Co-transfection of hepatocyte growth factor and truncated TGF-β type II receptor inhibit scar formation
Autor(a) principal: | |
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Data de Publicação: | 2020 |
Outros Autores: | , , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Brazilian Journal of Medical and Biological Research |
Texto Completo: | http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2020000100611 |
Resumo: | Wound scarring remains a major challenge for plastic surgeons. Transforming growth factor (TGF)-β plays a key role in the process of scar formation. Previous studies have demonstrated that truncated TGF-β type II receptor (t-TGF-βRII) is unable to continue signal transduction but is still capable of binding to TGF-β, thereby blocking the TGF-β signaling pathway. Hepatocyte growth factor (HGF) is a multifunctional growth factor that promotes tissue regeneration and wound healing. Theoretically, the combination of HGF and t-TGF-βRII would be expected to exert a synergistic effect on promoting wound healing and reducing collagen formation. In the present study, lentivirus-mediated transfection of the two genes (t-TGF-βRII/HGF) into fibroblasts in vitro and in a rat model in vivo was used. The results demonstrated that the expression of t-TGF-βRII and HGF in NIH-3T3 cells was successfully induced. The expression of both molecules significantly reduced collagen I and III expression, and also inhibited fibroblast proliferation. Furthermore, histological examination and scar quantification revealed less scarring in the experimental wound in a rat model. Moreover, on macroscopic inspection, the experimental wound exhibited less visible scarring compared with the control. Therefore, the present study demonstrated that the combination gene therapy of t-TGF-βRII and HGF promoted wound healing, with less scarring and more epithelial tissue formation, not only by suppressing the overgrowth of collagen due to its antifibrotic effect, but also by promoting tissue regeneration. |
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Co-transfection of hepatocyte growth factor and truncated TGF-β type II receptor inhibit scar formationWound healingTruncated transforming growth factor-β type II receptorHepatocyte growth factorScarRatLentivirusWound scarring remains a major challenge for plastic surgeons. Transforming growth factor (TGF)-β plays a key role in the process of scar formation. Previous studies have demonstrated that truncated TGF-β type II receptor (t-TGF-βRII) is unable to continue signal transduction but is still capable of binding to TGF-β, thereby blocking the TGF-β signaling pathway. Hepatocyte growth factor (HGF) is a multifunctional growth factor that promotes tissue regeneration and wound healing. Theoretically, the combination of HGF and t-TGF-βRII would be expected to exert a synergistic effect on promoting wound healing and reducing collagen formation. In the present study, lentivirus-mediated transfection of the two genes (t-TGF-βRII/HGF) into fibroblasts in vitro and in a rat model in vivo was used. The results demonstrated that the expression of t-TGF-βRII and HGF in NIH-3T3 cells was successfully induced. The expression of both molecules significantly reduced collagen I and III expression, and also inhibited fibroblast proliferation. Furthermore, histological examination and scar quantification revealed less scarring in the experimental wound in a rat model. Moreover, on macroscopic inspection, the experimental wound exhibited less visible scarring compared with the control. Therefore, the present study demonstrated that the combination gene therapy of t-TGF-βRII and HGF promoted wound healing, with less scarring and more epithelial tissue formation, not only by suppressing the overgrowth of collagen due to its antifibrotic effect, but also by promoting tissue regeneration.Associação Brasileira de Divulgação Científica2020-01-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersiontext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2020000100611Brazilian Journal of Medical and Biological Research v.53 n.1 2020reponame:Brazilian Journal of Medical and Biological Researchinstname:Associação Brasileira de Divulgação Científica (ABDC)instacron:ABDC10.1590/1414-431x20199144info:eu-repo/semantics/openAccessXu,Ji-HuaZhao,Wan-YiFang,Qing-QingWang,Xiao-FengZhang,Ding-DingHu,Yan-YanZheng,BinTan,Wei-Qiangeng2020-01-10T00:00:00Zoai:scielo:S0100-879X2020000100611Revistahttps://www.bjournal.org/https://old.scielo.br/oai/scielo-oai.phpbjournal@terra.com.br||bjournal@terra.com.br1414-431X0100-879Xopendoar:2020-01-10T00:00Brazilian Journal of Medical and Biological Research - Associação Brasileira de Divulgação Científica (ABDC)false |
dc.title.none.fl_str_mv |
Co-transfection of hepatocyte growth factor and truncated TGF-β type II receptor inhibit scar formation |
title |
Co-transfection of hepatocyte growth factor and truncated TGF-β type II receptor inhibit scar formation |
spellingShingle |
Co-transfection of hepatocyte growth factor and truncated TGF-β type II receptor inhibit scar formation Xu,Ji-Hua Wound healing Truncated transforming growth factor-β type II receptor Hepatocyte growth factor Scar Rat Lentivirus |
title_short |
Co-transfection of hepatocyte growth factor and truncated TGF-β type II receptor inhibit scar formation |
title_full |
Co-transfection of hepatocyte growth factor and truncated TGF-β type II receptor inhibit scar formation |
title_fullStr |
Co-transfection of hepatocyte growth factor and truncated TGF-β type II receptor inhibit scar formation |
title_full_unstemmed |
Co-transfection of hepatocyte growth factor and truncated TGF-β type II receptor inhibit scar formation |
title_sort |
Co-transfection of hepatocyte growth factor and truncated TGF-β type II receptor inhibit scar formation |
author |
Xu,Ji-Hua |
author_facet |
Xu,Ji-Hua Zhao,Wan-Yi Fang,Qing-Qing Wang,Xiao-Feng Zhang,Ding-Ding Hu,Yan-Yan Zheng,Bin Tan,Wei-Qiang |
author_role |
author |
author2 |
Zhao,Wan-Yi Fang,Qing-Qing Wang,Xiao-Feng Zhang,Ding-Ding Hu,Yan-Yan Zheng,Bin Tan,Wei-Qiang |
author2_role |
author author author author author author author |
dc.contributor.author.fl_str_mv |
Xu,Ji-Hua Zhao,Wan-Yi Fang,Qing-Qing Wang,Xiao-Feng Zhang,Ding-Ding Hu,Yan-Yan Zheng,Bin Tan,Wei-Qiang |
dc.subject.por.fl_str_mv |
Wound healing Truncated transforming growth factor-β type II receptor Hepatocyte growth factor Scar Rat Lentivirus |
topic |
Wound healing Truncated transforming growth factor-β type II receptor Hepatocyte growth factor Scar Rat Lentivirus |
description |
Wound scarring remains a major challenge for plastic surgeons. Transforming growth factor (TGF)-β plays a key role in the process of scar formation. Previous studies have demonstrated that truncated TGF-β type II receptor (t-TGF-βRII) is unable to continue signal transduction but is still capable of binding to TGF-β, thereby blocking the TGF-β signaling pathway. Hepatocyte growth factor (HGF) is a multifunctional growth factor that promotes tissue regeneration and wound healing. Theoretically, the combination of HGF and t-TGF-βRII would be expected to exert a synergistic effect on promoting wound healing and reducing collagen formation. In the present study, lentivirus-mediated transfection of the two genes (t-TGF-βRII/HGF) into fibroblasts in vitro and in a rat model in vivo was used. The results demonstrated that the expression of t-TGF-βRII and HGF in NIH-3T3 cells was successfully induced. The expression of both molecules significantly reduced collagen I and III expression, and also inhibited fibroblast proliferation. Furthermore, histological examination and scar quantification revealed less scarring in the experimental wound in a rat model. Moreover, on macroscopic inspection, the experimental wound exhibited less visible scarring compared with the control. Therefore, the present study demonstrated that the combination gene therapy of t-TGF-βRII and HGF promoted wound healing, with less scarring and more epithelial tissue formation, not only by suppressing the overgrowth of collagen due to its antifibrotic effect, but also by promoting tissue regeneration. |
publishDate |
2020 |
dc.date.none.fl_str_mv |
2020-01-01 |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2020000100611 |
url |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2020000100611 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
10.1590/1414-431x20199144 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
text/html |
dc.publisher.none.fl_str_mv |
Associação Brasileira de Divulgação Científica |
publisher.none.fl_str_mv |
Associação Brasileira de Divulgação Científica |
dc.source.none.fl_str_mv |
Brazilian Journal of Medical and Biological Research v.53 n.1 2020 reponame:Brazilian Journal of Medical and Biological Research instname:Associação Brasileira de Divulgação Científica (ABDC) instacron:ABDC |
instname_str |
Associação Brasileira de Divulgação Científica (ABDC) |
instacron_str |
ABDC |
institution |
ABDC |
reponame_str |
Brazilian Journal of Medical and Biological Research |
collection |
Brazilian Journal of Medical and Biological Research |
repository.name.fl_str_mv |
Brazilian Journal of Medical and Biological Research - Associação Brasileira de Divulgação Científica (ABDC) |
repository.mail.fl_str_mv |
bjournal@terra.com.br||bjournal@terra.com.br |
_version_ |
1754302947553968128 |