A new mechanically active adhesive fights muscle atrophy

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Mechanically Active Nitinol-Elastomer-Gel Tissue Adhesive (MAGENTA) Prototype Devices Made with a Nitinol Spring and Elastomer Insulation, Penny Per Scale [Photo courtesy of the Wyss Institute at Harvard University]

Harvard bioengineers have created a mechanically active adhesive that can prevent muscle wasting and support recovery from atrophy.

They call it MAGENTA, an acronym for Mechanically Active Nitinol-Elastomer-Gel Tissue Adhesive. Researchers from the Wyss Institute for Biologically Inspired Engineering at Harvard University and the Harvard John A. Paulson School of Engineering and Applied Science successfully tested MAGENTA in an animal model and published the study of it in materials from nature.

“With MAGENTA, we developed a new integrated multi-component system for muscle mechanical stimulation that can be placed directly into muscle tissue to activate key molecular pathways for growth,” lead author David Mooney, a founding member of the corps, said in a statement. Wyss teacher. Press release. “Although the study first provides [the] proof of concept that externally provided stretch and contraction movements can prevent atrophy in an animal model, we believe the core design of the device can be broadly adapted to various disease settings where atrophy is a significant problem.”

Nitinol does it again

The MAGENTA system uses a spring made of nitinol, a nickel-titanium alloy used in medical devices for its shape memory capacity. When heated, the nitinol spring acts rapidly, controlled by a microprocessor unit programmed with the frequency and duration of the stretch and contraction cycles.

An elastomeric material insulates the nitinol spring of the MAGENTA device, which is attached to muscle tissue with a “strong adhesive.” The device transmits mechanical force deep into the muscle when it aligns with the natural axis of muscle movement.

An illustration that explains the MAGENTA concept, from the device implanted in a future patient to a muscle to which it is attached and where it performs its work of extending and contracting the muscle throughout, to the composition and interface of the multifunctional material.  with muscle tissue.

[Illustration courtesy of the Wyss Institute at Harvard University]

The researchers implanted the device into the major calf muscles of mice without serious signs of tissue damage or inflammation. The device delivered a mechanical stress of around 15%, which the researchers said matched the natural deformation of the exercise.

The researchers then attached the device to the mouse’s paws and cast them for up to two weeks.

“Whereas untreated muscles and muscles treated with the device but not stimulated were significantly wasted during this period, actively stimulated muscles showed reduced muscle wasting,” first author and development fellow of the technology from Wyss, Sungmin Nam. “Our approach could also promote the recovery of muscle mass that had already been lost during a three-week immobilization period and induce activation of major biochemical mechanotransduction pathways known to trigger protein synthesis and muscle growth.

The MAGENTA device with its strong hydrogel adhesive surface (shown on the left) was implanted into the calf muscle of a mouse which, in the atrophy model, was then immobilized for a longer period of time to induce the muscle wasting.  Activating the device by turning on the electricity allows it to contract, generating mechanical stimulation to the underlying muscle, while turning off the electricity allows the device and muscle to relax (top row on the right).  Panels in the lower right show where muscle tissue is displaced as a result of MAGENTA contraction and relaxation with a color change from blue to red indicating displaced areas in muscle tissue.

These images show the MAGENTA device, what it looks like when implanted in the calf muscle of a mouse, and how much displacement the device causes. [Image courtesy of the Wyss Institute at Harvard University]

What’s next for the MAGENTA device?

The researchers also experimented with using light to activate the device, replacing the wires that connect the nitinol spring to the microprocessor. Laser light shone through the skin was able to activate the device, but failed to achieve the same frequencies, and fatty tissue apparently absorbed some of the light.

The researchers said they believe the device’s performance and light sensitivity can be improved.

“The general capabilities of MAGENTA and the fact that its assembly can be easily scaled from millimeters to several centimeters could make it interesting as a centerpiece of future mechanotherapy not only to treat atrophy, but perhaps also to accelerate regeneration in the skin, the heart and others. places that could benefit from this form of mechanotransduction,” Nam said.

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