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Acidification induces OGR1/Ca(2+)/calpain signaling in gingival fibroblasts

 Mi Seong Kim  ;  Dong Min Shin  ;  Min Seuk Kim 
 Biochemical and Biophysical Research Communications, Vol.496(2) : 693-699, 2018 
Journal Title
 Biochemical and Biophysical Research Communications 
Issue Date
Calcium/*metabolism ; Calpain/*metabolism ; Cell Line ; Fibroblasts/*cytology/metabolism ; Gingiva/*cytology/metabolism ; Humans ; Hydrogen-Ion Concentration ; Lysosomes/metabolism ; Matrix Metalloproteinase 1/metabolism ; G-Protein-Coupled/*metabolism Receptors ; *Signal Transduction ; Type C Phospholipases/metabolism ; Wound Healing
Gingivitis ; Hydrogen-ion concentration ; Lysosome ; Matrix metalloproteinase 1 ; Phospholipase C ; Wound healing
Gingivitis, the mildest form of periodontitis, is generally considered a consequence of prolonged exposure of the gingiva to periodontal pathogens. On the other hand, several epidemiologic reports have suggested that other etiologic factors such as oral acidification may also increase the susceptibility of the periodontium to destruction. However, the pathologic mechanism underlying the effects of oral acidification on the gingiva is still largely unknown. In this study, we analyzed molecular pathways mediating the influence of the acidic environment on human gingival fibroblasts (HGFs). Acidic extracellular pH caused biphasic increase of intracellular Ca(2+) level ([Ca(2+)]i) through activation of ovarian cancer G protein-coupled receptor 1, phospholipase C, and Ca(2+) release from the endoplasmic reticulum, but not through voltage-gated Ca(2+) channels or extracellular Ca(2+) influx via transient receptor potential cation channel subfamily V member 1. The acidic environment was also transiently cytotoxic for HGFs; however, the activation of pro-apoptotic proteins poly (ADP-ribose) polymerase-1 and BAX was not observed. Furthermore, we found that intracellular matrix metalloproteinase 1 was consistently upregulated in HGFs grown in regular medium, but significantly reduced in the acidic medium, which depended on [Ca(2+)]i increase, lysosomal pH homeostasis, and Ca(2+)-dependent protease calpain. Considering that HGFs, essential for oral wound healing, in the in vitro culture system are placed in wound repair-like conditions, our findings provide important insights into molecular mechanisms underlying HGF functional impairment and chronic damage to the gingiva caused by the acidic intraoral environment.
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2. College of Dentistry (치과대학) > Dept. of Oral Biology (구강생물학교실) > 1. Journal Papers
Yonsei Authors
Shin, Dong Min(신동민) ORCID logo https://orcid.org/0000-0001-6042-0435
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