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Modulation of bone remodeling via mechanically activated ion channelsA critical factor in the maintenance of bone mass is the physical forces imposed upon the skeleton. Removal of these forces, such as in a weightless environment, results in a rapid loss of bone, whereas application of exogenous mechanical strain has been shown to increase bone formation. Numerous flight and ground-based experiments indicate that the osteoblast is the key bone cell influenced by mechanical stimulation. Aside from early transient fluctuations in response to unloading, osteoclast number and activity seem unaffected by removal of strain. However, bone formation is drastically reduced in weightlessness and osteoblasts respond to mechanical strain with an increase in the activity of a number of second messenger pathways resulting in increased anabolic activity. Unfortunately, the mechanism by which the osteoblast converts physical stimuli into a biochemical message, a process we have termed biochemical coupling, remains elusive. Prior to the application of this grant, we had characterized a mechanosensitive, cation nonselective channel (SA-cat) in osteoblast-like osteosarcoma cells that we proposed is the initial signalling mechanism for mechanotransduction. During the execution of this grant, we have made considerable progress to further characterize this channel as well as to determine its role in the osteoblastic response to mechanical strain. To achieve these goals, we combined electrophysiologic techniques with cellular and molecular biology methods to examine the role of these channels in the normal function of the osteoblast in vitro.
Document ID
19960044614
Acquisition Source
Ames Research Center
Document Type
Contractor Report (CR)
Authors
Duncan, Randall L. (Indiana Univ. Medical Center Indianapolis, IN United States)
Date Acquired
September 6, 2013
Publication Date
January 1, 1996
Subject Category
Aerospace Medicine
Report/Patent Number
NASA-CR-201909
NAS 1.26:201909
Accession Number
96N32079
Funding Number(s)
CONTRACT_GRANT: NAG2-791
CONTRACT_GRANT: NAG2-1049
Distribution Limits
Public
Copyright
Work of the US Gov. Public Use Permitted.

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