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    Compressive remodeling alters fluid transport properties of collagen networks - implications for tumor growth

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    © The Author(s) 2019. Open Access. This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
    Date Issued
    2019-11-20
    Publisher Version
    10.1038/s41598-019-50268-z
    Author(s)
    Ferruzzi, Jacopo
    Sun, M.
    Gkousioudi, A.
    Pilvar, A.
    Roblyer, Darren
    Zhang, Yanhang
    Zaman, Muhammad H.
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    Permanent Link
    https://hdl.handle.net/2144/43610
    Version
    Published version
    Citation (published version)
    J. Ferruzzi, M. Sun, A. Gkousioudi, A. Pilvar, D. Roblyer, Y. Zhang, M.H. Zaman. 2019. "Compressive Remodeling Alters Fluid Transport Properties of Collagen Networks - Implications for Tumor Growth.." Sci Rep, Volume 9, Issue 1, pp. 17151 - ?. https://doi.org/10.1038/s41598-019-50268-z
    Abstract
    Biomechanical alterations to the tumor microenvironment include accumulation of solid stresses, extracellular matrix (ECM) stiffening and increased fluid pressure in both interstitial and peri-tumoral spaces. The relationship between interstitial fluid pressurization and ECM remodeling in vascularized tumors is well characterized, while earlier biomechanical changes occurring during avascular tumor growth within the peri-tumoral ECM remain poorly understood. Type I collagen, the primary fibrous ECM constituent, bears load in tension while it buckles under compression. We hypothesized that tumor-generated compressive forces cause collagen remodeling via densification which in turn creates a barrier to convective fluid transport and may play a role in tumor progression and malignancy. To better understand this process, we characterized the structure-function relationship of collagen networks under compression both experimentally and computationally. Here we show that growth of epithelial cancers induces compressive remodeling of the ECM, documented in the literature as a TACS-2 phenotype, which represents a localized densification and tangential alignment of peri-tumoral collagen. Such compressive remodeling is caused by the unique features of collagen network mechanics, such as fiber buckling and cross-link rupture, and reduces the overall hydraulic permeability of the matrix.
    Rights
    © The Author(s) 2019. Open Access. This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
    Collections
    • ENG: Biomedical Engineering: Scholarly Papers [294]
    • ENG: Mechanical Engineering: Scholarly Papers [262]
    • BU Open Access Articles [4751]


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