When it comes to aging skin, anti-aging creams promise miracles. But to date, the mechanism behind this inevitable process is not clear. Researchers at the University of California, San Diego have shed some light on the matter.
As we age, so does our skin. The process can be slowed by a healthy lifestyle. But it is still inevitable. And researchers at the University of California, San Diego are now revealing a little more about the underlying cellular mechanism.
To understand it, we need to know that certain fibroblasts found in our dermis have the ability to become fat cells. This is how they give our skin its plump, youthful appearance. At the same time, they produce a peptide that plays an essential role in fighting infections. “We have discovered that as we age, the skin loses its ability to produce fat,” says Richard Gallo, professor of dermatology.
Fighting infections better
The designated culprit: transforming growth factor beta (TGF-β). In the bats, the researchers chemically inhibited the production of this protein, and the fibroblasts began to be converted back into fat. The same was done in mice after the production of TGF-β was genetically switched off.
The researchers hope that their findings will help the skin fight infections like Staphylococcus aureus. Staphylococcus aureus is the leading cause of heart and skin infections and a contributing factor to eczema. And when it becomes resistant to antibiotics, it is one of the leading causes of death from infections.
The recognized regulator of skin aging
The skin ages, like all other organs. In fact, this natural process is under the control of a molecule called CD98hc, which contributes to the regeneration and healing of the epidermis.
The epidermis, the upper layer of the skin, is composed mainly of cells called keratinocytes, which in humans are constantly renewed in a 21-day cycle. These cells rest on a membrane composed of components of the extracellular matrix, which provides the connection to the dermis, the deep layer of the skin.
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The renewal of the epidermis is ensured by cell proliferation and differentiation, which maintains the balance of the adult tissue. The alteration of this balance (homeostasis), which is essential for the proper functioning of the tissues is responsible for the physical changes associated with aging.
CD98hc, a key molecule for skin balance
A team led by Chloé Féral, a researcher at Inserm, has studied the many cellular factors involved in maintaining this balance, in particular CD98hc, a molecule known for its interaction with receptors involved in skin aging. With age, the activity of the CD98hc transporter and integrins, these receptors linked to the components of the extracellular matrix, are affected. However, the mechanisms involved have not yet been fully understood.
With this work published in The Journal of Experimental Medicine, the researchers demonstrated in vivo in mice that the elimination of the Cd98hc gene (which encodes the CD98hc transporter) alters the balance of the skin and the healing process. By altering cell proliferation and migration, the removal of this gene also leads to a defect in the hair follicle cycle.
Skin regeneration under the control of CD98hc
The researchers deciphered all the complex mechanisms associated with CD98hc, in particular the deregulation of integrins triggered by the absence of this molecule in vivo. In particular, they confirmed what had already been described in vitro: the amino acid transporter CD98hc modulates integrin signaling, which is essential for skin renewal. In this way, CD98hc actively participates in skin renewal through effective and massive recruitment of epidermal cells when they are needed (e.g. in wound healing).
“Cd98hc seems to be necessary for a fast and efficient epidermal renewal. The decrease in its expression observed in vivo in older mice confirms its role in tissue maintenance, the hair follicle cycle, and healing, which are interrupted with age,” says Chloé Féral. The state of the CD98hc carrier in vivo could be an indicator of the skin’s ability to regenerate.