocytes,including gene expression,cell migratory and proliferative functions.Methods:Normal and keloid keratinocytes were isolated from discarded normal skin tissues and from resected keloid tissues,respectively.Cells were quiesced for 24 h without epidermal growth factor DS-Qi1MCDigital and were exposed to transforming growth factor-beta1(TGF-β1;10 ng/mL),with or without pirfenidone(400μg/mL),for an additional 24 h.The effects of pirfenidone on cytotoxicity,cell migration,cell proliferation,and on expression of genes and proteins involved in EMT were assayed.Statistical significance was determined by two-way ANOVA using Sigma Plot.Results:We found that pirfenidone did not elicit any cytotoxic effect at concentrations up to 1000μg/mL.A statistically significant dose-dependent decrease in basal cell proliferation rate was noted in both normal and keloid keratinocytes when exposed to pirfenidone at concentrations ranging from 200 to 1000μg/mL.Pirfenidone significantly decreased basal cell migration in both normal and keloid keratinocytes,but a significant decrease in TGF-β1-induced cell migration was seen only in keloid keratinocytes.Significant inhibition of the expression of TGF-β1-induced core EMT genes,namely hyaluronan synthase 2,vimentin,cadherin-11,and wingless-type MMTV integration site family,member 5A along with fibronectin-1,was observed in both normal and keloid keratinocytes treated with pirfenidone.In addition,the protein levels of vimentin and fibronectin were significantly reduced by pirfenidone(400μg/mL)in both normal and keloid keratinocytes.Conclusions:For the first time,this study shows the efficacy of pirfenidone in inhibiting the EMTlike phenotype in keratinocytes derived from keloids,suggesting that pirfenidone may counteract a critical contributor of keloid progression and recurrence. | Latha Satish Alexander Evdokiou Eleni Geletu Jennifer M.Hahn Dorothy M.Supp | 2020 | Burns & Trauma2020，8，1： | 3 |
| 2 | Classical cadherins control survival through the gp130/Stat3 axis显示文摘 | Geletu M Arulanandam R Chevalier S | 2013 | Biochim Biophys Acta2013，1833，8： | 1 |
| 3 | Activated Rac1 requires gp130 for Stat3 activation,cell proliferation and migration显示文摘 | Arulanandam R Geletu M Feracci H Raptis L | 2010 | Exp Cell Res2010，316，5： | 1 |
| 4 | Regulation of gap junctional, intercellular communication by the src oncogene product and its effectors显示文摘 | Geletu M Trotman GA Raptis L | 2012 | J Cell Sci Ther2012，5，： | 1 |
| 5 | Proteomie analysis of acute promyeloeytic leukemia:PML-RARalpha leads to decreased phosphoryIation of OPl8 at serine 63显示文摘 | Zada AA Geletu MH Pulikkan JA | 2006 | Proteomics2006，6，21： | 1 |
| 6 | Proteomic analysis of acute promyelocytic leukemia:PML-RARα leads to decreased phosphorylation of OP18 at sefine 63显示文摘 | Zada A Geletu M Pulikkan J | 2006 | Proteomics2006，6，21： | 1 |
| 7 | Effects of SRC and STAT3 upon gap junctional, intercellular communication in lung cancer lines 显示文摘 | Geletu M Guy S Raptis L | 2013 | Anticancer Res2013，33，10： | 1 |
| 8 | Circulating TNF - alpha, TGF - beta, and IL - 10 in tuberculosis patients and healthy contacts显示文摘 | OLOBO J O GELETU M DEMISSIE A | 2001 | Scand J Immunol2001，53，1： | 1 |
| 9 | Mind the gap;regulation of gap junctional,intercellular communication by the SRC oncogene product and its effectors显示文摘 | Geletu M Trotman-Grant A Raptis L | 2012 | Anticancer Res2012，32，： | 1 |
| 10 | Housekeeping genes; expression levels may change with density of cultured cells 显示文摘 | Greer S Honeywell R Geletu M | 2010 | Journal of Immunological Methods2010，355，12： | 1 |
| 11 | Proteomics of acute myeloid leukaemia:cytogenetic risk groups differ specifically in their proteome,interactome and post-translational protein modifications显示文摘 | Balkhi MY Trivedi AK Geletu M | 2006 | Oncogene2006，25，53： | 1 |
| 12 | Housekeeping genes; expression levels may change with density of cultured cells显示文摘 | Samantha Greer Rice Honeywell Mulu Geletu Rozanne Arulanandam Leda Raptis | 2010 | Journal of Immunological Methods2010，，1： | 1 |
| 13 | Activated Rac1 requires gp130 for Stat3 activation,cell proliferation and migration显示文摘 | Arulanandam R Geletu M Feracci H | 2010 | Exp Cell Res2010，316，5： | 1 |
| 14 | Effects of SRC and STAT3 upon gap junctional, intercellular communication in lung cancer lines 显示文摘 | Geletu M Guy S Raptis L | 2013 | Anticancer Res2013，33，10： | 1 |
| 15 | Proteomic analysis of acute promyelocytic leukemia: PML-RARα leads to decreased phosphorylation of op18 at serine 63显示文摘 | Zada A Geletu M Pulikkan J | 2006 | Proteomics2006，6，21： | 1 |
| 16 | The R(h)oads to Stat3: 5tat3 activation by the Rho GTPases显示文摘 | Raptis L Arulanandam R Geletu M | 2011 | Exp Cell Res2011，317，13： | 1 |
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