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:
https://lup.lub.lu.se/record/1035770
- author
- Franzén, Ahnders
LU
; Hultenby, Kjell
; Reinholt, Finn P
; Önnerfjord, Patrik
LU
and Heinegård, Dick
LU
- organization
- publishing date
- 2008
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Journal of Orthopaedic Research
- volume
- 26
- issue
- 5
- pages
- 721 - 728
- publisher
- John Wiley & Sons Inc.
- external identifiers
-
- pmid:18050311
- wos:000254960700016
- scopus:43649109028
- ISSN
- 1554-527X
- DOI
- 10.1002/jor.20544
- language
- English
- LU publication?
- yes
- additional info
- The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Connective Tissue Biology (013230151), Vessel Wall Biology (013212028)
- 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
- 2016-04-01 12:23:23
- date last changed
- 2022-01-27 03:05:21
@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 Inc.}},
series = {{Journal of Orthopaedic Research}},
title = {{Altered osteoclast development and function in osteopontin deficient mice.}},
url = {{http://dx.doi.org/10.1002/jor.20544}},
doi = {{10.1002/jor.20544}},
volume = {{26}},
year = {{2008}},
}