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Kruppel-like factor 4 attenuates osteoblast formation, function, and cross talk with osteoclasts
Kim, Jung Ha,Kim, Kabsun,Youn, Bang Ung,Lee, Jongwon,Kim, Inyoung,Shin, Hong-In,Akiyama, Haruhiko,Choi, Yongwon,Kim, Nacksung The Rockefeller University Press 2014 The Journal of cell biology Vol.204 No.6
<P>KLF4 controls bone homeostasis by negatively regulating both osteoclast and osteoblast differentiation.</P>
Pim-1 regulates RANKL-induced osteoclastogenesis via NF-관B activation and NFATc1 induction.
Kim, Kabsun,Kim, Jung Ha,Youn, Bang Ung,Jin, Hye Mi,Kim, Nacksung Williams Wilkins 2010 JOURNAL OF IMMUNOLOGY Vol.185 No.12
<P>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-관-activated kinase 1 (TAK1) and NF-관B as well as expression of NFATc1 during osteoclastogenesis. However, we found that overexpression of TAK1 in the presence of Pim-1 DN rescues NF-관B activation. Additionally, Pim-1 interacts with RANK as well as TAK1, indicating that Pim-1 is involved in RANKL-induced NF-관B 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.</P>
Piperine 유도체의 합성 및 중추억제작용에 관한 연구(I) 3,4-Methylenedioxycinnamic Acid 유도체
임중기(Joong Ki Rim),이동웅(Dong Ung Lee),이진영(Jin Young Lee),김연순(Youn Sun Kim),우원식(Won Sick Woo),이은방(Eun Bang Lee) 大韓藥學會 1982 약학회지 Vol.26 No.4
Piperine was reported to have a potential central nervous system (CNS) depressant activity in mice. In order to search a more active and less toxic compound than piperine and to elucidate the active group of piperine, the aromatic amides (10 compounds) and aromatic esters (10 compounds) of 3, 4-methylenedioxycinnamic acid were synthesized and evaluated on CNS depressant activity in comparison with piperine. The pharmacological tests conducted are as follows; (1) Acute toxicity, (2) Antagonism against strychnine induced conduced convulsion, (4) Antagonism against maximal electroshock seizure, (5) Rotarod test, (6) Potentiation of hexobarbital sleeping time. It was observed that 3, 4-methylendioxycinanamic acid derivatives were less toxic than piperine, and showed no significant CNS depressant activities. These facts indicate that the piperoyl group might be concerned with the pharmacological activity of piperine.
Silibinin Inhibits Osteoclast Differentiation Mediated by TNF Family Members
김정하,김갑순,Hye Mi Jin,송인선,Bang Ung Youn,Junwon Lee,Nacksung Kim 한국분자세포생물학회 2009 Molecules and cells Vol.28 No.3
Silibinin is a polyphenolic flavonoid compound isolated from milk thistle (páäóÄìã=ã~êá~åìã), with known hepatoprotective, anticarcinogenic, and antioxidant effects. Herein, we show that silibinin inhibits receptor activator of NF-κB ligand (RANKL)-induced osteoclastogenesis from RAW264.7 cells as well as from bone marrow-derived monocyte/macrophage cells in a dose-dependent manner. Silibinin has no effect on the expression of RANKL or the soluble RANKL decoy receptor osteoprotegerin (OPG) in osteoblasts. However, we demonstrate that silibinin can block the activation of NF-κB, c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein (MAP) kinase, and extracellular signal-regulated kinase (ERK) in osteoclast precursors in response to RANKL. Furthermore, silibinin attenuates the induction of nuclear factor of activated T cells (NFAT) c1 and osteoclast-associated receptor (OSCAR) expression during RANKL-induced osteoclastogenesis. We demonstrate that silibinin can inhibit TNF-α-induced osteoclastogenesis as well as the expression of NFATc1 and OSCAR. Taken together, our results indicate that silibinin has the potential to inhibit osteoclast formation by attenuating the downstream signaling cascades associated with RANKL and TNF-α.
The mechanism of osteoclast differentiation induced by IL-1.
Kim, Jung Ha,Jin, Hye Mi,Kim, Kabsun,Song, Insun,Youn, Bang Ung,Matsuo, Koichi,Kim, Nacksung Williams Wilkins 2009 JOURNAL OF IMMUNOLOGY Vol.183 No.3
<P>IL-1 is a potent cytokine that can induce bone erosion in inflammatory sites such as rheumatoid joint regions via activation of osteoclasts. Not only is IL-1 capable of activating osteoclasts, but it is also a key cytokine involved in the differentiation, multinucleation, and survival of osteoclasts. Herein, we show that IL-1 has the potential to drive osteoclast differentiation via a receptor activator of NF-kappaB ligand (RANKL)/RANK-independent mechanism. Although IL-1 has a synergistic effect on RANKL-induced osteoclast formation, IL-1 alone cannot induce osteoclast differentiation from osteoclast precursors (bone marrow-derived macrophages (BMMs)) due to a lack of IL-1 signaling potential in these cells. However, we demonstrate that overexpression of the IL-1RI receptor in BMMs or induction of IL-1RI by c-Fos overexpression enables IL-1 alone to induce the formation of authentic osteoclasts by a RANKL/RANK-independent mechanism. The expression of IL-1RI is up-regulated by RANKL via c-Fos and NFATc1. Furthermore, the addition of IL-1 to IL-1RI overexpressing BMMs (IL-1/IL-1RI) strongly activates NF-kappaB, JNK, p38, and ERK which is a hallmark gene activation profile of osteoclastogenesis. Interestingly, IL-1/IL-1RI does not induce expression of c-Fos or NFATc1 during osteoclast differentiation, although basal levels of c-Fos and NFATc1 seem to be required. Rather, IL-1/IL-1RI strongly activates MITF, which subsequently induces osteoclast-specific genes such as osteoclast-associated receptor and tartrate-resistant acid phosphatase. Together, these results reveal that IL-1 has the potential to induce osteoclast differentiation via activation of microphthalmia transcription factor under specific microenvironmental conditions.</P>
Silibinin inhibits osteoclast differentiation mediated by TNF family members
Kim, Jung Ha,Kim, Kabsun,Jin, Hye Mi,Song, Insun,Youn, Bang Ung,Lee, Junwon,Kim, Nacksung Springer-Verlag 2009 Molecules and cells Vol.28 No.3
<P>Silibinin is a polyphenolic flavonoid compound isolated from milk thistle (Silybum marianum), with known hepatoprotective, anticarcinogenic, and antioxidant effects. Herein, we show that silibinin inhibits receptor activator of NF-κB ligand (RANKL)-induced osteoclastogenesis from RAW264.7 cells as well as from bone marrow-derived monocyte/macrophage cells in a dose-dependent manner. Silibinin has no effect on the expression of RANKL or the soluble RANKL decoy receptor osteoprotegerin (OPG) in osteoblasts. However, we demonstrate that silibinin can block the activation of NF-κB, c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein (MAP) kinase, and extracellular signal-regulated kinase (ERK) in osteoclast precursors in response to RANKL. Furthermore, silibinin attenuates the induction of nuclear factor of activated T cells (NFAT) c1 and osteoclast-associated receptor (OSCAR) expression during RANKL-induced osteoclastogenesis. We demonstrate that silibinin can inhibit TNF-α-induced osteoclastogenesis as well as the expression of NFATc1 and OSCAR. Taken together, our results indicate that silibinin has the potential to inhibit osteoclast formation by attenuating the downstream signaling cascades associated with RANKL and TNF-α.</P>