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dc.contributor.authorBatista, Michael A.
dc.contributor.authorCox, Karen A.
dc.contributor.authorOrtiz, Christine
dc.contributor.authorGrodzinsky, Alan J.
dc.contributor.authorHan, Lin
dc.contributor.authorTavakoli Nia, Hadi
dc.contributor.authorOnnerfjord, Patrik
dc.contributor.authorHeinegard, Dick
dc.date.accessioned2014-08-22T15:25:42Z
dc.date.available2014-08-22T15:25:42Z
dc.date.issued2014-06
dc.date.submitted2014-05
dc.identifier.issn0945053X
dc.identifier.urihttp://hdl.handle.net/1721.1/88975
dc.description.abstractChondroadherin (CHAD), a class IV small leucine rich proteoglycan/protein (SLRP), was hypothesized to play important roles in regulating chondrocyte signaling and cartilage homeostasis. However, its roles in cartilage development and function are not well understood, and no major osteoarthritis-like phenotype was found in the murine model with CHAD genetically deleted (CHAD[superscript −/−]). In this study, we used atomic force microscopy (AFM)-based nanoindentation to quantify the effects of CHAD deletion on changes in the biomechanical function of murine cartilage. In comparison to wild-type (WT) mice, CHAD-deletion resulted in a significant ≈ 70–80% reduction in the indentation modulus, E[subscript ind], of the superficial zone knee cartilage of 11 weeks, 4 months and 1 year old animals. This mechanical phenotype correlates well with observed increases in the heterogeneity collagen fibril diameters in the surface zone. The results suggest that CHAD mainly plays a major role in regulating the formation of the collagen fibrillar network during the early skeletal development. In contrast, CHAD-deletion had no appreciable effects on the indentation mechanics of middle/deep zone cartilage, likely due to the dominating role of aggrecan in the middle/deep zone. The presence of significant rate dependence of the indentation stiffness in both WT and CHAD[superscript −/−] knee cartilage suggested the importance of both fluid flow induced poroelasticity and intrinsic viscoelasticity in murine cartilage biomechanical properties. Furthermore, the marked differences in the nanomechanical behavior of WT versus CHAD[superscript −/−] cartilage contrasted sharply with the relative absence of overt differences in histological appearance. These observations highlight the sensitivity of nanomechanical tools in evaluating structural and mechanical phenotypes in transgenic mice.en_US
dc.description.sponsorshipNational Science Foundation (U.S.) (Grant CMMI-0758651)en_US
dc.description.sponsorshipNational Institutes of Health (U.S.) (Grant AR60331)en_US
dc.description.sponsorshipUnited States. Dept. of Defense. Assistant Secretary of Defense for Research & Engineering (National Security Science and Engineering Faculty Fellowship Grant N00244-09-1-0064)en_US
dc.description.sponsorshipShriners Hospital for Childrenen_US
dc.language.isoen_US
dc.publisherElsevieren_US
dc.relation.isversionofhttp://dx.doi.org/10.1016/j.matbio.2014.05.008en_US
dc.rightsCreative Commons Attribution-NonCommercial-No Derivative Works 3.0en_US
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/en_US
dc.sourceElsevier Open Accessen_US
dc.titleNanomechanical phenotype of chondroadherin-null murine articular cartilageen_US
dc.typeArticleen_US
dc.identifier.citationBatista, Michael A., Hadi T. Nia, Patrik Onnerfjord, Karen A. Cox, Christine Ortiz, Alan J. Grodzinsky, Dick Heinegard, and Lin Han. “Nanomechanical Phenotype of Chondroadherin-Null Murine Articular Cartilage.” Matrix Biology (June 2014).en_US
dc.contributor.departmentMassachusetts Institute of Technology. Department of Biological Engineeringen_US
dc.contributor.departmentMassachusetts Institute of Technology. Department of Electrical Engineering and Computer Scienceen_US
dc.contributor.departmentMassachusetts Institute of Technology. Department of Materials Science and Engineeringen_US
dc.contributor.departmentMassachusetts Institute of Technology. Department of Mechanical Engineeringen_US
dc.contributor.mitauthorBatista, Michael A.en_US
dc.contributor.mitauthorTavakoli Nia, Hadien_US
dc.contributor.mitauthorOrtiz, Christineen_US
dc.contributor.mitauthorGrodzinsky, Alan J.en_US
dc.contributor.mitauthorHan, Linen_US
dc.relation.journalMatrix Biologyen_US
dc.eprint.versionFinal published versionen_US
dc.type.urihttp://purl.org/eprint/type/JournalArticleen_US
eprint.statushttp://purl.org/eprint/status/PeerRevieweden_US
dspace.orderedauthorsBatista, Michael A.; Nia, Hadi T.; Onnerfjord, Patrik; Cox, Karen A.; Ortiz, Christine; Grodzinsky, Alan J.; Heinegard, Dick; Han, Linen_US
dc.identifier.orcidhttps://orcid.org/0000-0003-3511-5679
dc.identifier.orcidhttps://orcid.org/0000-0003-1970-9901
dc.identifier.orcidhttps://orcid.org/0000-0002-4942-3456
mit.licensePUBLISHER_CCen_US


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