Tissue-Engineering Principals

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Science  03 Jul 2009:
Vol. 325, Issue 5936, pp. 13
DOI: 10.1126/science.325_13c
CREDIT: KILARSKI ET AL., NAT. MED. 15, 657 (2009)

If Robert Moses, the driving force behind the construction of the congested artery known as the Brooklyn-Queens Expressway, were alive today, he would marvel at the cellular engineers who relocate still-functioning blood vessels from nearby healthy tissue into healing wounds. After an injury, force-generating cells have previously been shown to reinforce the initial fibrin-based matrix and to latch onto and contract subsequently deposited extracellular matrix (ECM) components. Kilarski et al. show that myofibroblasts, in response to tensile stress and soluble growth factors, pull intact blood vessels with them as highly perfused granulation tissue (the reddish patch in a healing wound) migrates into the injured area [represented by a fibrin-collagen gel in an in vitro system or by a sutured cornea in an in vivo preparation (above)]. The mediating mechanisms are not yet precisely defined, but Legant et al. describe their microfabricated tissue gauge (or µTUG) and use it to quantitate the interplay between matrix mechanics and fibroblasts during remodeling of collagen mesh. Increasing matrix stiffness, both in vitro and in a computational model, elicited higher cellular contractility (which is roughly 20 nN per cell), whereas increasing mechanical stress evoked higher levels of expression of cytoskeletal and ECM proteins.

Nat. Med. 15, 657 (2009); Proc. Natl. Acad. Sci. U.S.A. 106, 10097 (2009).

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