Bimodal actions of reactive oxygen species in the differentiation and bone-resorbing functions of osteoclasts

Hyunsoo Kim, Ick Young Kim, Soo Young Lee, Daewon Jeong

Research output: Contribution to journalArticle

28 Citations (Scopus)

Abstract

In order to demonstrate that cellular redox status undergoes decreased reduction during osteoclast differentiation and further decreased reduction during osteoclastic bone resorption, we analyzed γ-glutamylcysteinyl synthetase activity, a glutathione synthesis rate-limiting enzyme, and total glutathione and thiol groups. Moderate and severe redox shifts towards a more oxidizing environment induced gradual increases and decreases in osteoclastogenesis. Moreover, while severe glutathione depletion inhibited bone resorption, moderate glutathione repletion enhanced bone resorption. In summary, our observations suggest that there is a threshold for redox status, representing biphasic patterns in osteoclast differentiation and function.

Original languageEnglish
Pages (from-to)5661-5665
Number of pages5
JournalFEBS Letters
Volume580
Issue number24
DOIs
Publication statusPublished - 2006 Oct 16

Fingerprint

Osteoclasts
Glutathione
Reactive Oxygen Species
Bone
Bone Resorption
Oxidation-Reduction
Bone and Bones
Ligases
Sulfhydryl Compounds
Osteogenesis
Enzymes

Keywords

  • Bone resorption
  • Glutathione
  • Osteoclast differentiation
  • Reactive oxygen species
  • Redox status

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

Cite this

Bimodal actions of reactive oxygen species in the differentiation and bone-resorbing functions of osteoclasts. / Kim, Hyunsoo; Kim, Ick Young; Lee, Soo Young; Jeong, Daewon.

In: FEBS Letters, Vol. 580, No. 24, 16.10.2006, p. 5661-5665.

Research output: Contribution to journalArticle

Kim, Hyunsoo ; Kim, Ick Young ; Lee, Soo Young ; Jeong, Daewon. / Bimodal actions of reactive oxygen species in the differentiation and bone-resorbing functions of osteoclasts. In: FEBS Letters. 2006 ; Vol. 580, No. 24. pp. 5661-5665.
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