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双光弹弹性成像检测 - 诱导的皮肤支架生物力学性质的改变。

Dual optical elastography detects -induced alterations in the biomechanical properties of skin scaffolds.

机构信息

University of Houston, Department of Biomedical Engineering, Houston, Texas, United States.

University of Sydney, Department of Mechanical Engineering, Sydney, New South Wales, Australia.

出版信息

J Biomed Opt. 2024 Sep;29(9):095002. doi: 10.1117/1.JBO.29.9.095002. Epub 2024 Sep 18.

DOI:10.1117/1.JBO.29.9.095002
PMID:39295639
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11409821/
Abstract

SIGNIFICANCE

The skin's mechanical properties are tightly regulated. Various pathologies can affect skin stiffness, and understanding these changes is a focus in tissue engineering. skin scaffolds are a robust platform for evaluating the effects of various genetic and molecular interactions on the skin. Transforming growth factor-beta ( ) is a critical signaling molecule in the skin that can regulate the amount of collagen and elastin in the skin and, consequently, its mechanical properties.

AIM

This study investigates the biomechanical properties of bio-engineered skin scaffolds, focusing on the influence of , a signaling molecule with diverse cellular functions.

APPROACH

The receptor I inhibitor, galunisertib, was employed to assess the mechanical changes resulting from dysregulation of . Skin scaffold samples, grouped into three categories (control, -treated, and + galunisertib-treated), were prepared in two distinct culture media-one with aprotinin (AP) and another without. Two optical elastography techniques, namely wave-based optical coherence elastography (OCE) and Brillouin microscopy, were utilized to quantify the biomechanical properties of the tissues.

RESULTS

Results showed significantly higher wave speed (with AP, ; without AP, ) and Brillouin frequency shift (with AP, ; without AP, ) in -treated group compared with the control group. The difference in wave speed between the control and + galunisertib with ( ) and without AP ( ) was not significant. Moreover, the + galunisertib-treated group exhibited lower wave speed without and with AP and reduced Brillouin frequency shift than the -treated group without AP, further strengthening the potential role of in regulating the mechanical properties of the samples.

CONCLUSIONS

These findings offer valuable insights into -induced biomechanical alterations in bio-engineered skin scaffolds, highlighting the potential of OCE and Brillouin microscopy in the development of targeted therapies in conditions involving abnormal tissue remodeling and fibrosis.

摘要

意义

皮肤的机械性能受到严格调控。各种病理状况会影响皮肤的硬度,了解这些变化是组织工程学的重点。皮肤支架是评估各种遗传和分子相互作用对皮肤影响的强大平台。转化生长因子-β(TGF-β)是皮肤中一种关键的信号分子,可调节皮肤中胶原蛋白和弹性蛋白的含量,从而影响其机械性能。

目的

本研究探讨了生物工程皮肤支架的生物力学特性,重点研究了信号分子 TGF-β的作用,该分子在细胞中有多种功能。

方法

使用 TGF-β受体 I 抑制剂 Galunisertib 评估由于 TGF-β失调导致的皮肤支架机械变化。将皮肤支架样本分为三组(对照组、TGF-β处理组和 TGF-β+Galunisertib 处理组),在两种不同的培养基中制备-一种含有抑肽酶(Aprotinin,AP),另一种不含 AP。采用两种光学弹性技术,即基于波的光学相干弹性成像(OCE)和布里渊显微镜,定量测量组织的生物力学特性。

结果

结果显示,与对照组相比,TGF-β处理组的波速(含 AP 时为 ;不含 AP 时为 )和布里渊频移(含 AP 时为 ;不含 AP 时为 )显著增加。对照组和 TGF-β+Galunisertib 组(含 AP 时为 ;不含 AP 时为 )的波速差异无统计学意义。此外,与不含 AP 的 TGF-β处理组相比,TGF-β+Galunisertib 处理组的波速更低,且不含和含 AP 时的布里渊频移均降低,进一步证实了 TGF-β在调节样本机械性能中的潜在作用。

结论

这些发现为生物工程皮肤支架中 TGF-β诱导的生物力学改变提供了有价值的见解,突显了 OCE 和布里渊显微镜在涉及异常组织重塑和纤维化的靶向治疗开发中的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dc5/11409821/3d8f059d675e/JBO-029-095002-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dc5/11409821/9b51ae0b00c2/JBO-029-095002-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dc5/11409821/48ecef2c0589/JBO-029-095002-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dc5/11409821/9f0e73cd33d8/JBO-029-095002-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dc5/11409821/ea9da3ec13e4/JBO-029-095002-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dc5/11409821/3d8f059d675e/JBO-029-095002-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dc5/11409821/9b51ae0b00c2/JBO-029-095002-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dc5/11409821/48ecef2c0589/JBO-029-095002-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dc5/11409821/9f0e73cd33d8/JBO-029-095002-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dc5/11409821/ea9da3ec13e4/JBO-029-095002-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7dc5/11409821/3d8f059d675e/JBO-029-095002-g005.jpg

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