29 April 2015

FOXO1 is the culprit of diabetic ulcers

Biologists have found out why wounds heal slowly in diabetics

RIA News

Cuts heal very slowly in diabetics due to the fact that the protein "conducting" the process of wound tightening "goes crazy" with an abnormally high concentration of glucose in the blood and begins to interfere with their healing, according to an article published in the Journal of Cell Biology (Zhang et al., FOXO1 differently regulates both normal and diabetic wound healing; briefly, Sugar saps FOXO1's healing power, the results of the work were retold by Mitch Leslie in the same issue of the magazine – VM).

The slightest skin damage in people suffering from diabetes can cause great trouble for them. Due to the fact that their wounds are extremely slow to heal, bacteria often get into them and non-healing ulcers occur, which often force doctors to amputate the affected limbs or perform life-threatening operations.

In recent years, scientists have been actively working on the creation of drugs that would stimulate the growth of skin tissues and help the body to tighten the wound. For example, in February last year, Swiss biochemists presented a drug based on a synthetic analogue of the hormone PIGF-2, which was able to make the wound on the body of a diabetic mouse heal in five days. However, the reasons for the slow regeneration of the skin in diabetics remained unknown.

Dana Graves from the University of Pennsylvania in Philadelphia (USA) and her colleagues discovered the mechanism of this problem by experimenting with mice that had damaged the FOXO1 gene responsible for the synthesis of a hormone that "conducts" the wound healing process.

Damage to this gene in the body of healthy mice leads to what scientists expected – the wounds began to slowly heal and ulcers began to appear on their body. When the authors of the article did the same with diabetic rodents, the effect was, very unexpectedly for them, completely the opposite - the problems with healing disappeared and the wounds began to heal.

Surprised scientists decided to find out what this was due to by following the work of FOXO1 molecules in keratinocytes – cells that make up most of the skin surface – in the body of healthy mice and diabetic rodents.

As it turned out, the reason for the unusual behavior of this hormone was glucose – its increased concentration in the blood and body of diabetics causes FOXO1 to connect not with the growth hormone TGF-alpha, but with the proteins CCL20 and SERPINB2, which inhibit the regeneration process. As a result, the healing process is not accelerated, but is inhibited in the body of diabetics.

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