The relationship between CTGF stimulated collagen accumulation and integrins
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Abstract
Drug induced gingival hyperplasia is a well documented side effect of dilantin, nifedipine, and cyclosporine A. Previous studies showed that CTGF is associated with dilantin-induced gingival hyperplasia. In the N5 cell cultures, domain 3 located on the C-terminal half of CTGF appears to participate in CTGF-stimulated collagen accumulation. The first objective of this study is to confirm the previous results. To extend these results, human gingival fibroblasts from different individuals were tested to establish the generality and consistency of these findings. Since previous data showed that anti-CTGF domain 3 monoclonal antibody blocks the CTGF dependent collagen accumulation, the anti-CTGF C-terminal polyclonal antibody should also inhibit this assay because CTGF domain 3 is located in the C-terminal half. On the other hand, the C-terminal half of CTGF itself should stimulate collagen production in gingival fibroblasts whereas the N-terminal half of CTGF should not. In HCTl 1 human gingival fibroblast cultures, the monoclonal antibody against CTGF domain 3 and the polyclonal antibody against C-terminal half of CTGF did block CTGF-stimulated collagen accumulation. On the other hand, the truncated C-terminal half of CTGF increased collagen deposition compared to the untreated controls (p>0.05). These results showed that C-terminal half, which contains domain 3, of CTGF stimulates collagen deposition in human gingival fibroblasts. In the second part of this study, the anti-integrin antibodies were used to test the relationship between CTGF and integrins because integrins sometimes serve as CTGF receptors. Results indicated that the aV antibody caused cell detachment. On the other hand, [alpha]6 and [beta]1 antibodies blocked CTGF-stimulated collagen deposition. In conclusion, [apha]6 and [beta]1 integrin might work with CTGF domain 3 to induce collagen accumulation.
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Thesis(M.S.D.)--Boston University, Henry M. Goldman School of Dental Medicine, 2003 (Periodontology and Oral Biology).
Includes bibliographical references (leaves 33-41).
Thesis(M.S.D.)--Boston University, Henry M. Goldman School of Dental Medicine, 2003 (Periodontology and Oral Biology).
Includes bibliographical references (leaves 33-41).
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