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Histone H3K27 Demethylase JMJD3 in Cooperation with NF-κB Regulates Keratinocyte Wound Healing
Na, Jungtae,Lee, Kwanghyun,Na, Wonho,Shin, Jee-Yoon,Lee, Min-Jung,Yune, Tae Young,Lee, Hae Kwang,Jung, Han-Sung,Kim, Won Sun,Ju, Bong-Gun Elsevier 2016 The Journal of investigative dermatology Vol.136 No.4
Lee, Kwanghyun,Na, Wonho,Lee, Jee Youn,Na, Jungtae,Cho, Heejung,Wu, Hongjin,Yune, Tae Young,Kim, Won‐,Sun,Ju, Bong‐,Gun Blackwell Publishing Ltd 2012 Journal of Neurochemistry Vol.122 No.2
<P><I>J. Neurochem.</I> (2012) <B>122</B>, 272–282.</P><P><B>Abstract</B></P><P>The inflammatory response contributes substantially to secondary injury cascades after spinal cord injury, with both neurotoxic and protective effects. However, epigenetic regulations of inflammatory genes following spinal cord injury have yet to be characterized thoroughly. In this study, we found that histone H3K27me3 demethylase Jmjd3 expression is acutely up‐regulated in blood vessels of the injured spinal cord. We also observed up‐regulation of <I>Jmjd3</I> gene expression in bEnd.3 endothelial cells that were subjected to oxygen‐glucose deprivation/reperfusion injury. When <I>Jmjd3</I> was depleted by siRNA, oxygen‐glucose deprivation/reperfusion injury‐induced up‐regulation of IL‐6 was significantly inhibited. In addition, Jmjd3 associated with NF‐κB (p65/p50) and CCAAT‐enhancer‐binding protein β at the <I>IL‐6</I> gene promoter. The recruitment of Jmjd3 coincided with decreased levels of tri‐methylated H3K27 as well as increased levels of mono‐methylated H3K27 at the <I>IL‐6</I> gene promoter. Furthermore, <I>Jmjd3</I> depletion did not result in significant changes of methylation level of H3K27 at the <I>IL‐6</I> gene promoter. Collectively, our findings imply that Jmjd3‐mediated H3K27me3 demethylation is crucial for <I>IL‐6</I> gene activation in endothelial cells, and this molecular event may regulate acute inflammatory response and integrity of the blood‐spinal cord barrier following spinal cord injury.</P>
자동차 충돌안전도 해석용 유한요소 인체 모델 개발 : Part Ⅱ 5% 성인 여성 모델
나상진(Sangjin Na),황대현(Daehyun Hwang),사성진(Sungjin Sah),이광희(Kwanghee Lee),영정태(Jungtae Yang),최형연(Hyoungyun Choi),이인혁(Inhyuk Lee),이진희(Jinhee Lee) 한국자동차공학회 2002 한국자동차공학회 Symposium Vol.2002 No.11
The Small female driver is much more vulnerable during the airbag deployment since they tend to sit on the fore side of seat while driving. In order to evaluate the aggressivity of airbag deployment on small female, so called "Out of Position" problem, it is very often to employ the Hybrid Ⅲ 5% dummy. The lack of biofidelity of Hybrid Ⅲ 5% dummy, however reveals the limits to the understanding of OOP related injury mechanism. Accordingly, a finite element model for small female(5%) has been proposed in this study. As a first step, multi-body rigid model, FARB(Female Articulated Rigid Body) has been developed and validated. Some parametric OOP simulation results will be also presented.
Bak, Dong-Ho,Na, Jungtae,Choi, Mi Ji,Lee, Byung Chul,Oh, Chang Taek,Kim, Jeom-Yong,Han, Hae Jung,Kim, Moo Joong,Kim, Tae Ho,Kim, Beom Joon D.A. Spandidos 2018 International journal of molecular medicine Vol.42 No.5
<P>Apoptosis and oxidative stress are essential for the pathogenesis of acute liver failure and fulminant hepatic failure. Human placental hydrolysate (hPH) has been reported to possess antioxidant and anti-inflammatory properties. In the present study, the protective effects of hPH against D-galactosamine (D-GalN)- and lipopolysaccharide (LPS)-induced hepatocyte apoptosis were investigated <I>in vivo</I>. In addition, the molecular mechanisms underlying the anti-apoptotic activities of hPH against D-GalN-induced cell death <I>in vitro</I> were examined. Male Sprague-Dawley rats were injected with D-GaIN/LPS with or without the administration of hPH. Rats were sacrificed 24 h after D-GaIN/LPS intraperitoneal injection, and the blood and liver samples were collected for future inflammation and hepatotoxicity analyses. Changes in cell viability, apoptosis protein expression, mitochondrial mass, mitochondrial membrane potential, reactive oxygen species generation, and the levels of proteins and mRNA associated with a protective mechanism were determined in HepG2 cells pretreated with hPH for 2 h prior to D-GalN exposure. The findings suggested that hPH treatment effectively protected against D-GalN/LPS-induced hepatocyte apoptosis by reducing the levels of alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase, interleukin-6, and tumor necrosis factor-α, and increasing the level of proliferating cell nuclear antigen. It was also found that hPH inhibited the apoptotic cell death induced by D-GalN. hPH activated the expression of antioxidant enzymes, including superoxide dismutase, glutathione peroxidase, and catalase, which were further upregulated by the Kelch-like ECH2-associated protein 1-p62-nuclear factor-erythroid 2-related factor 2 pathway, a component of oxidative stress defense mechanisms. Furthermore, hPH markedly reduced cytosolic and mitochondrial reactive oxygen species and rescued mitochondrial loss and dysfunction through the reduction of damage-regulated autophagy modulator, p53, and C/EBP homologous protein. Collectively, hPH exhibited a protective role in hepatocyte apoptosis by inhibiting oxidative stress and maintaining cell homeostasis. The underlying mechanisms may be associated with the inhibition of endoplasmic reticulum stress and minimization of the autophagy progress.</P>
( Ga Ram Ahn ),( Joon Seok ),( Jungtae Na ),( Beom Joon Kim ),( Chang Kwun Hong ) 대한피부과학회 2017 대한피부과학회 학술발표대회집 Vol.69 No.2
Background: Botulinum toxin A (BTX-A) is clinically used for muscular disorders, migraine, hyperhidrosis and cosmetics by preventing the release of neurotransmitter acetylcholine into synaptic cleft. Objectives: The aim of this study is to investigate the efficacy and safety of newly developed BTX-A product (Korea) compared to conventional BTX-A (USA) for the reduction of muscle hypertrophy in Myostatin-deficient (Mstn<sup>-/-</sup>) mouse. Methods: Two different BTX-As were injected on the hindlimb of Mstn<sup>-/-</sup>mouse. Since then, serial sciatic nerve conduction study (NCS), X-ray, 3D micro-CT and muscle biopsy was done. Results: Administration of BTX-A in both product group induced denervation-mediated atrophy and alleviated muscle hypertrophy generated in Mstn<sup>-/-</sup> mice. On day 56, newly developed BTX-A product group showed significant suppression in NCS compared with conventional BTX-A product group. Conclusion: In this study, the results suggest that both BTX-A regulate skeletal muscle size and the number and diameter of myofibers. Also, newly developed BTX-A product seems to have longer duration compared with conventional BTX-A product in the ability to act in a local area.
( Guk Jin Jeong ),( Jae Min Kim ),( Jungtae Na ),( Kapsok Li ),( Beom Joon Kim ) 대한피부과학회 2017 대한피부과학회 학술발표대회집 Vol.69 No.2
Background: Glycosaminoglycans (GAGs) are known to play an important role in the anti-aging process of skin. However, the exact molecular mechanism underlying the anti-aging effect of GAGs is not fully understood. Objectives: This study was conducted to investigate the influence of GAGs on proliferation, collagen synthesis, and collagen synthesis-related signaling pathways in human dermal fibroblasts (HDFs). Methods: HDFs obtained by skin biopsy were treated with differently concentrated GAGs. Viability and proliferation was determined using an MTT assay. RT-qPCR and ELISA were used for quantitative determination of collagen synthesis. Enzyme and gene expression related with collagen turnover process were evaluated by Western blot and immunocytochemistry. Results: GAGs stimulated fibroblast proliferation and the synthesis of type I collagen. Furthermore, GAGs consistently reduced MMP-1 and increased TIMP-1 via inhibition of ERK signaling as well as activation of TGF-β/SMAD signaling in HDFs. Conclusion: Our findings indicate the application of GAGs as potential effective anti-aging agents to reduce wrinkles.
( Sun Hye Shin ),( Jae Wan Park ),( Esther Lee ),( Byung Chul Lee ),( Jungtae Na ),( Kwang Ho Yoo ),( Beom Joon Kim ),( Myeung Nam Kim ) 대한피부과학회 2020 대한피부과학회 학술발표대회집 Vol.72 No.1
Background: Recent developments in material technology have revealed boehmite as a new therapeutic modality for use in wound healing and scar reduction, indicating its beneficial effects. However, the biological bases of the beneficial effects of boehmite remain unknown, and the use of boehmite to promote hair growth has not yet been studied. Objectives: This study was aimed to investigate the effect of boehmite on hair growth and the underlying mechanism. Methods: Minoxidil 3%, boehmite 1%, 3%, 5% and control vehicle cream were topically applied to the shaved dorsal skin of C3H/HeJ mice 5 days per week for 7 weeks. For in vitro model, we observed dose-dependent proliferation of human dermal papilla cell (hDPC). Reverse transcriptionquantitative polymerase chain reaction (qPCR) and western blot was carried out for expression analysis of hair growth related genes. Results: The length and size of hair follicle significantly increased in boehmite-treated mice. Boehmite increased hDPC viability, alkaline phosphatase (ALP) activity, AKT/GSK3/β-catenin pathway activity, anagen-related gene expression and VEGF secretion. In addition, it accelerated hair regrowth in a catagen-anagen transition model via upregulation of β-catenin signaling and follicular cell proliferation. Conclusion: Our results indicate that bohemite accelerates hair growth, partly via its effects on critical events in the active phase of the hair follicle cycle.