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Periostin increases migration and proliferation of human periodontal ligament fibroblasts challenged by tumor necrosis factor ‐α and Porphyromonas gingivalis lipopolysaccharides
Author(s) -
PadialMolina M.,
Volk S. L.,
Rios H. F.
Publication year - 2014
Publication title -
journal of periodontal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 83
eISSN - 1600-0765
pISSN - 0022-3484
DOI - 10.1111/jre.12120
Subject(s) - periostin , porphyromonas gingivalis , protein kinase b , periodontal fiber , proinflammatory cytokine , pi3k/akt/mtor pathway , cancer research , chemistry , tumor necrosis factor alpha , cell migration , microbiology and biotechnology , cell growth , immunology , signal transduction , biology , cell , medicine , periodontitis , extracellular matrix , inflammation , dentistry , biochemistry
Background In the chronic established periodontal lesion, the proliferation and migration potential of periodontal ligament ( PDL ) cells are significantly compromised. Thus, the progressive loss of tissue integrity is favored and normal healing and regeneration compromised. Periostin, a known PDL marker, modulates cell–matrix interactions, cell behavior, as well as the matrix biomechanics and PDL homeostasis. Objective To evaluate whether periostin restores the regenerative potential of PDL cells in terms of proliferation, migration, and activation of survival signaling pathways after being challenged by Porphyromonas gingivalis lipopolysaccharides and tumor n ecrosis f actor a lpha α. Methods Human PDL (hPDL) cells were cultured under different conditions: control, periostin (50 or 100 ng/mL), and fibroblast growth factor 2 (10 ng/mL) to evaluate cell proliferation (by Ki67), cell migration (by scratch assays) and PI3K/AKT/mTOR pathway activation (by western blot analyses of total AKT, phospho‐AKT and PS6). A different set of cultures was challenged by adding tumor necrosis factor alpha α (10 ng/mL) and P. gingivalis lipopolysaccharides (200 ng/mL) to evaluate the effects of periostin as described above. Results Periostin significantly increased cell proliferation (twofold), migration (especially at earlier time points and low dose) and activation of survival signaling pathway (higher phosphorylation of AKT and PS 6). Furthermore, periostin promoted similar cellular effects even after being challenged with proinflammatory cytokines and bacterial virulence factors. Conclusion Periostin acts as an important modulator of hPDL cell–matrix dynamics. It modulates h PDL proliferation, migration and PI 3 K / AKT /m TOR pathway. It also helps in overcoming the altered biological phenotype that chronic exposure to periodontal pathogens and proinflammatory cytokines produce in h PDL cells.
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