Osteoporosis induced in mice by overproduction of interleukin 4

D. B. Lewis, H. D. Liggitt, E. L. Effmann, S. T. Motley, S. L. Teitelbaum, K. J. Jepsen, S. A. Goldstein, J. Bonadio, J. Carpenter, R. M. Perlmutter

Research output: Contribution to journalArticlepeer-review

142 Scopus citations

Abstract

Osteoporosis is a common disease in which loss of bone mass results in skeletal fragility. The development of therapies for this disorder has been hampered by the lack of a convenient animal model. Here we describe a disorder in bone homeostasis in transgenic mice that inappropriately express the cytokine interleukin 4 (IL-4) under the direction of the lymphocyte- specific proximal promoter for the lck gene. Bone disease in lck-IL-4 mice appeared to result from markedly decreased bone formation by osteoblasts, features strikingly similar to those observed in cases of severe low-turnover human involutional osteoporosis. By 2 months of age, female and male lck-IL- 4 mice invariably developed severe osteoporosis of both cortical and trabecular bone. Osteoporosis was observed in two independently derived founder animals, indicating that this phenotype was directly mediated by the IL-4 transgene.

Original languageEnglish
Pages (from-to)11618-11622
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Volume90
Issue number24
DOIs
StatePublished - 1993

Keywords

  • lck promoter
  • osteoblasts
  • osteoclasts
  • osteopenia
  • transgenic mice

Fingerprint

Dive into the research topics of 'Osteoporosis induced in mice by overproduction of interleukin 4'. Together they form a unique fingerprint.

Cite this