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Dissecting the Effects of Cigarette Smoke Components on Delay of Wound Healing
Author(s) -
Wong L.S.,
Sielaff R.L.,
Yuan H.,
Bhattacharya M.,
Zafarani M.,
MartinsGreen M.
Publication year - 2008
Publication title -
wound repair and regeneration
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.847
H-Index - 109
eISSN - 1524-475X
pISSN - 1067-1927
DOI - 10.1111/j.1067-1927.2005.130215p.x
Subject(s) - wound healing , smoke , granulation tissue , myofibroblast , chemistry , cell migration , contraction (grammar) , microbiology and biotechnology , cigarette smoke , in vivo , cell , biophysics , surgery , pathology , medicine , biochemistry , biology , toxicology , fibrosis , organic chemistry
Exposure to cigarette smoke has detrimental effects on the early stages of wound repair but not much is known about the effects of smoke on the development of the healing (granulation) tissue. Cell proliferation, migration, differentiation, and deposition of ECM are critical processes for normal granulation tissue (GT) formation. Here we investigate the effects of MSW (“first‐hand smoke”) and SSW (the main component of “secondhand smoke”) smoke on wound healing in mice that have been smoking for 9 months. We show that both MSW and SSW smoke adversely affect wound contraction and closure. The keratinocytes accumulate at the edge of the wound and the GT is deficient in fibroblasts and ECM. Moreover, by immunolabeling for α‐SMA, we found that the myofibroblasts remained at the edges of the wound rather than penetrating the GT, potentially contributing to the lack of wound contraction. To test the possibility that smoke inhibits cell migration, we plated primary human fibroblasts in between two interstitial collagen gels, treated the cultures with the smoke solutions and found that cell migration into the gels was inhibited. Furthermore, using the collagen gel contraction assay, we showed that cigarette smoke components inhibit gel contraction. To further decipher which components of the smoke contribute to delayed wound closure, we fractionated SSW smoke solutions into polar and nonpolar components using solid phase extraction cartridges. We show that both the polar and nonpolar fractions delay wound closure in vivo and that the nonpolar fraction inhibits cell migration whereas the polar faction increases cell survival. We are currently pursuing these studies by further fractionation of these two phases with the goal of identifying the specific component(s) in each fraction that cause these effects on cell migration and survival. Identification of the components in cigarette smoke that lead to delayed wound healing and eliminating them from cigarettes could help those exposed to secondhand smoke heal faster.