New clues into causes of scleroderma

sease that we can use to potentially slow down or reverse the process of tissue damage."

One of the most characteristic effects of the disease is the gradual formation of fibrotic tissue, which leaves patients with disfiguring and painful tightening of the skin. Additionally, the disease tends to slowly destroy small blood vessels and capillaries, which are not only present in skin, but also in internal organs, leaving them vulnerable to function failure.

It is known that the excessive fibrosis seen in scleroderma patients is in part the result of an inappropriate activation of transforming growth factor-beta (TGF-beta), a substance called a cytokine that regulates the intensity and duration of the immune response. Too much TGF-beta activity can occur in the presence of destabilized microtubules, which give structural support to cells and are involved in the movement of genetic material during cell division. When microtubules become destabilized, a complex process ensues which leads to the excessive TGF-beta pathway activation, and consequent accumulation of collagen, the primary component of fibrotic tissue.

"We've learned in our previous studies that the treatment of individual cells with paclitaxel helps stabilize microtubules, thereby blocking the excessive activity of TGF-beta," Dong explained. "So in our latest studies, we were interested in determining whether or not paclitaxel would have any effect on tissue with scleroderma."

For their experiments, the Duke team used mice bred to have no immune system. They transplanted skin samples from humans with and without scleroderma onto the backs of these mice. Some of the skin samples were pre-treated for 30 minutes with paclitaxel.

"We found that the skin samples from scleroderma patients that were pre-treated with paclitaxel prior to transplantation significantly suppressed the activity of TGF-beta and lessened the formation of fibrotic tissue," Dong said.

Just as i

Contact: Richard Merritt
Duke University Medical Center

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