Cigarette smoke condensate inhibits collagen gel contraction and prostaglandin E2 production in human gingival fibroblasts. (29th July 2014)

• Record Type: Journal Article
• Authors: Romero, A.; Cáceres, M.; Arancibia, R.; Silva, D.; Couve, E.; Martínez, C.; Martínez, J.; Smith, P. C.
• Is Part Of: Journal of periodontal research. Volume 50:Number 3(2015:Jun.)
• Page Start: 371
• Page End: 379
• Publication Date: 2014-07-29
• Subjects: collagen -- fibroblast -- prostaglandin -- smoking; Periodontics -- Periodicals; 617.632
• DOI: 10.1111/jre.12216
• Languages: English
• ISSNs: 0022-3484

Abstract

Abstract : Background: Granulation tissue remodeling and myofibroblastic differentiation are critically important events during wound healing. Tobacco smoking has a detrimental effect in gingival tissue repair. However, studies evaluating the effects of cigarette smoke on these events are lacking. Material and Methods: We used gingival fibroblasts cultured within free‐floating and restrained collagen gels to simulate the initial and final steps of the granulation tissue phase during tissue repair. Collagen gel contraction was stimulated with serum or transforming growth factor‐β1. Cigarette smoke condensate (CSC) was used to evaluate the effects of tobacco smoke on gel contraction. Protein levels of alpha‐smooth muscle actin, β1 integrin, matrix metalloproteinase‐3 and connective tissue growth factor were evaluated through Western blot. Prostaglandin E2 (PGE2 ) levels were determined through ELISA. Actin organization was evaluated through confocal microscopy. Results: CSC reduced collagen gel contraction induced by serum and transforming growth factor‐β1 in restrained collagen gels. CSC also altered the development of actin stress fibers in fibroblasts cultured within restrained collagen gels. PGE2 levels were strongly diminished by CSC in three‐dimensional cell cultures. However, other proteins involved in granulation tissue remodeling and myofibroblastic differentiation such as alpha‐smooth muscle actin, β1 integrin, matrix metalloproteinase‐3 and connective tissue growth factor, were unmodified by CSC. Conclusions: CSC may alter the capacity of gingival fibroblasts to remodel and contract a collagen matrix. Inhibition of PGE2 production and alterations of actin stress fibers in these cells may impair proper tissue maturation during wound healing in smokers.