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Differential gene expression of collagen‐binding small leucine‐rich proteoglycans and lysyl hydroxylases, during mineralization by MC3T3‐E1 cells cultured on titanium implant material
Author(s) -
Takashi Matsuura,
Tsubaki Satoshi,
Tsuzuki Takashi,
Duarte Wagner R.,
Yamauchi Mitsuo,
Sato Hironobu
Publication year - 2005
Publication title -
european journal of oral sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.802
H-Index - 93
eISSN - 1600-0722
pISSN - 0909-8836
DOI - 10.1111/j.1600-0722.2005.00208.x
Subject(s) - mineralization (soil science) , chemistry , titanium , gene expression , biochemistry , collagen, type i, alpha 1 , microbiology and biotechnology , gene , anatomy , biology , extracellular matrix , organic chemistry , nitrogen
Titanium implants create a unique ultrastructure (composed of a collagenous zone with relatively disorganized fibril morphology) at the bone–implant interface. The objective of this study was to investigate the temporal mRNA expression patterns, using real‐time polymerase chain reaction, of type I collagen (COLI) and regulators for collagen fibrillogenesis, collagen‐binding small leucine‐rich proteoglycans (SLRPs) and lysyl hydroxylases (LHs), during mineralization, by MC3T3‐E1 cells cultured on titanium (Ti). Lysates of the cultures on Ti and on plastic wells (Pl) for 10–50 d were used for the quantification of calcium and mRNA. Although the onset of calcium accumulation in the cultures on Ti (30–40 d) was slower than that of cultures on Pl (20–30 d), the gene expression patterns during mineralization were similar in cells cultured on either material. COLI and fibromodulin were up‐regulated just before the onset of mineralization and then down‐regulated. Lumican and LH1 were up‐regulated just before the onset of mineralization and then returned to the baseline level. Decorin and LH2 were up‐regulated at the late mineralization stage. Biglycan was down‐regulated once at the early mineralization stage and then returned to the original level. LH3 was maintained at a steady level throughout. This study suggests actual but distinct roles of SLRPs and LHs in the formation of a unique ultrastructure at the bone–implant interface.