RIVERSIDE, Calif. – Cigarette smoke, whether first- or second-hand, complicates the careful cellular choreography of wound healing, according to a paper by University of California, Riverside researchers that was included in the 2004 Press Book of the 44th Annual Meeting of the American Society For Cell Biology (ASCB).
Cigarette smoke delays the formation of healing tissue and sets the stage for increased scarring at the edges of a wound according to the paper titled Smoke Gets In Your Wounds, one of 15 from a field of more than 1,200 submissions to the ASCB Annual Meeting Press Book.
UCR Professor of Cell Biology and Neuroscience Manuela Martins-Green will present her findings Sunday, Dec. 5, at the annual meeting, which is scheduled to begin Saturday, Dec. 4, in Washington D.C. and will run through Wednesday, Dec. 8.
The press book is the ASCB’s major effort to open cell biology research to a wider audience by helping science journalists discover the meeting’s most exciting and significant new work, according to an association statement.
Martins-Green, and student Lina Wong are part of a team of researchers who have published several papers on the subject. Similar findings were announced in the journals BMC Cell Biology in April and Wound Repair and Regeneration in August. Those papers also examined the role of fibroblasts, the cells that play a major role in wound healing.
Wound healing is a highly choreographed, biological drama of clotting, inflammation, cell proliferation and tissue remodeling. It features an exotic cast of clotting and growth factors, specialized cells and structural proteins, each of which must time their entrance and exit perfectly. Nothing messes up this timing like cigarette smoke. Clinical studies have consistently shown that individuals exposed to cigarette smoke – whether “first-” or “second-hand”– heal poorly and are more likely to develop scarring and associated diseases.
The negative effects of smoking on cells during the inflammatory phase of tissue repair are well documented. However the effects of cigarette smoke on the phase in which fibroblasts proliferate and migrate to create healing tissue, are less understood.
Using doses of cigarette smoke equivalent to “first-hand” and “second-hand” exposure in humans, Martins-Green and her colleagues focused on the structure and function of fibroblasts, both in mice and in human tissue culture.
Fibroblasts secrete many proteins that compose a matrix of connective tissue outside of the cells and are critical in orchestrating tissue repair and remodeling. Surprisingly, smoke, at levels found in tissues of smokers, did not kill the fibroblasts, but instead injured them in a way that allowed them to turn on certain genes that improved their survival. However, it was cell survival at the wrong time and in the wrong place, in terms of properly forming healing tissue.
During normal development of wound healing tissue, the fibroblasts at the site of the wound produce proteins that form a matrix into which fibroblasts and endothelial cells (which form linings of, among other things, blood and lymph vessels and the heart) migrate from outside the wounded tissue. These cells then knit the healing tissue together.
While smoke stimulates these cells to stay alive, it impairs their ability to move, causing them to bunch up at the margin of the wound, which promotes scarring. Both the mouse studies and human cell culture models of wound healing gave the same results, according to Martins-Green.
“Taken together, our results suggest that tobacco smoke may delay wound repair because of the inability of the fibroblasts to migrate into the wounded area, leading to an accumulation of these cells at the edge of the wound, thus preventing the formation of the healing tissue,” she said.
Martins-Green added that: “We’re now trying to isolate the component or components in smoke that inhibit cell migration.”
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