Folia histochemica et cytobiologica · 2025
Enhanced migration and adhesion protein expression by polyethylene glycol 4-modified SVVYGLR peptide in an in vitro human gingival fibroblast wound healing model.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Xiong Peiying, Yu Chengcheng, Chen Zhihui, Chen Luyuan, Hong Yonglong, Wu Buling
Аннотация
INTRODUCTION: This study was aimed at exploring the effect of four units of polyethylene glycol (PEG4)-modified Ser-Val-Val-Tyr-Gly-Leu-Arg (SVVYGLR) peptide (SV peptide) on the proliferative potential and migrative capability of human gingival fibroblasts (HGFs) and the activation of adhesion-related proteins.
MATERIAL AND METHODS: PEG4-SV peptide was synthesised using peptide solid phase synthesis. The proliferative response of HGFs to varying concentrations of PEG4-SV peptide was quantitatively evaluated using a Cell Counting Kit-8 (CCK-8) assay. The migratory capacity of HGFs in response to PEG4-SV peptide treatment was evaluated using an in vitro wound healing assay. The expression levels of adhesion-related genes, including collagen type I (COL-1), vinculin (VCL), focal adhesion kinase (FAK), and integrin β1(ITGB1), were quantitatively analysed using qRT-PCR. To assess the aforementioned adhesion-related proteins, immunofluorescence and Western blotting were performed.
RESULTS: Primary HGFs were isolated through enzymatic digestion using dispase, and subsequently characterised by positive immunoreactivity for both vimentin and CD90 (Thy-1) markers. Compared to the control group, PEG4-SV at concentrations of 10, 20, and 40 μg/mL significantly promoted the proliferation of HGFs. The wound area in the SV group exhibited a significantly smaller size in the monolayer cell culture at 24 and 48 h. The expression of adhesion-related genes and proteins (collagen type I, vinculin, FAK and integrin β1), were significantly upregulated after treatment with 20 μg/mL PEG4-SV.
CONCLUSIONS: These results demonstrate that PEG4-SV peptide may have the ability to promote soft tissue healing around an implant surface and form tight soft tissue sealing on the transmucosal part of the implant.
MATERIAL AND METHODS: PEG4-SV peptide was synthesised using peptide solid phase synthesis. The proliferative response of HGFs to varying concentrations of PEG4-SV peptide was quantitatively evaluated using a Cell Counting Kit-8 (CCK-8) assay. The migratory capacity of HGFs in response to PEG4-SV peptide treatment was evaluated using an in vitro wound healing assay. The expression levels of adhesion-related genes, including collagen type I (COL-1), vinculin (VCL), focal adhesion kinase (FAK), and integrin β1(ITGB1), were quantitatively analysed using qRT-PCR. To assess the aforementioned adhesion-related proteins, immunofluorescence and Western blotting were performed.
RESULTS: Primary HGFs were isolated through enzymatic digestion using dispase, and subsequently characterised by positive immunoreactivity for both vimentin and CD90 (Thy-1) markers. Compared to the control group, PEG4-SV at concentrations of 10, 20, and 40 μg/mL significantly promoted the proliferation of HGFs. The wound area in the SV group exhibited a significantly smaller size in the monolayer cell culture at 24 and 48 h. The expression of adhesion-related genes and proteins (collagen type I, vinculin, FAK and integrin β1), were significantly upregulated after treatment with 20 μg/mL PEG4-SV.
CONCLUSIONS: These results demonstrate that PEG4-SV peptide may have the ability to promote soft tissue healing around an implant surface and form tight soft tissue sealing on the transmucosal part of the implant.