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Growth factor modulation of mitogenic responses and proteoglycan synthesis by human periodontal fibroblasts
Author(s) -
Haase Helen R.,
Clarkson Richard W.,
Waters Michael J.,
Bartold P. Mark
Publication year - 1998
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/(sici)1097-4652(199803)174:3<353::aid-jcp9>3.0.co;2-n
Subject(s) - proteoglycan , microbiology and biotechnology , growth factor , modulation (music) , chemistry , cancer research , biology , biochemistry , extracellular matrix , receptor , philosophy , aesthetics
Abstract In order to understand the relationship between specific growth factors and matrix synthesis by periodontal cells, we have investigated the effects of platelet‐derived growth factor BB (PDGF‐BB), insulin‐like growth factor‐I (IGF‐1), and growth hormone on DNA and proteoglycan synthesis by cultured human gingival and periodontal ligament fibroblasts in vitro. PDGF‐BB and IGF‐1, but not growth hormone, were mitogenic for both periodontal ligament fibroblasts and gingival fibroblasts, although the periodontal ligament cells responded more strongly. The mitogenic response was accompanied by alterations in expression of matrix proteoglycan mRNA. For both the gingival and periodontal ligament cells, there was a decrease in mRNA for decorin and an increase in mRNA for versican following exposure to IGF‐1 and PDGF‐BB. Although no change was seen in response to PDGF, biglycan mRNA level was increased by IGF‐1 in periodontal ligament fibroblasts. With the gingival fibroblats, biglycan mRNA levels were unaffected by IGF‐1, PDGF‐BB, or growth hormone. These findings suggest variable responses of fibroblasts to growth factors depending upon anatomical site within the periodontium. Moreover, there appears to be a correlation between cell proliferation and the types of proteoglycan synthesised with decorin expression being suppressed, and versican being increased during fibroblast proliferation. J. Cell. Physiol. 174:353–361, 1998. © 1998 Wiley‐Liss, Inc.

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