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Effects of substance P on osteoblastic differentiation and heme oxygenase‐1 in human periodontal ligament cells
Author(s) -
Kook YoonAh,
Lee SunKyung,
Son DaeHyung,
Kim Youngho,
Kang KyungHwa,
Cho JinHyung,
Kim SangCheol,
Kim YoungSuk,
Lee HwaJeong,
Lee SukKeun,
Kim EunCheol
Publication year - 2009
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1016/j.cellbi.2008.12.007
Subject(s) - bone sialoprotein , osteopontin , osteonectin , osteocalcin , chemistry , runx2 , heme oxygenase , microbiology and biotechnology , osteoprotegerin , cellular differentiation , bone resorption , osteoclast , p38 mitogen activated protein kinases , downregulation and upregulation , periodontal ligament stem cells , periodontal fiber , blot , osteoblast , alkaline phosphatase , mapk/erk pathway , endocrinology , heme , signal transduction , biology , biochemistry , activator (genetics) , receptor , enzyme , medicine , in vitro , gene , dentistry
Although substance P (SP) is associated with osteoclast differentiation and bone resorption, little is known about the osteogenic differentiation‐inducing effects of SP in periodontal ligament (PDL) cells. This study investigated whether PDL cells could differentiate into osteoblastic‐like cells by SP. The expression of osteoblastic differentiation markers such as osteopontin (OPN), osteonectin (ON), osteocalcin (OCN) and bone sialoprotein (BSP) were evaulated by Western blotting. Additionally, SP‐mediated heme oxygenase‐1 (HO‐1) pathways were further clarified. SP increased HO‐1 and osteogenic differentiation in concentration‐ and time‐dependent manners, as determined by OPN, ON, OCN and BSP expression. Furthermore, treatment with inhibitors of p38, ERK MAPK, and NF‐κB abolished SP‐induced osteogenic differentiation and HO‐1 expression. SP‐induced translocation of Nrf‐2 was also observed. The combined results suggest that SP activates the stress‐response enzymes HO‐1 and Nrf‐2, subsequently leading to upregulation of osteogenic differentiation in human PDL cells.