Silibinin Inhibits Osteoclast Differentiation Mediated by TNF Family Members

Kim, Jung Ha; Kim, Kabsun; Jin, Hye-Mi; Song, In-Sun; Youn, Bang Ung; Lee, Junwon; Kim, Nacksung

doi:10.1007/s10059-009-0123-y

Cited by 38 publications

(50 citation statements)

References 26 publications

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“…Consistent with previous results (22,23), RANKL induced degradation of IkB and activation of ERK, p38 MAPK, and JNK in control vector-infected BMMs. However, RANKL-induced IkB degradation was blocked by overexpression of Pim-1 DN, while other signaling pathways, including activation of ERK, JNK, and p38 MAPK, were not significantly affected (Fig.…”

Section: Activation Of Pim-1 Plays a Role In Rankl-induced Nf-kb Actisupporting

confidence: 93%

Pim-1 Regulates RANKL-Induced Osteoclastogenesis via NF-κB Activation and NFATc1 Induction

Kim

Youn

et al. 2010

The Journal of Immunology

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Pim kinases are emerging as important mediators of cytokine signaling pathways in hematopoietic cells. In this study, we demonstrate that Pim-1 positively regulates RANKL-induced osteoclastogenesis and that Pim-1 expression can be upregulated by RANKL signaling during osteoclast differentiation. The silencing of Pim-1 by RNA interference or overexpression of a dominant negative form of Pim-1 (Pim-1 DN) in bone marrow-derived macrophage cells attenuates RANKL-induced osteoclast formation. Overexpression of Pim-1 DN blocks RANKL-induced activation of TGF-β–activated kinase 1 (TAK1) and NF-κB as well as expression of NFATc1 during osteoclastogenesis. However, we found that overexpression of TAK1 in the presence of Pim-1 DN rescues NF-κB activation. Additionally, Pim-1 interacts with RANK as well as TAK1, indicating that Pim-1 is involved in RANKL-induced NF-κB activation via TAK1. Furthermore, we demonstrate that Pim-1 also regulates NFATc1 transcription activity and subsequently induces osteoclast-associated receptor expression, an osteoclast-specific gene. Taken together, our results reveal that Pim-1 positively regulates RANKL-induced osteoclastogenesis.

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Section: Activation Of Pim-1 Plays a Role In Rankl-induced Nf-kb Actisupporting

confidence: 93%

Pim-1 Regulates RANKL-Induced Osteoclastogenesis via NF-κB Activation and NFATc1 Induction

Kim

Youn

et al. 2010

The Journal of Immunology

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“…Osteoclast formation and TRAP staining Murine osteoclasts were prepared from bone marrow cells as previously described (Kim et al, 2009). In brief, femurs were aseptically removed from 6-8-week-old ICR mice, and bone marrow cells were flushed out with a sterile 21-gauge syringe.…”

Section: Methodsmentioning

confidence: 99%

SLAT Negatively Regulates RANKL-Induced Osteoclast Differentiation

Youn

Kim

et al. 2013

Molecules and Cells

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RANKL induces the formation of osteoclasts, which are responsible for bone resorption. Herein, we investigated the role of SWAP-70-like adapter of T cells (SLAT) in RANKL-induced osteoclastogenesis. Expression levels of SLAT were reduced during RANKL-induced osteoclastogenesis. Overexpression of SLAT in BMMs inhibited TRAP-positive multinuclear osteoclast formation and attenuated the expression of NFATc1, which is an important modulator in osteoclastogenesis. Furthermore, silencing of SLAT by RNA interference enhanced osteoclast formation as well as NFATc1 expression. In addition, SLAT was involved in RANKL-induced JNK activation in osteoclasts. Taken together, our data suggest that SLAT acts as a negative modulator of RANKL-induced osteoclastogenesis.

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“…On the other hand, Hartree-Fock and Dirac-Hartree-Fock methods are more general, faster, and easier to use for open-shell systems, so in the foreseeable future they are unlikely to be superseded, except perhaps for closed-shell or alkali-like elements [154]. In the present work an overview has been given on the current status of the Dirac-Hartree-Fock theory.…”

Section: Discussionmentioning

confidence: 99%

Ab initioMCDHF calculations of electron–nucleus interactions

et al. 2015

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1 AbstractWe present recent advances in the development of atomic ab initio multiconfiguration Dirac-HartreeFock (MCDHF) theory, implemented in the GRASP relativistic atomic structure code. For neutral atoms, the deviations of properties calculated within the Dirac-Hartree-Fock method (based on independent particle model of an atomic cloud) are usually dominated by electron correlation effects, i. e. the non-central interactions of individual electrons. We present the recent advances in accurate calculations of electron correlation effects in small, medium, and heavy neutral atoms. We describe methods of systematic development of multiconfiguration expansions leading to systematic, controlled improvement of the accuracy of the ab initio calculations. These methods originate from the concept of the Complete Active Space model within the Dirac-Hartree-Fock theory, which, at least in principle, permits fully relativistic calculations with full account of electron correlation effects. The calculations within the Complete Active Space model on currently available computer systems are feasible only for very light systems. For heavier atoms or ions with more than a few electrons, restrictions have to be imposed on the multiconfiguration expansions. We present methods and tools, which are designed to extend the numerical calculations in a controlled manner, where multiconfiguration expansions account for all leading electron correlation effects. We show examples of applications of the GRASP code to calculations of hyperfine structure constants, but the code may be used for calculations of arbitrary bound-state atomic properties. In recent years it has been applied to calculations of atomic and ionic spectra (transition energies and rates), to determinations of nuclear electromagnetic moments, as well as to calculations related to interactions of bound electrons with nuclear electromagnetic moments leading to violations of discrete symmetries.

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Silibinin Inhibits Osteoclast Differentiation Mediated by TNF Family Members

Cited by 38 publications

References 26 publications

Pim-1 Regulates RANKL-Induced Osteoclastogenesis via NF-κB Activation and NFATc1 Induction

Pim-1 Regulates RANKL-Induced Osteoclastogenesis via NF-κB Activation and NFATc1 Induction

SLAT Negatively Regulates RANKL-Induced Osteoclast Differentiation

Ab initioMCDHF calculations of electron–nucleus interactions

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