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Endoplasmic reticulum stress and mineralization inhibition mechanism by the resinous monomer HEMA
Author(s) -
Diamanti E.,
Mathieu S.,
Jeanneau C.,
Kitraki E.,
Panopoulos P.,
Spyrou G.,
About I.
Publication year - 2013
Publication title -
international endodontic journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.988
H-Index - 119
eISSN - 1365-2591
pISSN - 0143-2885
DOI - 10.1111/j.1365-2591.2012.02103.x
Subject(s) - endoplasmic reticulum , osteonectin , chemistry , unfolded protein response , microbiology and biotechnology , odontoblast , cytoplasm , secretion , chaperone (clinical) , downregulation and upregulation , pulp (tooth) , biochemistry , biology , medicine , dentistry , pathology , alkaline phosphatase , osteocalcin , enzyme , gene
Aim To investigate the expression of two endoplasmic reticulum (ER) ‐resident key chaperone proteins, ER dj5 and BiP, under the influence of resinous monomers and its relationship with the inhibition of mineralization caused by the monomer 2‐hydroxyethyl methacrylate ( HEMA ). Methodology The ER dj5 and BiP expression was studied in vitro , in primary human pulp cell cultures after treatment with three different HEMA concentrations at different time periods. Subsequently, the expression of both the odontoblast markers dentine sialoprotein ( DSP ) and osteonectin ( OSN ) was studied in human pulp cells under the same conditions. Results The ER dj5 and BiP expression was upregulated in the pulp cells. DSP and OSN were largely dispersed in the cytoplasm in control cell cultures but accumulated in a perinuclear area after exposure to HEMA . Their expression levels were not affected. Conclusions The increased expression of ER dj5 and BiP may reflect activation of ER stress. DSP and OSN accumulation into the cells may lead to their secretion arrest and inhibition of dentine matrix formation. These events may elucidate the mechanism by which HEMA inhibits the mineralization process.