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Lee Bonggi,An Hye Jin,Kim Dae Hyun,Lee Min-Kyeong,Jeong Hyeon Hak,Chung Ki Wung,고영훈,Seo Arnold Y.,Kim Il Yong,Seong Je Kyung,Yu Byung Pal,LEE, JAE-WON,Im Eunok,Lee In-Kyu,Lee Myung-Shik,Yamada Ken-ich 생화학분자생물학회 2022 Experimental and molecular medicine Vol.54 No.-
The vitamin-C-synthesizing enzyme senescent marker protein 30 (SMP30) is a cold resistance gene in Drosophila, and vitamin C concentration increases in brown adipose tissue post-cold exposure. However, the roles of SMP30 in thermogenesis are unknown. Here, we tested the molecular mechanism of thermogenesis using wild-type (WT) and vitamin C-deficient SMP30-knockout (KO) mice. SMP30-KO mice gained more weight than WT mice without a change in food intake in response to short-term high-fat diet feeding. Indirect calorimetry and cold-challenge experiments indicated that energy expenditure is lower in SMP30-KO mice, which is associated with decreased thermogenesis in adipose tissues. Therefore, SMP30-KO mice do not lose weight during cold exposure, whereas WT mice lose weight markedly. Mechanistically, the levels of serum FGF21 were notably lower in SMP30-KO mice, and vitamin C supplementation in SMP30-KO mice recovered FGF21 expression and thermogenesis, with a marked reduction in body weight during cold exposure. Further experiments revealed that vitamin C activates PPARα to upregulate FGF21. Our findings demonstrate that SMP30-mediated synthesis of vitamin C activates the PPARα/FGF21 axis, contributing to the maintenance of thermogenesis in mice.
Small RNAs induce the activation of the pro‐inflammatory TLR7 signaling pathway in aged rat kidney
Lee, Eun Kyeong,Chung, Ki Wung,Kim, Ye Ra,Ha, Sugyeong,Kim, Sung Dae,Kim, Dae Hyun,Jung, Kyung Jin,Lee, Bonggi,Im, Eunok,Yu, Byung Pal,Chung, Hae Young John Wiley and Sons Inc. 2017 Aging cell Vol.16 No.5
<P><B>Summary</B></P><P>We have recently reported that TLR‐related genes, including TLR7, are upregulated during aging. However, the role of TLR7 and its endogenous ligand in inflammation related to aging is not well defined. Here, we established that small RNAs trigger age‐related renal inflammation <I>via</I> TLR7 signaling pathway. We first investigated the expression changes of nine different TLRs in kidney of 6‐month‐old young rats and 20‐month‐old aged rats. The results revealed that the expression of TLR7 was the highest among nine TLRs in kidney of old rats compared to the young aged rats. Next, to assess the role of cellular RNA as a TLR7 ligand, we treated a renal tubular epithelial cell line with total RNA isolated from the kidney of young and old rats. The results showed that RNA isolated from old rats showed higher expression of TLR7, IL1β, and TNFα compared to that from young rats. Furthermore, RNA isolated from old rats induced IKKα/β/JNK/NF‐κB activation. To identify RNA that activates TLR7, we isolated small and large RNAs from old rat kidney and found that small RNAs increased TLR7 expression in cells. Finally, to investigate the local inflammatory response by small RNA, C57B/L6 mice were intraperitoneally injected with small RNAs isolated from young and old rats; thereby, RNA isolated from old rats induced higher inflammatory responses. Our study demonstrates that renal small RNAs from aged rats induce pro‐inflammatory processes <I>via</I> the activation of the TLR7/IKKα/β/JNK/NF‐κB signaling pathway, and highlights its causative role as a possible therapeutic target in age‐related chronic renal inflammation.</P>
Lee, Jonghwan,Park, Cheolmin,Dao, Vinh Ai,Lee, Youn-Jung,Ryu, Kyungyul,Choi, Gyuho,Kim, Bonggi,Ju, Minkyu,Jeong, Chaehwan,Yi, Junsin American Scientific Publishers 2013 Journal of Nanoscience and Nanotechnology Vol.13 No.11
<P>In this paper, we present a detailed study on the local back contact (LBC) formation of rear-surface-passivated silicon solar cells, where both the LBC opening and metallization are realized by one-step alloying of a dot of fine pattern screen-printed aluminum paste with the silicon substrate. Based on energy dispersive spectrometer (EDS) and scanning electron microscopy (SEM) characterizations, we suggest that the aluminum distribution and the silicon concentration determine the local-back-surface-field (Al-p+) layer thickness, resistivity of the Al-p+ and hence the quality of the Al-p+ formation. The highest penetration of silicon concentration of 78.17% in aluminum resulted in the formation of a 5 microm-deep Al-p+ layer, and the minimum LBC resistivity of 0.92 x 10-6 omega cm2. The degradation of the rear-surface passivation due to high temperature of the LBC formation process can be fully recovered by forming gas annealing (FGA) at temperature and hydrogen content of 450 degrees C and 15%, respectively. The application of the optimized LBC of rear-surface-passivated by a dot of fine pattern screen(-) printed aluminum paste resulted in efficiency of up to 19.98% for the p-type czochralski (CZ) silicon wafers with 10.24 cm2 cell size at 649 mV open circuit voltage. By FGA for rear-surface passivation recovery, efficiencies up to 20.35% with a V(OC) of 662 mV, FF of 82%, and J(SC) of 37.5 mA/cm2 were demonstrated.</P>
이은경(Eun Kyeong Lee),김주현(Ju Hyun Kim),문경미(Kyoung Mi Moon),하수경(Sugyeong Ha),노상균(Sang-Gyun Noh),김대현(Dae Hyun Kim),이봉기(Bonggi Lee),김도현(Do Hyun Kim),김수정(Su Jeong Kim),울라술탄(Sultan Ullah),문형룡(Hyung Ryong Moo 한국생명과학회 2017 생명과학회지 Vol.27 No.2
본 연구에서는 (E)-2-(substituted benzylidene)-2,3-dihydro-1H-cyclopenta[a]naphthalen-1-one 유도체들을 합성했으며, 합성된 유도체들이 멜라닌 생성과정의 주요 효소인 tyrosinase 활성을 저해할 수 있는지에 대하여 확인하였다. 19종류의 유도체들의 tyrosinase 저해활성을 측정해본 결과, MHY3655 (IC50 = 0.1456 μM)가 가장 큰 저해활성을 나타냈으며 이는 대조군인 코직산(IC50 = 17.2 μM) 보다 큰 효능을 보였다. 게다가, Lineweaver-Burk 분석법을 이용하여 MHY3655가 경쟁적 저해 기전으로 tyrosinase 활성을 저해하였고, docking simulation으로 MHY3655가 tyrosinase에 직접 결합함을 재확인하였다. 마지막으로, B16F10 melanoma 세포에서 MHY3655의 세포독성을 평가한 결과 1-20 μM 사이의 MHY3655는 세포독성을 나타내지 않았다. 이상의 결과에서, 신물질 MHY3655은 우수한 tyrosinase 저해활성을 나타내며, 이는 미백 화장품 소재로서 활용할 가치가 있으리라 사료된다. The inhibition of tyrosinase, a key enzyme in mammalian melanin synthesis, plays an important role in preventing skin pigmentation and melanoma. Therefore, tyrosinase inhibitors are very important in the fields of medicine and cosmetics. However, only a few tyrosinase inhibitors are currently available because of their toxic effects on skin or lack of selectivity and stability. Therefore, we synthesized a novel series of (E)-2-(substituted benzylidene)-2,3-dihydro-1H-cyclopenta[a]naphthalen-1-one derivatives and evaluated their inhibitory effects on mushroom tyrosinase, with the aim of discovering a novel tyrosinase inhibitor. Among 19 derivatives, MHY3655 (IC50 = 0.1456 μM) showed the strongest inhibitory effect on tyrosinase activity compared to kojic acid (IC50 = 17.2 μM), a well-known tyrosinase inhibitor. In addition, MHY3655 showed competitive inhibition on Lineweaver-Burk plots. We confirmed that MHY3655 strongly interacts with mushroom tyrosinase residues through the docking simulation. Substitutions with a hydroxy group at both R2 and R4 in the phenyl ring indicated that these groups play a major role in the high binding affinity to tyrosinase. Further, MHY3655 did not show cytotoxicity at the concentrations tested in B16F10 melanoma cells. In conclusion, the novel compound MHY3655 potentially shows tyrosinase inhibitory activity, and it could be used as an ingredient in whitening cosmetics.
Heeyeon Ryu,Hyeon Hak Jeong,Seungjun Lee,Min-Kyeong Lee,Myeong-Jin Kim,Bonggi Lee The Korean Society for Microbiology and Biotechnol 2024 Journal of microbiology and biotechnology Vol.34 No.2
Macrophages are versatile immune cells that play crucial roles in tissue repair, immune defense, and the regulation of immune responses. In the context of skeletal muscle, they are vital for maintaining muscle homeostasis but macrophage-induced chronic inflammation can lead to muscle dysfunction, resulting in skeletal muscle atrophy characterized by reduced muscle mass and impaired insulin regulation and glucose uptake. Although the involvement of macrophage-secreted factors in inflammation-induced muscle atrophy is well-established, the precise intracellular signaling pathways and secretion factors affecting skeletal muscle homeostasis require further investigation. This study aimed to explore the regulation of macrophage-secreted factors and their impact on muscle atrophy and glucose metabolism. By employing RNA sequencing (RNA-seq) and proteome array, we uncovered that factors secreted by lipopolysaccharide (LPS)-stimulated macrophages upregulated markers of muscle atrophy and pro-inflammatory cytokines, while concurrently reducing glucose uptake in muscle cells. The RNA-seq analysis identified alterations in gene expression patterns associated with immune system pathways and nutrient metabolism. The utilization of gene ontology (GO) analysis and proteome array with macrophage-conditioned media revealed the involvement of macrophage-secreted cytokines and chemokines associated with muscle atrophy. These findings offer valuable insights into the regulatory mechanisms of macrophage-secreted factors and their contributions to muscle-related diseases.
Chung, Ki Wung,Kim, Kyung Mok,Choi, Yeon Ja,An, Hye Jin,Lee, Bonggi,Kim, Dae Hyun,Lee, Eun Kyeong,Im, Eunok,Lee, Jaewon,Im, Dong Soon,Yu, Byung Pal,Chung, Hae Young Informa UK (TaylorFrancis) 2017 AUTOPHAGY Vol.13 No.7
<P>Macroautophagy/autophagy is a central mechanism by which cells maintain integrity and homeostasis, and endotoxin-induced autophagy plays important roles in innate immunity. Although TLR4 stimulation mediated by lipopolysaccharide (LPS) also upregulates autophagy in hepatocytes and liver, its physiological role remains elusive. The objective of this study was to determine the role of LPS-induced autophagy in the regulation of liver lipid metabolism. LPS treatment (5 mg/kg) increased autophagy, as detected by LC3 conversion and transmission electron microscopy (TEM) analysis in C57BL6 mouse livers. AC2F hepatocytes also showed increased autophagic flux after LPS treatment (1 mu g/ml). To investigate the role of LPS-induced autophagy further, liver lipid metabolism changes in LPS-treated mice and fasted controls were compared. Interestingly, LPS-treated mice showed less lipid accumulation in liver than fasted mice despite increased fatty acid uptake and lipid synthesis-associated genes. In vitro analysis using AC2F hepatocytes demonstrated LPS-induced autophagy influenced the degradation of lipid droplets. Inhibition of LPS-induced autophagy using bafilomycin A(1) or Atg7 knockdown significantly increased lipid accumulation in AC2F hepatocytes. In addition, pretreatment with chloroquine aggravated LPS-induced lipid accumulation and inflammation in C57BL6 mouse livers. The physiological importance of autophagy was verified in LPS-treated young and aged rats. Autophagic response was diminished in LPS-treated aged rats and lipid metabolism was impaired during sepsis, indicating autophagy response is important for regulating lipid metabolism after endotoxin challenge. Our findings demonstrate endotoxin-induced autophagy is important for the regulation of lipid metabolism, and suggest that autophagy helps maintain lipid metabolism homeostasis during sepsis.</P>
Kim, Min Jo,An, Hye Jin,Kim, Dae Hyun,Lee, Bonggi,Lee, Hye Jin,Ullah, Sultan,Kim, Su Jeong,Jeong, Hyoung Oh,Moon, Kyoung Mi,Lee, Eun Kyeong,Yang, Jungho,Akter, Jinia,Chun, Pusoon,Moon, Hyung Ryong,Chu Elsevier 2018 Bioorganic & medicinal chemistry letters Vol.28 No.4
<P><B>Abstract</B></P> <P>The NAD<SUP>+</SUP>-dependent deacetylase SIRT1, which is associated with the improvement of metabolic syndromes, such as type 2 diabetes, is a well-known longevity-related gene. Several <I>in vitro</I> and <I>in vivo</I> studies have shown the known protective effects of SIRT1 activators, such as resveratrol and SRT1720, on diabetes- or obesity-induced fatty liver and insulin resistance. Here, we newly synthesized 18 benzoxazole hydrochloride derivatives based on the structure of resveratrol and SRT1720. We performed an <I>in vitro</I> SIRT1 activity assay to identify the strongest SIRT1 activator. The assay confirmed MHY2233 to be the strongest SIRT1 activator (1.5-fold more potent than resveratrol), and docking simulation showed that the binding affinity of MHY2233 was higher than that of resveratrol and SRT1720. To investigate its beneficial effects, db/db mice were orally administered MHY2233 for 1 month, and various metabolic parameters were assessed in the serum and liver tissues. MHY2233 markedly ameliorated insulin signaling without affecting body weight in db/db mice. In particular, the mRNA expression of lipogenic genes, such as acetyl CoA carboxylase, fatty acid synthase, and sterol regulatory element-binding protein, which increased in db/db mice, decreased following oral treatment with MHY2233.</P> <P>In conclusion, the novel SIRT1 activator MHY2233 reduced lipid accumulation and improved insulin resistance. This finding may contribute toward therapeutic approaches for fatty liver disease and glucose tolerance.</P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
송봉기(Bonggi Song),신성환(Seonghwan Shin),권민석(Minsuk Kwon),이인호(Inho Lee),양태형(Taehyoung Yang),송현석(Hyunseok Song) 한국자동차공학회 2016 한국자동차공학회 학술대회 및 전시회 Vol.2016 No.11
The smart headrest can detect gap between driver`s head and headrest. It is required that a technique calculate an optimal target distance. In this paper we study the characteristics of the sensor the underlying technology that can detect the distance between the driver`s head and the headrest. We suggest the 2 Channel sensor and 3 channel sensor using capacitive sensor. We use upper sensor, lower sensor and shoulder sensor. The 2 channel sensor consists of only upper sensor and lower sensor. We compare and evaluate the properties of each sensor. By the result, We know that the 2 channel pattern detection area is large and it was confirmed to be suitable for smart headrest.