08 September 2020

They take such people as astronauts

Myostatin Inhibitor helped Mice keep bones and muscles in space

Svetlana Yastrebova, N+1

The loss of bone and muscle mass caused by prolonged exposure to microgravity can be prevented by introducing a myostatin protein inhibitor – a decoy receptor (modification of the activin type II receptor, ACVR2B), according to the Proceedings of the National Academy of Sciences. This was shown by experiments on mice, some of which spent 33 days on the International Space Station, and some spent the same time in a laboratory on Earth. Normally, myostatin limits muscle growth.

Reduced gravity on the ISS and in similar conditions leads to the fact that part of the muscle mass and bone substance is lost, which makes a person weak and his bones become more fragile. Although they try to combat this with physical exercises (astronauts on the ISS devote two hours on average to them almost every day), it is not possible to completely prevent losses.

Probably, pharmacological methods can help in this, namely, the suppression of the myostatin protein. It is known that it suppresses muscle growth: in animals with the "switched off" Mstn gene, muscle mass is significantly greater than in wild-type individuals, while the proportion of adipose tissue is very low. Blocking myostatin is already used in cattle breeding and discussed in bodybuilding (although there are no effective and approved for use by people myostatin blockers yet).

Researchers led by Emily L. Germain-Leeg from the University of Connecticut School of Medicine have tested how the neutralization of myostatin affects changes in bone and muscle mass that occur due to a long stay in microgravity. The experiments were conducted on mice injected with a myostatin blocker – a molecule based on a receptor for myostatin and activin ACVR2B, in which not the real "body" of ACVR2B was attached to the binding sites with these proteins, but a crystallizing fragment of immunoglobulin Fc. Thus, myostatin, binding to the decoy receptor, did not trigger a cascade of reactions in the cell, which it normally should cause.

In addition to such rodents, scientists used mice in which the Mstn gene was knocked out, and wild-type individuals acted as controls.

myostatin.jpg

A mouse with a knockout Mstn gene and a wild-type mouse.

Some of the individuals (40 females) lived on the ISS, and the main experiment with them lasted 33 days. Some of them returned to Earth, the rest were killed. Another 24 females were tested in the laboratory in parallel with them during the same period. In all groups from the ISS, biologists measured the mass of muscles and bones before the onset of microgravity, during and after it.

During 33 days in orbit, wild-type mice lost 8-18 percent of the mass of most large muscles: the triceps of the shoulder, quadriceps of the thigh, calf muscle and others (comparison with the control group). In mice with a non-functioning myostatin gene, muscle mass increased over the same time, but in those who had been in microgravity, muscle growth was weaker.

A similar effect was observed in the case of rodents that received a decoy receptor. In addition, the mice injected with the modified ACVR2B practically did not suffer from bone loss due to the action of microgravity (and their musculoskeletal system recovered faster after returning from the ISS), since this receptor affects metabolism not only in muscles, but also in bones.

It turns out that inhibitors of cascades of reactions triggered in cells by myostatin and activin can theoretically be used to reduce the loss of bone and muscle tissue in microgravity and accelerate the recovery of these tissues after space flight. The authors of the work suggest that the use of "deceptive" ACVR2B and similar molecules is not limited to this. It is necessary to prevent the degradation of muscles and bones not only in astronauts, but also in everyone who has been without movement for a long time (people confined to a wheelchair or bed), as well as in the elderly.

Portal "Eternal youth" http://vechnayamolodost.ru


Found a typo? Select it and press ctrl + enter Print version