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Modulating Myofibroblastic Differentiation of Fibroblasts through Actin-MRTF Signaling Axis by Micropatterned Surfaces for Suppressed Implant-Induced Fibrosis

Myofibroblasts, the primary effector cells for implant-induced fibrosis, contribute to this process by secreting excessive collagen-rich matrix and contracting. Thus, approaches that suppress myofibroblasts may achieve desirable suppression effects in the fibrotic process. As one of the important ph...

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Autores principales: Han, Weiju, Chu, Qi, Li, Junliang, Dong, Zixuan, Shi, Xuetao, Fu, Xiaoling
Formato: Online Artículo Texto
Lenguaje:English
Publicado: AAAS 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10076024/
https://www.ncbi.nlm.nih.gov/pubmed/37040480
http://dx.doi.org/10.34133/research.0049
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author Han, Weiju
Chu, Qi
Li, Junliang
Dong, Zixuan
Shi, Xuetao
Fu, Xiaoling
author_facet Han, Weiju
Chu, Qi
Li, Junliang
Dong, Zixuan
Shi, Xuetao
Fu, Xiaoling
author_sort Han, Weiju
collection PubMed
description Myofibroblasts, the primary effector cells for implant-induced fibrosis, contribute to this process by secreting excessive collagen-rich matrix and contracting. Thus, approaches that suppress myofibroblasts may achieve desirable suppression effects in the fibrotic process. As one of the important physical properties of materials, material topographical structures have been proven to affect various aspects of cell behaviors, so is it possible to manipulate the formation of myofibroblasts by tailoring the topographical properties of medical devices? In this study, polycaprolactone (PCL) surfaces with typical micropatterns (micro column and micro pit) were fabricated. The regulatory effects of surface micropatterns on the myofibroblastic differentiation of fibroblasts were investigated. Compared to the flat surfaces and surfaces with micro pit, surfaces with micro columns triggered the F- to G-actin transition, inhibiting the nuclear transfer of myocardin-related transcription factor-A. Subsequently, the downstream gene α-smooth muscle actin, which is a marker of myofibroblasts, was suppressed. Further in vivo investigation showed that PCL implants with micro-column-patterned surfaces inhibited the formation of peri-implant fibrotic capsules. Our results demonstrate that surface topographical properties are a potent regulator of fibroblast differentiation into myofibroblasts and highlight the antifibrotic potential of modifying surfaces with micro-column patterns.
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spelling pubmed-100760242023-04-06 Modulating Myofibroblastic Differentiation of Fibroblasts through Actin-MRTF Signaling Axis by Micropatterned Surfaces for Suppressed Implant-Induced Fibrosis Han, Weiju Chu, Qi Li, Junliang Dong, Zixuan Shi, Xuetao Fu, Xiaoling Research (Wash D C) Research Article Myofibroblasts, the primary effector cells for implant-induced fibrosis, contribute to this process by secreting excessive collagen-rich matrix and contracting. Thus, approaches that suppress myofibroblasts may achieve desirable suppression effects in the fibrotic process. As one of the important physical properties of materials, material topographical structures have been proven to affect various aspects of cell behaviors, so is it possible to manipulate the formation of myofibroblasts by tailoring the topographical properties of medical devices? In this study, polycaprolactone (PCL) surfaces with typical micropatterns (micro column and micro pit) were fabricated. The regulatory effects of surface micropatterns on the myofibroblastic differentiation of fibroblasts were investigated. Compared to the flat surfaces and surfaces with micro pit, surfaces with micro columns triggered the F- to G-actin transition, inhibiting the nuclear transfer of myocardin-related transcription factor-A. Subsequently, the downstream gene α-smooth muscle actin, which is a marker of myofibroblasts, was suppressed. Further in vivo investigation showed that PCL implants with micro-column-patterned surfaces inhibited the formation of peri-implant fibrotic capsules. Our results demonstrate that surface topographical properties are a potent regulator of fibroblast differentiation into myofibroblasts and highlight the antifibrotic potential of modifying surfaces with micro-column patterns. AAAS 2023-02-21 2023 /pmc/articles/PMC10076024/ /pubmed/37040480 http://dx.doi.org/10.34133/research.0049 Text en Copyright © 2023 Weiju Han et al. https://creativecommons.org/licenses/by/4.0/Exclusive licensee Science and Technology Review Publishing House. No claim to original U.S. Government Works. Distributed under a Creative Commons Attribution License 4.0 (CC BY 4.0) (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Research Article
Han, Weiju
Chu, Qi
Li, Junliang
Dong, Zixuan
Shi, Xuetao
Fu, Xiaoling
Modulating Myofibroblastic Differentiation of Fibroblasts through Actin-MRTF Signaling Axis by Micropatterned Surfaces for Suppressed Implant-Induced Fibrosis
title Modulating Myofibroblastic Differentiation of Fibroblasts through Actin-MRTF Signaling Axis by Micropatterned Surfaces for Suppressed Implant-Induced Fibrosis
title_full Modulating Myofibroblastic Differentiation of Fibroblasts through Actin-MRTF Signaling Axis by Micropatterned Surfaces for Suppressed Implant-Induced Fibrosis
title_fullStr Modulating Myofibroblastic Differentiation of Fibroblasts through Actin-MRTF Signaling Axis by Micropatterned Surfaces for Suppressed Implant-Induced Fibrosis
title_full_unstemmed Modulating Myofibroblastic Differentiation of Fibroblasts through Actin-MRTF Signaling Axis by Micropatterned Surfaces for Suppressed Implant-Induced Fibrosis
title_short Modulating Myofibroblastic Differentiation of Fibroblasts through Actin-MRTF Signaling Axis by Micropatterned Surfaces for Suppressed Implant-Induced Fibrosis
title_sort modulating myofibroblastic differentiation of fibroblasts through actin-mrtf signaling axis by micropatterned surfaces for suppressed implant-induced fibrosis
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10076024/
https://www.ncbi.nlm.nih.gov/pubmed/37040480
http://dx.doi.org/10.34133/research.0049
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