NDLI: Smad3 deficiency alters key structural elements of the extracellular matrix and mechanotransduction of wound closure

Content Provider	PubMed Central
Author	Arany, Praveen R. Flanders, Kathleen C. Kobayashi, Tetsu Kuo, Catherine K. Christina, Stuelten Desai, Kartiki V. Tuan, Rocky Rennard, Stephen I. Roberts, Anita B.
Copyright Year	2006
Abstract	The loss of TGFβ or its downstream mediator, Smad3, key players in tissue repair, accelerates closure of incisional wounds in mice. In contrast, we now report that excisional ear wounds in mice lacking Smad3 enlarge compared with wild-type controls resulting from changes in extracellular matrix molecules, which alter the mechanotransduction properties of these wounds. Specifically, levels of elastin and glycosoaminoglycans are increased, collagen fibers are more compactly organized, and matrix modulators like integrins, TGFβ1, and matrix metalloproteinases (MMPs) are altered both basally and after wounding in Smad3 knockout mice. Mechanical testing of dorsal skin correlates these changes in matrix composition with functional parameters, specifically an increased elastic modulus, suggesting an imbalance of tissue forces. We propose that the altered mechanical elastic properties translate into a persistent retractile force that is opposed by decreased wound contractile forces contributing to the enlarging ear wound in Smad3 knockout mice. These studies highlight a previously undescribed role for Smad3 in the mechanotransduction of matrix unsupported ear wound closure.
Related Links	http://dx.doi.org/10.1073/pnas.0602473103
Ending Page	9255
Page Count	6
Starting Page	9250
File Format	PDF
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	24
Volume Number	103
Language	English
Publisher	National Academy of Sciences
Publisher Date	2006-06-13
Access Restriction	Open
Rights Holder	National Academy of Sciences
Subject Keyword	General Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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