Abstract
During skin healing, periostin facilitates myofibroblast differentiation through a β1 integrin/FAK dependent mechanism and continued expression is associated with scarring. In contrast to skin, gingival tissue does not typically scar upon injury, but the role of periostin in gingival healing has never been investigated. Using a rat gingivectomy model, we show that the gingival architecture is re-established within 14 days of wounding. Periostin mRNA levels peak at day 7 post-wounding, with persistence of periostin protein in the connective tissue through day 14. Collagen type I and lysyl oxidase mRNA levels peak at day 7 post wounding, which corresponded with the peak of fibroblast proliferation. Although α-smooth muscle actin mRNA levels increased 200-fold in the tissue, no myofibroblasts were detected in the regenerating tissue. In vitro, human gingival fibroblast adhesion on periostin, but not collagen, was inhibited by blocking β1 integrins. Fibroblasts cultured on periostin exhibited similar rates of proliferation and myofibroblast differentiation to cells cultured on collagen only. However, human gingival fibroblasts cultured in the presence of periostin exhibited significantly increased fibronectin and collagen mRNA levels. Increases in fibronectin production were attenuated by pharmacological inhibition of FAK and JNK signaling in human gingival fibroblasts. In vivo, mRNA levels for fibronectin peaked at day 3 and 7 post wounding, with protein immunoreactivity highest at day 7, suggesting periostin is a modulator of fibronectin production during gingival healing.
Highlights
Periostin is a non-structural secreted matricellular protein that is highly expressed in collagen-rich tissues[1], with its role in tissue development, repair, and remodeling becoming increasingly determined
Scarring in skin is characterized by the persistence of myofibroblasts, cells expressing α-SMA, which our lab has shown is modulated by periostin through β1 integrin and focal adhesion kinase (FAK) dependent manner[15]
To investigate the gingival healing process temporally, we assessed the regeneration of the gingival connective tissue and oral epithelium in rats at days 1, 3, 7, and 14 post-wounding, with unwounded gingiva serving as a structural baseline control (Fig. 1)
Summary
Periostin is a non-structural secreted matricellular protein that is highly expressed in collagen-rich tissues[1], with its role in tissue development, repair, and remodeling becoming increasingly determined. Successful healing of soft tissues such as skin follows a precise and predictable series of overlapping events encompassing inflammation, proliferation, re-epithelialization, and matrix remodeling[17]. This results in re-establishment of the epithelium and underlying connective tissue restoring barrier function. With the use of knockout mice, periostin has been shown to regulate collagen synthesis[6], myofibroblast differentiation[15], and fibroblast proliferation[22] during healing. Studies have shown that gingival fibroblasts exhibit less of a pro-fibrotic or scarring phenotype in three-dimensional culture; increased synthesis of levels of genes associated with ECM remodeling and inflammation[30]. We conclude that periostin regulates extracellular matrix synthesis during gingival healing
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