Advanced

Altered osteoclast development and function in osteopontin deficient mice.

Franzén, Ahnders LU ; Hultenby, Kjell; Reinholt, Finn P; Önnerfjord, Patrik LU and Heinegård, Dick LU (2008) In Journal of Orthopaedic Research 26(5). p.721-728
Abstract
The role of osteopontin in bone resorption was elucidated by studies of mice with knock out of the osteopontin gene generated by a different approach compared to previous models. Thus, a targeting vector with the promoter region as well as exons 1, 2, and 3 of the osteopontin gene was replaced by a loxP-flanked Neo-TK cassette, and this cassette was eliminated through transient expression of Cre recombinase. The recombined ES cells were used to create mice lacking expression of the osteopontin gene. Tissues from these mice were subjected structural and molecular analyses including morphometry and proteomics. The bone of the null mice contained no osteopontin but showed no significant alterations with regard to other bone proteins. The bone... (More)
The role of osteopontin in bone resorption was elucidated by studies of mice with knock out of the osteopontin gene generated by a different approach compared to previous models. Thus, a targeting vector with the promoter region as well as exons 1, 2, and 3 of the osteopontin gene was replaced by a loxP-flanked Neo-TK cassette, and this cassette was eliminated through transient expression of Cre recombinase. The recombined ES cells were used to create mice lacking expression of the osteopontin gene. Tissues from these mice were subjected structural and molecular analyses including morphometry and proteomics. The bone of the null mice contained no osteopontin but showed no significant alterations with regard to other bone proteins. The bone volume was normal in young null animals but in the lower metaphysis, the volume and number of osteoclasts were increased. Notably, the volume and length of the osteoclast ruffled border was several folds lower, indicating a lower resorptive capacity. The null mice did not develop the bone loss characteristic for osteoporosis demonstrated in old wild-type female animals. This quantitative study demonstrates a bone phenotype in the osteopontin null mice of all ages. The data provides further evidence for a role of osteopontin in osteoclast activity. (c) 2007 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res. (Less)
Please use this url to cite or link to this publication:
author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Journal of Orthopaedic Research
volume
26
issue
5
pages
721 - 728
publisher
John Wiley & Sons
external identifiers
  • pmid:18050311
  • wos:000254960700016
  • scopus:43649109028
ISSN
1554-527X
DOI
10.1002/jor.20544
language
English
LU publication?
yes
id
fb2000ac-e108-46fa-8653-3754ff2804c5 (old id 1035770)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/18050311?dopt=Abstract
date added to LUP
2008-04-01 11:28:24
date last changed
2017-09-24 03:44:02
@article{fb2000ac-e108-46fa-8653-3754ff2804c5,
  abstract     = {The role of osteopontin in bone resorption was elucidated by studies of mice with knock out of the osteopontin gene generated by a different approach compared to previous models. Thus, a targeting vector with the promoter region as well as exons 1, 2, and 3 of the osteopontin gene was replaced by a loxP-flanked Neo-TK cassette, and this cassette was eliminated through transient expression of Cre recombinase. The recombined ES cells were used to create mice lacking expression of the osteopontin gene. Tissues from these mice were subjected structural and molecular analyses including morphometry and proteomics. The bone of the null mice contained no osteopontin but showed no significant alterations with regard to other bone proteins. The bone volume was normal in young null animals but in the lower metaphysis, the volume and number of osteoclasts were increased. Notably, the volume and length of the osteoclast ruffled border was several folds lower, indicating a lower resorptive capacity. The null mice did not develop the bone loss characteristic for osteoporosis demonstrated in old wild-type female animals. This quantitative study demonstrates a bone phenotype in the osteopontin null mice of all ages. The data provides further evidence for a role of osteopontin in osteoclast activity. (c) 2007 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res.},
  author       = {Franzén, Ahnders and Hultenby, Kjell and Reinholt, Finn P and Önnerfjord, Patrik and Heinegård, Dick},
  issn         = {1554-527X},
  language     = {eng},
  number       = {5},
  pages        = {721--728},
  publisher    = {John Wiley & Sons},
  series       = {Journal of Orthopaedic Research},
  title        = {Altered osteoclast development and function in osteopontin deficient mice.},
  url          = {http://dx.doi.org/10.1002/jor.20544},
  volume       = {26},
  year         = {2008},
}