http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
조골세포내 cAMP농도 변화가 파골세포 형성에 미치는 영향
전윤나(Yunna Chun),임미정(Mijung Yim) 대한약학회 2005 약학회지 Vol.49 No.1
In the present study, treatment of IBMX, a phosphodiesterase (PDE) inhibitor, alone induced osteoclast formation in co-cultures of mouse bone marrow cells and calvarial osteoblasts. However, treatment of IBMX in combination with prostaglandin E₂(PGE₂) inhibited osteoclast formation in a dose-dependent manner. Among various isozyme-specific PDE inhibitors, a PDE4 specific inhibitor rolipram, showed similar effects as IBMX on osteoclast formation. To address the involvement of cyclic adenosine monophosphate (cAMP) in osteoclast formation, cAMP concentration in calvarial osteo- blasts was investigated. When calvarial osteoblasts were co-cultured with IBMX alone or in combination with PGE₂, the patterns of cAMP concentration in calvarial osteoblasts were differ each other, suggesting that cAMP in calvarial osteoblasts subtly regulates osteoclast formation.
노아롱새미(A Long Saemi Noh),임미정(Mijung Yim) 대한약학회 2010 약학회지 Vol.54 No.6
We investigated the role of L-type Ca2+ channel in receptor activator of nuclear factor-kappaB ligand (RANKL)-induced osteoclast formation. BayK 8644, a L-type Ca2+ channel agonist, was shown to increase the RANKLinduced osteoclastogenesis and actin ring formation in mouse bone marrow-dereived macrophage (BMM) culture system. BayK 8644 stimulated RANKL-induced extracellular signal-regulated kinase (ERK) and p38 MAP kinase (MAPK) activation, which leads to increased nuclear factor of activated T cells (NFAT)c1 expression. Taken together, these data indicate that L-type Ca2+ channel regulates osteoclast formation possibly through ERK- and p38-mediated NFATc1 expression.
박효정(Hyojung Park),노아롱새미(A Long Saemi Noh),이정민(Jung-Min Lee),임미정(Mijung Yim) 대한약학회 2010 약학회지 Vol.54 No.5
We explored the role of phosphodiesterase 4 (PDE4) on parathyroid (PTH)-induced signaling in osteoblasts. PTH was shown to increase the activity of PDE, mainly PDE4, in osteoblasts, which is partly attributable to elevated PDE4B and PDE4D mRNA expression. The use of PDE4 inhibitor strengthened the PTH-induced extracellular signal-regulated kinase (ERK) and p38 MAP kinase (MAPK) activation. Furthermore, the PDE4 inhibitor stimulated PTH-induced receptor activator of nuclear factor-κB ligand (RANKL) expression in osteoblasts, which in turn increased osteoclast formation. Taken together, these data suggest the negative role of PDE4 on PTH-induced signaling in osteoblasts.
양미혜(Mihye Yang),박효정(Hyojung Park),이동석(Dong-Seok Lee),임미정(Mijung Yim) 大韓藥學會 2009 약학회지 Vol.53 No.4
We explored the role of reactive oxygen species (ROS) in LPS-induced bone loss. LPS was shown to increase the concentration of ROS in osteoclast precursors. The antioxidant decreased osteoclast formation by LPS. Furthermore, the antioxidant decreased NFATc1 expression by LPS, suggesting that ROS mediates NFATc1 expression in the regulation of LPS-induced osteoclast formation. Finally, the antioxidant decreased LPS-induced RANKL mRNA expression in osteoblasts. Taken together, these data indicate that LPS mediates ROS to induce bone loss.
5-Lipoxygenase에 의한 성숙 파골세포의 조절
노아롱새미(A Long Sae Mi Noh),문미란(Miran Moon),정지은(Ji-Eun Jeong),임미정(Mijung Yim) 대한약학회 2012 약학회지 Vol.56 No.6
5-Lipoxygenase (5-LO) catalyzes the formation of two major groups of leukotrienes, LTB4 and cysteinyl leukotrienes (CysLT), and it has been implicated as a promising drug target to treat various inflammatory diseases. Since its role in mature osteoclasts (mOCs) had not been reported, we investigated the effect of 5-LO inhibitors on mOCs. We showed that 5-LO inhibitors dose-dependently decreases the number of mOCs. The effects of 5-LO inhibitors were reversible, suggesting that they did not cause any cellular damages in mOCs. We further demonstrated that the suppression of mOCs by 5-LO inhibitors was caused mainly by disruption of the actin ring formation. Similar effects were shown with CysLT receptor (CysLTR)1 antagonist in mOCs. The mRNA expression of CysLTR1 and the production of CysLT were increased in mOCs. These results indicate that CysLTR1 mediates the suppression of mOCs by 5-LO inhibitors. Taken together, this study demonstrated that 5-LO plays important role in mOCs and possibly a novel therapeutic target for bone resorption diseases.
H₁수용체 길항체 Pyrilamine이 파골세포 형성에 미치는 영향
임미정 숙명여자대학교 약학연구소 2005 약학논문집-숙명여자대학교 Vol.22 No.-
Osteoclasts, the multinucleated giant cells that resorb bone, develop from hemopoietic cells of monocyte-macrophage lineage. Differentiation of osteoclasts is strictly regulated by osteoblasts, which deposit bone. In the present study, pyrilamine, an H₁ receptor antagonist, inhibited osteoclast formation in co-cultures of mouse bone marrow cells and calvarial osteoblasts in the presence of 1,25-dihydroxyvitamine D₃ and PGE₂. Pyrilamine also inhibited osteoclastic differentiation of RAW264.7 cells in the presence of TRANCE, suggesting that H₁ receptor-mediated signals crosstalk with TRANCE signals. Further studies will elucidate the precise role of H₁ receptor in TRANCE-mediated osteoclast formation.
IL-1 의 신호전달에 관여하는 TRAF6 결합 motif의 기능적 중요성
임미정 숙명여자대학교 약학연구소 2002 약학논문집-숙명여자대학교 Vol.18 No.-
Crystal structure of TRAF6 in complex with TRAF6-binding sites from CD40 was previously determined. The structure revealed a distinct TRAF6-binding groove of CD40, the key structural determinant of interaction. The structural information leads to a proposed TRAF6-binding motif. This allows the identification of TRAF6-binding sequences in the hIRAK protein, whose functional requirement in IL-1 mediated signal transduction is further demonstrated using site-directed mutagenesis. The mutational effects of hIRAK on the down-stream NF-kB signaling shows the importance of the TRAF6 interface for signaling by IL-1.
골수세포를 이용한 파괄세포 분화 유도계에서 나타나는 세균 대사산물의 분화 억제 효과
임미정 숙명여자대학교 약학연구소 2003 약학논문집-숙명여자대학교 Vol.19 No.-
Bone turnover normally occurs in a highly regulated manner throughout life. It involves two different kinds of cells, osteoclasts and osteoblasts. Osteoclasts, the monocyte-macrophage lineage cells, resorb bone and osteoblasts deposit bone. Perturbations to these processes underlie skeletal disorders, such as osteoporosis. To understand the cellular and molecular mechanisms of bone biology and for the identification and characterization of new drug targets and therapies, a mouse co-culture system of osteoblasts and hematopoietic cells is established, in which osteoclasts are formed in response to 1 a ,25-dihydroxyvitamin D3 (1 a ,25(OH)₂D₃) and prostaglandin E₂ (PGE₂). Using this co-culture system, the bacterial metabolite n-butyrate, which has well-known anti-inflammatory effects, is shown to stimulate or inhibit osteoclastogenesis depending on the concentration. These results demonstrate a novel property of w-butyrate that may modulate osteoclastogenesis via osteoblasts.
Prostaglandin E₂가 파골세포 형성에 미치는 영향
조은숙,임미정 숙명여자대학교 약학연구소 2004 약학논문집-숙명여자대학교 Vol.21 No.-
Osteoclasts, the multinucleated giant cells that resorb bone, develop from hemopoietic cells of monocyte-macrophage lineage. Differentiation of osteoclasts is strictly regulated by osteoblasts, which deposit bone. In the present study, prostaglandin E₂ (PGE₂) induced osteoclast formation in co-cultures of mouse bone marrow cells and calvarial osteoblasts. This activity was not observed in the absence of calvarial osteoblasts, suggesting that calvarial osteoblasts are likely target cells of PGE₂. Northern blot analysis revealed that the effect of PGE₂ is associated with increased expression of the osteoclast differentiation factor TNF-related activation-induced cytokine (TRANCE, identical to RANKL, ODF, and OPGL) in mouse calvarial osteoblasts. Induction of TRANCE expression by PGE₂ was partially suppressed by the inhibitors of ERK and p38 MAPK, suggesting that activation of ERK and p38 MAPK is involved in TRANCE expression by PGE₂.
파골세포 분화에 관여하는 Phosphodiesterase Isozyme 의 규명
조은숙,임미정 숙명여자대학교 약학연구소 2004 약학논문집-숙명여자대학교 Vol.21 No.-
Phosphodiesterases (PDEs) are enzymes that degrade intracellular cAMP and cGMP. In the present study, inhibition of PDE4 was demonstrated to influence osteoclast formation in co-cultures of mouse bone marrow cells and calvarial osteoblasts. Furthermore, PDE4 was shown to modulate mRNA expression of EP4, TRANCE, and COX-2 in calvarial osteoblasts. These results suggest that PDE4 is a key regulator of EP4, TRANCE, and COX-2 expression in osteoblasts, which in turn controls osteoclast formation.