Advanced glycation end-products enhance calcification in cultured rat dental pulp cells. 2013

Yukiko Nakajima, and Yuji Inagaki, and Yuka Hiroshima, and Jun-ichi Kido, and Toshihiko Nagata
Department of Periodontology and Endodontology, Institute of Health Biosciences, University of Tokushima Graduate School, Tokushima, Japan.

BACKGROUND Amorphous calcification frequently appears in dental pulp tissues of diabetic patients; however, its pathologic process has not been fully elucidated. We previously found that pulp stones and thickened predentin occurred more frequently in diabetic rats. Recent findings demonstrated that accumulation of advanced glycation end-products (AGE) might be involved in vascular calcification complicated with diabetes. The aim of this study was to determine the effect of AGE on calcified nodule formation by rat dental pulp cells in culture. METHODS Rat dental pulp cells and gingival fibroblasts were independently cultured with 50 and 100 μg/mL AGE. Alkaline phosphatase activity and calcified nodule formation were measured. Expressions of receptor for AGE, osteopontin (OPN), and osteocalcin (OCN) mRNA were determined by quantitative real-time polymerase chain reaction. Protein levels of OPN and OCN secreted in culture medium were quantified by enzyme-linked immunosorbent assay. RESULTS AGE (50 and 100 μg/mL) markedly increased both alkaline phosphatase activity and calcified nodule formation in dental pulp cells (P < .01), whereas it did not affect those in gingival fibroblasts. Real-time polymerase chain reaction analysis revealed that AGE increased mRNA expressions of receptor for AGE, OPN, and OCN in dental pulp cells (P < .05). Enzyme-linked immunosorbent assay analysis revealed that the protein levels of OPN and OCN produced by dental pulp cells were higher in AGE-treated than in untreated cells (P < .05). CONCLUSIONS AGE enhanced the calcification potentials of rat dental pulp cells, suggesting that it may stimulate pathologic calcification of diabetic dental pulp tissues.

UI MeSH Term Description Entries
D008297 Male Males
D011971 Receptors, Immunologic Cell surface molecules on cells of the immune system that specifically bind surface molecules or messenger molecules and trigger changes in the behavior of cells. Although these receptors were first identified in the immune system, many have important functions elsewhere. Immunologic Receptors,Immunologic Receptor,Immunological Receptors,Receptor, Immunologic,Receptors, Immunological
D002478 Cells, Cultured Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others. Cultured Cells,Cell, Cultured,Cultured Cell
D003782 Dental Pulp A richly vascularized and innervated connective tissue of mesodermal origin, contained in the central cavity of a tooth and delimited by the dentin, and having formative, nutritive, sensory, and protective functions. (Jablonski, Dictionary of Dentistry, 1992) Dental Pulps,Pulp, Dental,Pulps, Dental
D003784 Dental Pulp Calcification CALCINOSIS of the DENTAL PULP or ROOT CANAL. Dental Pulp Stones,Denticle,Anomalous Dysplasia of Dentin,Calcification, Dental Pulp,Coronal Dentin Dysplasia,Dental Pulp Stone,Denticles,Dentin Dyspalsia, Shields Type 2,Dentin Dysplasia, Coronal,Dentin Dysplasia, Shields Type II,Dentin Dysplasia, Type II,Pulp Calcification, Dental,Pulp Stone, Dental,Pulp Stones,Pulp Stones, Dental,Pulpal Dysplasia,Stone, Dental Pulp,Stones, Dental Pulp,Calcifications, Dental Pulp,Coronal Dentin Dysplasias,Dental Pulp Calcifications,Dentin Anomalous Dysplasia,Dentin Anomalous Dysplasias,Dentin Dysplasias, Coronal,Dysplasia, Coronal Dentin,Dysplasia, Pulpal,Dysplasias, Coronal Dentin,Dysplasias, Pulpal,Pulp Calcifications, Dental,Pulp Stone,Pulpal Dysplasias,Stone, Pulp,Stones, Pulp
D005347 Fibroblasts Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules. Fibroblast
D005881 Gingiva Oral tissue surrounding and attached to TEETH. Gums,Interdental Papilla,Papilla, Interdental,Gum
D000067759 Receptor for Advanced Glycation End Products A single-pass transmembrane CELL SURFACE RECEPTOR that binds ADVANCED GLYCATION END PRODUCTS to mediate cellular responses to both acute and chronic vascular inflammation in conditions such as ATHEROSCLEROSIS and DIABETES MELLITUS, TYPE 2. Advanced Glycation End Product Receptor,Advanced Glycation End Product Receptors,Receptor For Advanced Glycation End Product,Receptor for Advanced Glycation Endproduct,AGE Receptor,AGER Protein,Amphoterin Receptor,RAGE (Receptor for Advanced Glycation End Products),Receptor for Advanced Glycation End Products (RAGE),Receptor for Advanced Glycation Endproducts,Receptor, Amphoterin
D000469 Alkaline Phosphatase An enzyme that catalyzes the conversion of an orthophosphoric monoester and water to an alcohol and orthophosphate. EC 3.1.3.1.
D000818 Animals Unicellular or multicellular, heterotrophic organisms, that have sensation and the power of voluntary movement. Under the older five kingdom paradigm, Animalia was one of the kingdoms. Under the modern three domain model, Animalia represents one of the many groups in the domain EUKARYOTA. Animal,Metazoa,Animalia

Related Publications

Yukiko Nakajima, and Yuji Inagaki, and Yuka Hiroshima, and Jun-ichi Kido, and Toshihiko Nagata
April 2022, Oral diseases,
Yukiko Nakajima, and Yuji Inagaki, and Yuka Hiroshima, and Jun-ichi Kido, and Toshihiko Nagata
January 2009, The Journal of international medical research,
Yukiko Nakajima, and Yuji Inagaki, and Yuka Hiroshima, and Jun-ichi Kido, and Toshihiko Nagata
March 2013, BMC cardiovascular disorders,
Yukiko Nakajima, and Yuji Inagaki, and Yuka Hiroshima, and Jun-ichi Kido, and Toshihiko Nagata
May 2014, Zhonghua nan ke xue = National journal of andrology,
Yukiko Nakajima, and Yuji Inagaki, and Yuka Hiroshima, and Jun-ichi Kido, and Toshihiko Nagata
January 2011, Contributions to nephrology,
Yukiko Nakajima, and Yuji Inagaki, and Yuka Hiroshima, and Jun-ichi Kido, and Toshihiko Nagata
January 2008, Journal of gastroenterology,
Yukiko Nakajima, and Yuji Inagaki, and Yuka Hiroshima, and Jun-ichi Kido, and Toshihiko Nagata
April 2003, The American journal of pathology,
Yukiko Nakajima, and Yuji Inagaki, and Yuka Hiroshima, and Jun-ichi Kido, and Toshihiko Nagata
December 2000, Journal of neuropathology and experimental neurology,
Yukiko Nakajima, and Yuji Inagaki, and Yuka Hiroshima, and Jun-ichi Kido, and Toshihiko Nagata
January 2013, Molecular medicine reports,
Yukiko Nakajima, and Yuji Inagaki, and Yuka Hiroshima, and Jun-ichi Kido, and Toshihiko Nagata
August 2016, International journal of molecular sciences,
Copied contents to your clipboard!