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Mechanism of alveolar bone loss in a collagen‐induced arthritis model in mice
Park, Jungx2010,Chul,Su, Chuanxin,Jung, Imx2010,Hee,Choi, Seongx2010,Ho,Cho, Kyoox2010,Sung,Kim, Chongx2010,Kwan,Park, Yongx2010,Beom,Lee, Soox2010,Kon,Kim, Changx2010,Sung Blackwell Publishing Ltd 2011 Journal of Clinical Periodontology Vol.38 No.2
<P>Park J‐C, Su C, Jung I‐H, Choi S‐H, Cho K‐S, Kim C‐K, Park Y‐B, Lee S‐K, Kim C‐S: Mechanism of alveolar bone loss in a collagen‐induced arthritis model in mice. J Clin Periodontol 2011; 38: 122–130. doi: 10.1111/j.1600‐051X.2010.01645.x</P><P><B>Abstract</B></P><P><B>Objective: </B> The aim of this study was to understand the cellular/molecular mechanisms of periodontal breakdown in a collagen‐induced arthritis (CIA) model in mice to enhance the understanding of rheumatoid arthritis (RA)‐associated alveolar bone loss in humans.</P><P><B>Materials and Methods: </B> All analyses were performed on paired samples from CIA and control group mice. Mandibles were retrieved for micro‐computed tomography (micro‐CT), histomorphometric analysis, and isolation of alveolar bone cells (ABCs). In vitro osteoclastogenic/osteogenic/adipogenic potentials of ABCs were evaluated and the mRNA expression of downstream effector genes was assessed. Bone formation of ABCs was assessed using an ectopic transplantation model.</P><P><B>Results: </B> Histomorphometric and micro‐CT data showed that alveolar bone loss was significantly increased in the CIA group (<I>p</I><0.05). Osteoclastogenesis was significantly increased in the CIA group in vivo (<I>p</I><0.05), with upregulated mRNA expressions of osteoclastogenesis‐associated genes. Osteoblasts appeared to undergo increased apoptosis, and the bone‐forming activity of ABCs concomitantly decreased with in vitro osteogenic differentiation and in vivo ectopic transplantation (<I>p</I><0.05). Also, adipogenesis‐associated mRNA expression was highly expressed in the CIA group, resulting in significantly enhanced adipocyte differentiation in vitro (<I>p</I><0.05).</P><P><B>Conclusions: </B> These data demonstrate that increased osteoclastic activity, decreased bone‐forming activity and enhanced adipogenesis promote alveolar bone loss in a CIA model in mice, and they suggest that these mechanisms could account for the same outcome in human RA.</P>
Jeong, Jix2010,Hak,Jeong, Yunx2010,Jeong,Cho, Hyunx2010,Ji,Shin, Jaex2010,Moon,Kang, Jeongx2010,Han,Park, Kwan‐,Kyu,Park, Yoonx2010,Yub,Chung, Ilx2010,Kyung,Chang, Hyeunx2010,Woo Wiley Subscription Services, Inc., A Wiley Company 2012 Journal of cellular biochemistry Vol.113 No.4
<P><B>Abstract</B></P><P>Ascochlorin, a non‐toxic prenylphenol compound derived from the fungus <I>Ascochyta viciae</I>, has been shown recently to have anti‐cancer effects on various human cancer cells. However, the precise molecular mechanism of this anti‐cancer activity remains to be elucidated. Here, we investigated the effects of ascochlorin on hypoxia‐inducible factor‐1α (HIF‐1α) and vascular endothelial growth factor (VEGF) expression in human epidermoid cervical carcinoma CaSki cells. Ascochlorin inhibited epidermal growth factor (EGF)‐induced HIF‐1α and VEGF expression through multiple potential mechanisms. First, ascochlorin selectively inhibited HIF‐1α expression in response to EGF stimulation, but not in response to hypoxia (1% O<SUB>2</SUB>) or treatment with a transition metal (CoCl<SUB>2</SUB>). Second, ascochlorin inhibited EGF‐induced ERK‐1/2 activation but not AKT activation, both of which play essential roles in EGF‐induced HIF‐1α protein synthesis. Targeted inhibition of epidermal growth factor receptor (EGFR) expression using an EGFR‐specific small interfering RNA (siRNA) diminished HIF‐1α expression, which suggested that ascochlorin inhibits HIF‐1α expression through suppression of EGFR activation. Finally, we showed that ascochlorin functionally abrogates in vivo tumor angiogenesis induced by EGF in a Matrigel plug assay. Our data suggest that ascochlorin inhibits EGF‐mediated induction of HIF‐1α expression in CaSki cells, providing a potentially new avenue of development of anti‐cancer drugs that target tumor angiogenesis. J. Cell. Biochem. 113: 1302–1313, 2012. © 2011 Wiley Periodicals, Inc.</P>
Han, Kyungx2010,Ah,Chon, Suk,Chung, Choon Hee,Lim, Soo,Lee, Kwan‐,Woo,Baik, SeiHyun,Jung, Chang Hee,Kim, Dongx2010,Sun,Park, Kyong Soo,Yoon, Kunx2010,Ho,Lee, Inx2010,Kyu,Cha, Bongx2010 Blackwell Publishing Ltd 2018 DIABETES OBESITY AND METABOLISM Vol.20 No.10
<P><B>Aim</B></P><P>To evaluate the efficacy and safety of ipragliflozin vs placebo as add‐on therapy to metformin and sitagliptin in Korean patients with type 2 diabetes mellitus (T2DM).</P><P><B>Methods</B></P><P>This double‐blind, placebo‐controlled, multi‐centre, phase III study was conducted in Korea in 2015 to 2017. Patients were randomized to receive either ipragliflozin 50 mg/day or placebo once daily for 24 weeks in addition to metformin and sitagliptin. The primary endpoint was the change in glycated haemoglobin (HbA1c) from baseline to end of treatment (EOT).</P><P><B>Results</B></P><P>In total, 143 patients were randomized and 139 were included in efficacy analyses (ipragliflozin: 73, placebo: 66). Baseline mean (SD) HbA1c levels were 7.90 (0.69)% for ipragliflozin add‐on and 7.92 (0.79)% for placebo. The corresponding mean (SD) changes from baseline to EOT were −0.79 (0.59)% and 0.03 (0.84)%, respectively, in favour of ipragliflozin (adjusted mean difference −0.83% [95% CI −1.07 to −0.59]; <I>P</I> < .0001). More ipragliflozin‐treated patients than placebo‐treated patients achieved HbA1c target levels of <7.0% (44.4% vs 12.1%) and < 6.5% (12.5% vs 1.5%) at EOT (<I>P</I> < .05 for both). Fasting plasma glucose, fasting serum insulin, body weight and homeostatic model assessment of insulin resistance decreased significantly at EOT, in favour of ipragliflozin (adjusted mean difference −1.64 mmol/L, −1.50 μU/mL, −1.72 kg, and −0.99, respectively; <I>P</I> < .05 for all). Adverse event rates were similar between groups (ipragliflozin: 51.4%; placebo: 50.0%). No previously unreported safety concerns were noted.</P><P><B>Conclusions</B></P><P>Ipragliflozin as add‐on to metformin and sitagliptin significantly improved glycaemic variables and demonstrated a good safety profile in Korean patients with inadequately controlled T2DM.</P>
Cho, Hyunx2010,Ji,Kang, Jeongx2010,Han,Kim, Teoan,Park, Kwangx2010,Kyun,Kim, Cheorlx2010,Ho,Lee, Inx2010,Seon,Min, Kwan‐,Sik,Magae, Junji,Nakajima, Hiroo,Bae, Youngx2010,Seuk,Chang, Wiley Subscription Services, Inc., A Wiley Company 2009 Journal of cellular biochemistry Vol.107 No.2
<P><B>Abstract</B></P><P>Fibrosis in glomerulosclerosis causes progressive loss of renal function. Transforming growth factor (TGF)‐β, one of the major profibrotic cytokines, induces the synthesis of plasminogen activator inhibitor (PAI)‐1, a factor that plays a crucial role in the development of fibrosis. Here, we found that an isoprenoid antibiotic, ascofuranone, suppresses expression of profibrotic factors including matrix proteins and PAI‐1 induced by TGF‐β in renal fibroblasts. Ascofuranone selectively inhibits phosphorylation of epidermal growth factor receptor (EGFR), and downstream kinases such as Raf‐1, MEK‐1/2, and ERK‐1/2. PAI‐1 transcription also is suppressed by treatment with kinase inhibitors for MEK‐1/2 or EGFR, and with small interfering RNA for EGFR. Ascofuranone inhibits cellular metalloproteinase activity, and an inhibitor of metalloproteinases suppresses EGFR phosphorylation and PAI‐1 transcription. These results suggest that ascofuranone suppresses expression of profibrotic factors through the inhibition of an EGFR‐dependent signal transduction pathway activated by metalloproteinases. J. Cell. Biochem. 107: 335–344, 2009. © 2009 Wiley‐Liss, Inc.</P>
Min, Cheonx2010,Ki,Wikesjö,, Ulf M. E.,Park, Jungx2010,Chul,Chae, Gyungx2010,Joon,Pippig, Susanne D.,Bastone, Patrizia,Kim, Changx2010,Sung,Kim, Chongx2010,Kwan Blackwell Publishing Ltd 2011 Journal of Clinical Periodontology Vol.38 No.3
<P>Min C‐K, Wikesjö UME, Park J‐C, Chae G‐J, Pippig SD, Bastone P, Kim C‐S, Kim C‐K. Wound healing/regeneration using recombinant human growth/differentiation factor‐5 in an injectable poly‐lactide‐co‐glycolide‐acid composite carrier and a one‐wall intra‐bony defect model in dogs. J Clin Peridontol 2011; 38: 261–268. 38: 261–268. doi: 10.1111/j.1600‐051X.2010.01691.x.</P><P><B>Abstract</B></P><P><B>Objective: </B> The purpose of this study was to evaluate the effect of recombinant human growth/differentiation factor‐5 (rhGDF‐5) on periodontal wound healing/regeneration using an injectable poly‐lactide‐co‐glycolide‐acid (PLGA) composite carrier and an established defect model.</P><P><B>Methods: </B> Bilateral 4 × 5 mm (width × depth) one‐wall, critical‐size, intra‐bony periodontal defects were surgically created at the second and the fourth mandibular pre‐molar teeth in 15 Beagle dogs. The animals were randomized to receive (using a split‐mouth design; defect sites in the same jaw quadrant getting the same treatment) rhGDF‐5 high dose (188 <I>μ</I>g/defect) <I>versus</I> sham‐surgery control (five animals), rhGDF‐5 mid dose (37 <I>μ</I>g/defect) <I>versus</I> carrier control (five animals), and rhGDF‐5 low dose (1.8 <I>μ</I>g/defect) <I>versus</I> treatment reported elsewhere (five animals). The animals were euthanized for histometric analysis following an 8‐week healing interval.</P><P><B>Results: </B> Clinical healing was uneventful. The rhGDF‐5/PLGA construct was easy to assemble and apply. The rhGDF‐5 high dose supported significantly increased bone formation compared with the low‐dose, sham‐surgery, and carrier controls (<I>p</I><0.05) and induced significantly increased cementum formation compared with the controls (<I>p</I><0.05). Root resorption/ankylosis or other aberrant healing events were not observed.</P><P><B>Conclusion: </B> rhGDF‐5 appears to effectively support periodontal wound healing/regeneration in a dose‐dependent order; the PLGA composite appears to be an effective ease‐of‐use candidate for carrier technology.</P>
An, Hyunx2010,Jin,Kim, Jungx2010,Yeon,Kim, Woonx2010,Hae,Gwon, Mix2010,Gyeong,Gu, Hye Min,Jeon, Min Ji,Han, Sangx2010,Mi,Pak, Sok Cheon,Lee, Chongx2010,Kee,Park, In Sook,Park, Kwan‐ John Wiley and Sons Inc. 2018 British journal of pharmacology Vol.175 No.23
<P><B>Background and Purpose</B></P><P>Atopic dermatitis (AD) is a multifactorial skin condition with complex interactions of innate and adaptive immune responses. There are several existing therapies for AD, including topical glucocorticosteroids, emollients, phototherapies, calcineurin inhibitors and immunosuppressants, such as cyclosporine A. Although these therapies reduce inflammation, they also cause serious side effects. Therefore, it is necessary to develop new therapeutic approaches for AD treatment without side effects. There are several studies on natural materials or toxins, such as herbs, ginseng extract and snake venom, for AD treatment. However, treatment of AD with bee venom and its major component, melittin has rarely been studied.</P><P><B>Experimental Approach</B></P><P>Effects of bee venom and melittin were studied in a model of AD <I>in vivo</I> induced by 1‐chloro‐2,4‐dinitrobenzene (DNCB) in female Balb/c mice and in cultures of human keratinocytes, stimulated by TNF‐α/IFN‐γ. The potential pharmacological effects of bee venom and melittin on these <I>in vivo</I> and <I>in vitro</I> AD‐like skin disease models were studied.</P><P><B>Key Results</B></P><P>Bee venom and melittin exhibited potent anti‐atopic activities, shown by decreased AD‐like skin lesions, induced by DNCB in mice. <I>In vitro</I> studies using TNF‐α/IFN‐γ‐stimulated human keratinocytes showed that bee venom and melittin inhibited the increased expression of chemokines, such as CCL17 and CCL22, and pro‐inflammatory cytokines, including IL‐1β, IL‐6 and IFN‐γ, through the blockade of the NF‐κB and STAT signalling pathways.</P><P><B>Conclusions and Implications</B></P><P>Our results suggest that bee venom and melittin would be suitable for epicutaneous application, as topical administration is often appropriate for the treatment of AD.</P>
Park, Sang Kyu,Cho, Illhun,Gierschner, Johannes,Kim, Jin Hong,Kim, Jong H.,Kwon, Ji Eon,Kwon, Oh Kyu,Whang, Dong Ryeol,Park, Jungx2010,Hwa,An, Byeongx2010,Kwan,Park, Soo Young WILEY‐VCH Verlag 2016 Angewandte Chemie Vol.55 No.1
<P><B>Abstract</B></P><P>We report on a molecularly tailored 1:1 donor–acceptor (D‐A) charge‐transfer (CT) cocrystal that manifests strongly red‐shifted CT luminescence characteristics, as well as noteworthy reconfigurable self‐assembling behaviors. A loosely packed molecular organization is obtained as a consequence of the noncentrosymmetric chemical structure of molecule <B>A1</B>, which gives rise to considerable free volume and weak intermolecular interactions. The stacking features of the CT complex result in an external stimuli‐responsive molecular stacking reorganization between the mixed and demixed phases of the D‐A pair. Accordingly, high‐contrast fluorescence switching (red↔blue) is realized on the basis of the strong alternation of the electronic properties between the mixed and demixed phases. A combination of structural, spectroscopic, and computational studies reveal the underlying mechanism of this stimuli‐responsive behavior.</P>
Park, Jimin,Du, Ping,Jeon, Jinx2010,Kyung,Jang, Gun Hyuk,Hwang, Mintai Peter,Han, Hyungx2010,Seop,Park, Kwideok,Lee, Kwan Hyi,Lee, Jeex2010,Wook,Jeon, Hojeong,Kim, Yux2010,Chan,Park, Jong Woon WILEY‐VCH Verlag 2015 Angewandte Chemie Vol.127 No.49
<P><B>Abstract</B></P><P>Although the use of reactive oxygen species (ROS) has been extensively studied, current systems employ external stimuli such as light or electrical energy to produce ROS, which limits their practical usage. In this report, biocompatible metals were used to construct a novel electrochemical system that can spontaneously generate H<SUB>2</SUB>O<SUB>2</SUB> without any external light or voltage. The corrosion of Mg transfers electrons to Au‐decorated oxidized Ti in an energetically favorable process, and the spontaneous generation of H<SUB>2</SUB>O<SUB>2</SUB> in an oxygen reduction reaction was revealed to occur at titanium by combined spectroscopic and electrochemical analyses. The controlled release of H<SUB>2</SUB>O<SUB>2</SUB> noticeably enhanced in vitro angiogenesis even in the absence of growth factors. Finally, a new titanium implant prototype was developed by Mg incorporation, and its potential for promoting angiogenesis was demonstrated.</P>
Yun, Sun Woo,Kim, Jong H.,Shin, Seunghoon,Yang, Hoichang,An, Byeongx2010,Kwan,Yang, Lin,Park, Soo Young WILEY‐VCH Verlag 2012 Advanced Materials Vol.24 No.7
<P><B>Novel π–conjugated cyanostilbene‐based semiconductors</B> (Hex‐3,5‐TFPTA and Hex‐4‐TFPTA) with tight molecular stacking and optimized energy levels are synthesized. Hex‐4‐TFPTA exhibits high‐performance n‐type organic field‐effect transistor (OFET) properties with electron mobilities as high as 2.14 cm<SUP>2</SUP> V<SUP>−1</SUP>s<SUP>−1</SUP> and on‐off current ratios >10<SUP>6</SUP>.</P>
Lee, Youjin,Jung, Jieun,Cho, Kyung Jin,Lee, Seoungx2010,Kwan,Park, Jongx2010,Wan,Oh, ILx2010,Hoan,Kim, Gi Jin Wiley Subscription Services, Inc., A Wiley Company 2013 Journal of cellular biochemistry Vol.114 No.1
<P><B>Abstract</B></P><P>Hypoxia triggers physiological and pathological cellular processes, including proliferation, differentiation, and death, in several cell types. Mesenchymal stem cells (MSCs) derived from various tissues have self‐renewal activity and can differentiate towards multiple lineages. Recently, it has been reported that hypoxic conditions tip the balance between survival and death by hypoxia‐induced autophagy, although the underlying mechanism is not clear. The objectives of this study are to compare the effect of hypoxia on the self‐renewal of bone marrow‐derived mesenchymal stem cells (BM‐MSCs) and placental chorionic plate‐derived mesenchymal stem cells (CP‐MSCs) and to investigate the regulatory mechanisms of self‐renewal in each MSC type during hypoxia. The expression of self‐renewal markers (e.g., Oct4, Nanog, Sox2) was assessed in both cell lines. PI3K and stem cell factor (SCF) expression gradually increased in CP‐MSCs but were markedly downregulated in BM‐MSCs by hypoxia. The phosphorylation of ERK and mTOR was augmented by hypoxia in CP‐MSCs compared to control. Also, the expression of LC3 II, a component of the autophagosome and the hoof‐shaped autophagosome was detected more rapidly in CP‐MSCs than in BM‐MSCs under hypoxia. Hypoxia induced the expression of SCF in CP‐MSCs and increased SCF/c‐kit pathway promotes the self‐renewal activities of CP‐MSCs via an autocrine/paracrine mechanism that balances cell survival and cell death events by autophagy. These activities occur to a greater extent in CP‐MSCs than in BM‐MSCs through regulating the phosphorylation of mTOR. These findings will provide useful guidelines for better understanding the function of SCF/c‐kit in the self‐renewal and autophagy‐regulated mechanisms that promote of MSC survival. J. Cell. Biochem. 114: 79–88, 2012. © 2012 Wiley Periodicals, Inc.</P>