Send to

Choose Destination
Adv Sci (Weinh). 2019 Mar 14;6(9):1801780. doi: 10.1002/advs.201801780. eCollection 2019 May 3.

Collagen Fibrils Mechanically Contribute to Tissue Contraction in an In Vitro Wound Healing Scenario.

Author information

Julius Wolff Institute Charité-Universitätsmedizin Berlin 13353 Berlin Germany.
Berlin-Brandenburg School for Regenerative Therapies Charité-Universitätsmedizin Berlin 13353 Berlin Germany.
Berlin-Brandenburg Center for Regenerative Therapies Charité-Universitätsmedizin Berlin 13353 Berlin Germany.
Center for Musculo-Skeletal Surgery Charité-Universitätsmedizin Berlin 13353 Berlin Germany.


Wound contraction is an ancient survival mechanism of vertebrates that results from tensile forces supporting wound closure. So far, tissue tension was attributed to cellular forces produced by tissue-resident (myo-)fibroblasts alone. However, difficulties in explaining pathological deviations from a successful healing path motivate the exploration of additional modulatory factors. Here, it is shown in a biomaterial-based in vitro wound healing model that the storage of tensile forces in the extracellular matrix has a significant, so-far neglected contribution to macroscopic tissue tension. In situ monitoring of tissue forces together with second harmonic imaging reveal that the appearance of collagen fibrils correlates with tissue contraction, indicating a mechanical contribution of tensioned collagen fibrils in the contraction process. As the re-establishment of tissue tension is key to successful wound healing, the findings are expected to advance the understanding of tissue healing but also underlying principles of misregulation and impaired functionality in scars and tissue contractures.


cell force; collagen; extracellular matrix; second harmonic imaging; tension; tissue regeneration; traction force microscopy; wound contraction

Conflict of interest statement

The authors declare no conflict of interest.

Supplemental Content

Full text links

Icon for PubMed Central
Loading ...
Support Center