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Effect of Acellular Amnion With Increased TGF-β and bFGF Levels on the Biological Behavior of Tenocytes

The human amniotic membrane has been a subject for clinical and basic research for nearly 100 years, but weak rejection has been reported. The purpose of this research is to remove the cellular components of the amnion for eliminating its immune-inducing activity to the utmost extent. The amniotic m...

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Autores principales: Sang, Rongli, Liu, Yuanyuan, Kong, Lingyu, Qian, Ligang, Liu, Chunjie
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7240037/
https://www.ncbi.nlm.nih.gov/pubmed/32478059
http://dx.doi.org/10.3389/fbioe.2020.00446
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author Sang, Rongli
Liu, Yuanyuan
Kong, Lingyu
Qian, Ligang
Liu, Chunjie
author_facet Sang, Rongli
Liu, Yuanyuan
Kong, Lingyu
Qian, Ligang
Liu, Chunjie
author_sort Sang, Rongli
collection PubMed
description The human amniotic membrane has been a subject for clinical and basic research for nearly 100 years, but weak rejection has been reported. The purpose of this research is to remove the cellular components of the amnion for eliminating its immune-inducing activity to the utmost extent. The amniotic membrane treated by acid removed the epithelial cell, fibroblast, and sponge layers and retained only the basal and dense layers. In vitro, biological effects of the new material on tenocytes were evaluated. The levels of transforming growth factor (TGF-β1), fibroblast growth factor (bFGF) proteins were measured. In vivo, the tendon injury model of chickens was constructed to observe effects on tendon adhesion and healing. The acellular amniotic membrane effectively removed the cell components of the amnion while retaining the fibrous reticular structure. Abundant collagen fibers enhanced the tensile strength of amnion, and a 3D porous structure provided enough 3D space structure for tenocyte growth. In vitro, acellular amnion resulted in the fast proliferation trend for tenocytes with relatively static properties by releasing TGF-β1 and bFGF. In vivo, the experiment revealed the mechanism of acellular amnion in promoting endogenous healing and barrier exogenous healing by evaluating tendon adhesion, biomechanical testing, and labeling fibroblasts/tendon cells and monocytes/macrophages with vimentin and CD68. The acellular amnion promotes endogenous healing and barrier exogenous healing by releasing the growth factors such as TGF-β1 and bFGF, thereby providing a new direction for the prevention and treatment of tendon adhesion.
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spelling pubmed-72400372020-05-29 Effect of Acellular Amnion With Increased TGF-β and bFGF Levels on the Biological Behavior of Tenocytes Sang, Rongli Liu, Yuanyuan Kong, Lingyu Qian, Ligang Liu, Chunjie Front Bioeng Biotechnol Bioengineering and Biotechnology The human amniotic membrane has been a subject for clinical and basic research for nearly 100 years, but weak rejection has been reported. The purpose of this research is to remove the cellular components of the amnion for eliminating its immune-inducing activity to the utmost extent. The amniotic membrane treated by acid removed the epithelial cell, fibroblast, and sponge layers and retained only the basal and dense layers. In vitro, biological effects of the new material on tenocytes were evaluated. The levels of transforming growth factor (TGF-β1), fibroblast growth factor (bFGF) proteins were measured. In vivo, the tendon injury model of chickens was constructed to observe effects on tendon adhesion and healing. The acellular amniotic membrane effectively removed the cell components of the amnion while retaining the fibrous reticular structure. Abundant collagen fibers enhanced the tensile strength of amnion, and a 3D porous structure provided enough 3D space structure for tenocyte growth. In vitro, acellular amnion resulted in the fast proliferation trend for tenocytes with relatively static properties by releasing TGF-β1 and bFGF. In vivo, the experiment revealed the mechanism of acellular amnion in promoting endogenous healing and barrier exogenous healing by evaluating tendon adhesion, biomechanical testing, and labeling fibroblasts/tendon cells and monocytes/macrophages with vimentin and CD68. The acellular amnion promotes endogenous healing and barrier exogenous healing by releasing the growth factors such as TGF-β1 and bFGF, thereby providing a new direction for the prevention and treatment of tendon adhesion. Frontiers Media S.A. 2020-05-14 /pmc/articles/PMC7240037/ /pubmed/32478059 http://dx.doi.org/10.3389/fbioe.2020.00446 Text en Copyright © 2020 Sang, Liu, Kong, Qian and Liu. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Bioengineering and Biotechnology
Sang, Rongli
Liu, Yuanyuan
Kong, Lingyu
Qian, Ligang
Liu, Chunjie
Effect of Acellular Amnion With Increased TGF-β and bFGF Levels on the Biological Behavior of Tenocytes
title Effect of Acellular Amnion With Increased TGF-β and bFGF Levels on the Biological Behavior of Tenocytes
title_full Effect of Acellular Amnion With Increased TGF-β and bFGF Levels on the Biological Behavior of Tenocytes
title_fullStr Effect of Acellular Amnion With Increased TGF-β and bFGF Levels on the Biological Behavior of Tenocytes
title_full_unstemmed Effect of Acellular Amnion With Increased TGF-β and bFGF Levels on the Biological Behavior of Tenocytes
title_short Effect of Acellular Amnion With Increased TGF-β and bFGF Levels on the Biological Behavior of Tenocytes
title_sort effect of acellular amnion with increased tgf-β and bfgf levels on the biological behavior of tenocytes
topic Bioengineering and Biotechnology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7240037/
https://www.ncbi.nlm.nih.gov/pubmed/32478059
http://dx.doi.org/10.3389/fbioe.2020.00446
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