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Longer‐term in vitro exposure to high glucose levels mimicking diabetes upregulates LPA1 on human gingival (GF) but not periodontal ligament (PDLF) fibroblasts
Author(s) -
Cerutis D. Roselyn,
McLaughlin Matthew,
RochaSanchez Sonia Maria,
McVaney Timothy P.,
Parrish Lawrence C.,
Mattson John S.
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a749-c
Subject(s) - periodontal fiber , receptor , wound healing , microbiology and biotechnology , blot , cell culture , platelet derived growth factor receptor , confocal microscopy , lysophosphatidic acid , in vitro , medicine , endocrinology , biology , chemistry , pathology , immunology , biochemistry , growth factor , dentistry , gene , genetics
Background: Diabetic patients experience problems with wound healing. LPA 1–3 receptors bind lysophosphatidic acid, which plays an important role in regulating wound healing. We have published that these receptors regulate the healing responses of human GF and their responses to PDGF; however, no information is available about the expressed levels of LPA 1–3 or of the PDGF receptors (PDGFR) on these fibroblasts under conditions of exposure to high glucose concentrations. Methods: GF and PDLF were seeded onto tissue culture plates in complete media and allowed to grow to confluence. The media was then changed to complete media containing glucose to a final concentration of 10 mg/ml, and the media changed every 3 days. Cells were harvested for analysis by western blotting (WB) on days 3, 6, and 9. Cell lysates were run on SDS‐PAGE and subjected to WB for levels of LPA 1–3 and PDGFR‐β. LPA 1–3 localization was also examined by confocal microscopy. Results: This treatment did not produce significant changes for any of either class of receptors on PDLF. PDGFR‐β levels were also unchanged for GF; however, a 2.5‐fold increase in LPA 1 was found on day 9. LPA 1 was also found associated with the nucleus. Conclusions: LPA 1 has been implicated in controlling LPA‐dependent cell migration, and in regulating inflammatory gene expression. Thus, the up‐regulation and perinuclear/nuclear localization seen for this receptor may represent a compensatory action by the cells and/or may potentially contribute to dysregulation of the wound‐healing response seen in diabetics. Support: Nebraska Society for Periodontology Summer Student Fellowship (M.M) #211293‐732100‐110 and 1 R15 DE016855 ‐01 (D.R.C).