Studies of chain substitution caused sub-fibril level differences in stiffness and ultrastructure of wildtype and oim/oim collagen fibers using multifrequency-AFM and molecular modeling
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Author(s)
Li, Tao
Rodriguez-Florez, Naiara
Shefelbine, Sandra
Zeng, Kaiyang
Chang, Shu-Wei
Buehler, Markus J
Dao, Ming
Date Issued
August 2016
Journal
Biomaterials
Publisher
Elsevier BV
Citation
Li, Tao et al. “Studies of Chain Substitution Caused Sub-Fibril Level Differences in Stiffness and Ultrastructure of Wildtype and Oim/oim Collagen Fibers Using Multifrequency-AFM and Molecular Modeling.” Biomaterials 107 (November 2016): 15–22 © 2016 Elsevier Ltd
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Author's final manuscript
Abstract
Molecular alteration in type I collagen, i.e., substituting the α2 chain with α1 chain in tropocollagen molecule, can cause osteogenesis imperfecta (OI), a brittle bone disease, which can be represented by a mouse model (oim/oim). In this work, we use dual-frequency Atomic Force Microscopy (AFM) and incorporated with molecular modeling to quantify the ultrastructure and stiffness of the individual native collagen fibers from wildtype (+/+) and oim/oim diseased mice humeri. Our work presents direct experimental evidences that the +/+ fibers have highly organized and compact ultrastructure and corresponding ordered stiffness distribution. In contrast, oim/oim fibers have ordered but loosely packed ultrastructure with uncorrelated stiffness distribution, as well as local defects. The molecular model also demonstrates the structural and molecular packing differences between +/+ and oim/oim collagens. The molecular mutation significantly altered sub-fibril structure and mechanical property of collagen fibers. This study can give the new insight for the mechanisms and treatment of the brittle bone disease.
MIT Department
Massachusetts Institute of Technology. Department of Civil and Environmental Engineering
Massachusetts Institute of Technology. Department of Materials Science and Engineering
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DOI of Published Version
https://doi.org/10.1016/J.BIOMATERIALS.2016.08.038
