Advanced Glycation End Products (AGEs), but not High Glucose, Inhibit the Osteoblastic Differentiation of Mouse Stromal ST2 Cells Through the Suppression of Osterix Expression, and Inhibit Cell Growth and Increasing Cell Apoptosis

Diabetes mellitus is known to be associated with osteoporotic fractures through a decrease in osteoblastic bone formation rather than an increase in osteoclastic bone resorption. However, its precise mechanism is unknown, and we examined whether or not high glucose or advanced glycation end products...

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Bibliographic Details
Published in:Calcified tissue international 2012-10, Vol.91 (4), p.286-296
Main Authors: Okazaki, Kyoko, Yamaguchi, Toru, Tanaka, Ken-ichiro, Notsu, Masakazu, Ogawa, Noriko, Yano, Shozo, Sugimoto, Toshitsugu
Format: Article
Language:English
Subjects:
Advanced glycosylation end products
Alkaline phosphatase
Animals
Apoptosis
Biochemistry
Biomedical and Life Sciences
Bone density
Bone Morphogenetic Protein 2 - genetics
Bone Morphogenetic Protein 2 - metabolism
Bone resorption
Cbfa-1 protein
Cell Biology
Cell Differentiation
Cell Proliferation
Cells, Cultured
Cellular biology
Diabetes
Diabetes mellitus
Differentiation
Endocrinology
Fractures
Gene expression
Glucose
Glucose - metabolism
Glucose - pharmacology
Glycation End Products, Advanced - metabolism
Humans
Life Sciences
Mice
Mineralization
Original Research
Orthopedics
Osteoblastogenesis
Osteoblasts
Osteoblasts - cytology
Osteoblasts - metabolism
Osteocalcin
Osteogenesis
Osteoporosis
Polymerase chain reaction
Sp7 Transcription Factor
stromal cells
Stromal Cells - cytology
Stromal Cells - metabolism
Transcription Factors - antagonists & inhibitors
Transcription Factors - genetics
Transcription Factors - metabolism
Western blotting
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Summary:Diabetes mellitus is known to be associated with osteoporotic fractures through a decrease in osteoblastic bone formation rather than an increase in osteoclastic bone resorption. However, its precise mechanism is unknown, and we examined whether or not high glucose or advanced glycation end products (AGEs), which play key roles in the pathogenesis and complications of diabetes, would affect the osteoblastic differentiation, growth, and apoptosis of mouse stromal ST2 cells. Ten to 200 μg/mL AGE2 or AGE3 alone dose-dependently inhibited the mineralization. AGE2 or AGE3 alone (200 μg/mL) significantly inhibited alkaline phosphatase (ALP) activities as well as the mineralization of the cells ( p  
ISSN:0171-967X
1432-0827
DOI:10.1007/s00223-012-9641-2