Does LOXL2 and JNK MAP kinase activation mediate CCN2CTGF-induced collagen accumulation in gingival fibroblasts?
Date
2014
DOI
Authors
Cabrera, Vianca Elize
Version
OA Version
Citation
Abstract
CCN2/CTGF is a member of the CCN family of matricellular proteins, functioning in
collaboration with other factors and extracellular matrix components. CCN proteins bind
receptors including low-density lipoprotein related proteins and integrins (Heng et al., 2006).
Even after all that has been discovered about CCN2/CTGF over the last two decades, not
everything is known today, for example the mechanism by which CCN2/CTGF stimulates
collagen deposition (Crean et al., 2002).
Gingival fibrosis is defined by accumulation of excess gingival tissue and is characterized
by excess extracellular matrix accumulation and elevated levels of cytokines in the absence of
periodontal bone loss. Drug-induced gingival fibrosis is the adverse effect of three types of
medications: 1) calcium channel blockers, 2) immunosuppressive cyclosporine A, and 3) antiseizure
drugs. After culturing gingival fibroblasts (GFs), evidence revealed notable levels of
CCN2/CTGF up-regulated by TGF-beta1. CCN2/CTGF stimulated collagen deposition but not
collagen synthesis; the collagen mRNA was not increased, suggesting the responsibility of posttranslational
events for deposition. It is also important to state that lysyl oxidase activity is
enhanced by CCN2/CTGF in cultures of GFs (Hong et al., 1999). Another important finding
suggests that CCN2/CTGF effects can be regulated by the MAP kinase pathway, which showed ... [TRUNCATED]
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Thesis (MSD) --Boston University, Henry M. Goldman School of Dental Medicine, 2014 (Department of Molecular and Cell Biology).
Includes bibliography: leaves 60-63.
Thesis (MSD) --Boston University, Henry M. Goldman School of Dental Medicine, 2014 (Department of Molecular and Cell Biology).
Includes bibliography: leaves 60-63.
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This work is protected by copyright. Downloading is restricted to the BU community. If you are the author of this work and would like to make it publicly available, please contact open-help@bu.edu.