Biomedical Materials · uk
Wounds Pull Their Own Switch: Force-Sensing Dressing Accelerates Repair in Mice and Ex Vivo Human Skin
The material first captures growth factors already present in the body, then releases them locally in response to pulling forces from repair cells; early results show faster wound closure, but multiple hurdles remain before it can be used for complex chronic wounds such as diabetic foot wounds.
The signals needed for wound healing are not always in short supply. Sometimes the real challenge is enabling them to act at the right place and time. A team at Imperial College London has designed a material that responds to cellular pulling forces, allowing cells involved in repair to trigger the local release of growth factors themselves. In both mouse skin wounds and ex vivo human skin, the strategy showed early signs of promoting repair.
The technology, published in *Nature Materials*, is called traction-force-activated payloads (TrAPs). Each TrAP consists of a DNA aptamer that can bind a specific growth factor, a tethering end anchored to a scaffold, and a handle for cell adhesion. The aptamer first captures growth factors from cells, injured tissue, or platelet lysate, temporarily restricting their activity. The factors are released nearby only when repair cells attach and exert pulling forces.
The researchers created constructs targeting VEGF-A, HGF, FGF-2, and PDGF-BB, and tested them using primary human cells, animal wounds, and ex vivo tissue. Unlike continuously supplying an externally administered drug across the entire wound, the system seeks to harness molecular resources already present in the tissue and convert mechanical forces generated by cells into delivery signals. As a result, the required growth-factor doses can be several orders of magnitude lower than those used in current clinical delivery methods; however, the two approaches have not yet been directly compared in human trials.
In a small mouse study, a sponge-like material carrying capture components for all four growth factors produced a smaller normalized wound diameter by day 10 than both a TrAP that could not be activated by pulling forces and a standard scaffold control. Experiments with ex vivo human skin also showed improved repair, but the tissue came from only three donors, and the ex vivo model lacked blood circulation, an immune system, and the patients’ overall health conditions, so it cannot be equated with clinical treatment outcomes.
The platform increased blood-vessel formation in a rat femoral injury model but did not produce bone growth, showing that activating a biological signal is not necessarily sufficient to achieve tissue regeneration. For skin wounds, the existing animal experiments also did not use diabetic or infected wounds. These common clinical situations involve inadequate blood flow, persistent inflammation, and microbial burden, making them far more complex than controlled acute wounds.
The next steps, in addition to determining whether the material can be manufactured and stored reliably, include assessing the toxicity, immune responses, and degradation of the DNA aptamers and scaffold, as well as the strength, scarring, and long-term function of the healed skin. The research currently includes no in vivo human data, and some of the inventors are affiliated with Traxion Biotech. It should therefore be regarded as a preclinical materials platform with a novel mechanism, not a smart dressing proven for use in patients.