NDLI: A comprehensive investigation of skeletal dynamics in the aging rat

Content Provider	IEEE Xplore Digital Library
Author	Buhl, K.M. Jacobs, C.R. Donahue, H.J.
Copyright Year	1998
Description	Author affiliation: Musculoskeletal Res. Lab., Pennsylvania State Coll. of Med., Hershey, PA, USA (Buhl, K.M.)
Abstract	The authors hypothesize that the age-related decline in bone formation will be reflected in an altered pattern of gene expression for proteins found in the extracellular matrix (ECM) of bone. Further, this decline in bone formation and altered ECM composition contribute to a decreased mechanical competence. Previous studies have investigated age-related changes in bone mechanics and bone metabolism independently. Further, these studies have used different strains of rats with varied growth rates and life spans making interpretation difficult. The present study is the first comprehensive investigation of the effect of aging on bone at the molecular, cellular and whole organ levels. The results showed that the decline in bone formation and material properties was associated with a corresponding decrease in the steady-state levels of type I collagen, osteopontin and osteocalcin mRNA. The abundance and orientation of collagen fibers contribute to the material properties of bone, as may the abundance of osteopontin and osteocalcin. Therefore, the authors' results suggest a decrease in ECM production and composition may contribute to age-related changes in bone material properties.
Starting Page	58
Ending Page	60
File Size	288902
Page Count	3
File Format	PDF
ISBN	0780345444
DOI	10.1109/NEBC.1998.664876
Language	English
Publisher	Institute of Electrical and Electronics Engineers, Inc. (IEEE)
Publisher Date	1998-04-10
Publisher Place	USA
Access Restriction	Subscribed
Rights Holder	Institute of Electrical and Electronics Engineers, Inc. (IEEE)
Subject Keyword	Aging Bones Electrochemical machining Material properties Gene expression Proteins Extracellular Biochemistry Capacitive sensors Rats
Content Type	Text
Resource Type	Article

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