Scientist discovers why skin turns leathery

Apr 21 2004

“The reason our skin becomes more leathery and thick as we age might be due to a loss of elasticity in the cells,” says Igor Sokolov of Clarkson University, who presented his latest research findings during a session on bio-imaging techniques at the Annual American Physical Society (APS) March meeting in Montreal.

Researchers hope Sokolov’s discovery can provide a new direction for research into treatment of age-related diseases that involve loss of elasticity in epithelial tissues.

Scientists have known for a long time that human epithelial tissues lose elasticity with aging. It has been implicated in the pathogenesis of many progressive diseases of aging, including hardening of the arteries, joint stiffness, cataracts, Alzheimer’s and dementia. However, previous researchers believed the reason for the loss was only the “glue” that seals the epithelial tissues, so called extra cellular proteins, rather than the cells themselves. Many treatments of diseases caused by cell elasticity loss have been based on this assumption.

But now, Igor Sokolov of Clarkson University and his colleagues, Craig Woodworth and Tamara Berdyyeva, have found that individual epithelial cells themselves become more rigid with age. By developing a new atomic force microscopy (AFM) method for studying cells, they found that the Young’s modulus, a measure of the epithelial cells’ rigidity, is two-to-ten times higher in old (close to senescence) age than in young cells. This helps to explain why skin often looks and feels more leathery as we age. The research also allows scientists to look at the problem of elasticity loss from new positions.

Sokolov is using AFM to study individual human epithelial cells. Those cells are found in skin, as well as other tissues that line the surfaces of the body, including blood vessels, kidneys, liver, the brain, eyes, etc.

To study the effect of aging and elasticity, Sokolov and his colleagues used fast aging in in-vitro epithelial cells under physiological conditions, and then probed the elasticity of those cells. “However, a typical rigid AFM probe is too sharp to measure the cells quickly while they are alive, and to get reliable statistical data,” says Sokolov. So he added a five-micron silica ball to the AFM tip. “This ball presses slowly against the cell being studied, while the AFM detects the deformation caused by the applied pressure. The less deformation is detected, the more rigid cell we observe,” he explained.

Can we discover what causes this loss of elasticity? Sokolov hypothesized that the secret lays in the cell cytoskeleton, the most rigid part of the cell, and imaged it using AFM. Sokolov says, “We developed a nice, simple way to image cellular cytoskeleton with the AFM. Typically, this is difficult to do because the cytoskeleton is hidden inside the cell and the AFM can image only the surface.”

Sokolov and his colleagues found a way to expose the cytoskeleton to the surface by removing and washing out the entire cell content, apart from the cytoskeleton. After doing that, the scientists discovered that the increase of rigidity in the older cells strongly correlates with the amount of cytoskeleton surface fibers per unit area (surface density). “It is worth noting,” Sokolov added. “No other method allows us to obtain this kind of information.”

Sokolov is an assistant physics and chemistry professor at Clarkson University and a member of the University’s Center for Advanced Materials Processing (CAMP). His research was partially funded by a grant from the New York State Office of Science, Technology and Academic Research (NYSTAR).