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Provedor de dados:  BJMBR
País:  Brazil
Título:  Co-transfection of hepatocyte growth factor and truncated TGF-β type II receptor inhibit scar formation
Autores:  Xu,Ji-Hua
Zhao,Wan-Yi
Fang,Qing-Qing
Wang,Xiao-Feng
Zhang,Ding-Ding
Hu,Yan-Yan
Zheng,Bin
Tan,Wei-Qiang
Data:  2020-01-01
Ano:  2020
Palavras-chave:  Wound healing
Truncated transforming growth factor-β type II receptor
Hepatocyte growth factor
Scar
Rat
Lentivirus
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.
Tipo:  Info:eu-repo/semantics/article
Idioma:  Inglês
Identificador:  http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2020000100611
Editor:  Associação Brasileira de Divulgação Científica
Relação:  10.1590/1414-431x20199144
Formato:  text/html
Fonte:  Brazilian Journal of Medical and Biological Research v.53 n.1 2020
Direitos:  info:eu-repo/semantics/openAccess
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