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Baek, Yi-Yong,Cho, Dong Hui,Choe, Jongseon,Lee, Hansoo,Jeoung, Dooil,Ha, Kwon-Soo,Won, Moo-Ho,Kwon, Young-Guen,Kim, Young-Myeong Elsevier 2012 european journal of pharmacology Vol.674 No.2
<P><B>Abstract</B></P><P>Taurine, a non essential sulfur-containing amino acid, plays a critical role in cardiovascular functions. We here examined the effect of taurine on angiogenesis and its underlying signal pathway. Taurine treatment increased angiogenesis <I>in vitro</I> and <I>in vivo</I>, which was followed by activation of the phosphatidylinositol 3-kinase (PI3K)/Akt, MEK/ERK, and Src/FAK signaling pathways. Further, taurine promoted endothelial cell cycle progression to the S and G2/M phases by up-regulating the positive cell cycle proteins, particularly cyclins D1 and B, as well as down-regulating the negative cell cycle proteins, p53 and p21<SUP>WAF1/CIP1</SUP>, resulting in Rb phosphorylation. This angiogenic event was inhibited by inhibitors of PI3K and MEK. In addition, a PI3K inhibitor blocked the activation of Akt and ERK, while Akt knockdown did not affect taurine-induced ERK activation, indicating that PI3K is an upstream mediator of both MEK and Akt. Taurine-induced endothelial cell migration was suppressed by Src inhibitor, but not by other inhibitors, suggesting that the increase in cell migration is regulated by Src-dependent pathway. Moreover, inhibition of cellular taurine uptake by β-alanine and taurine transporter knockdown promoted taurine-induced cell proliferation, ERK and Akt activation, and <I>in vivo</I> angiogenesis, suggesting that extracellular taurine induces angiogenesis. However, taurine did not induce vascular inflammation and permeability <I>in vitro</I> and <I>in vivo</I>. These data demonstrate that extracellular taurine promotes angiogenesis by Akt- and ERK-dependent cell cycle progression and Src/FAK-mediated cell migration without inducing vascular inflammation, indicating that it is potential use for the treatment of vascular dysfunction-associated human diseases.</P>
Baek Jung-Hwan,Kim Myung Sup,Jung Hye Ryeon,Hwang Min-Seon,Lee Chan-ho,Han Dai Hoon,Lee Yong-ho,Yi Eugene C.,Im Seung-Soon,Hwang Ilseon,Kim Kyungeun,Chung Joon-Yong,Chun Kyung-Hee 생화학분자생물학회 2023 Experimental and molecular medicine Vol.55 No.-
Nonalcoholic fatty liver disease (NAFLD) occurs due to the accumulation of fat in the liver, leading to fatal liver diseases such as nonalcoholic steatohepatitis (NASH) and cirrhosis. Elucidation of the molecular mechanisms underlying NAFLD is critical for its prevention and therapy. Here, we observed that deubiquitinase USP15 expression was upregulated in the livers of mice fed a high-fat diet (HFD) and liver biopsies of patients with NAFLD or NASH. USP15 interacts with lipid-accumulating proteins such as FABPs and perilipins to reduce ubiquitination and increase their protein stability. Furthermore, the severity of NAFLD induced by an HFD and NASH induced by a fructose/palmitate/cholesterol/trans-fat (FPC) diet was significantly ameliorated in hepatocyte-specific USP15 knockout mice. Thus, our findings reveal an unrecognized function of USP15 in the lipid accumulation of livers, which exacerbates NAFLD to NASH by overriding nutrients and inducing inflammation. Therefore, targeting USP15 can be used in the prevention and treatment of NAFLD and NASH.
Baek, Jayeon,Park, Soomin,Song, Chyan Kyung,Kim, Tae Yong,Nam, Inho,Lee, Jong Min,Han, Jeong Woo,Yi, Jongheop The Royal Society of Chemistry 2015 Chemical communications Vol.51 No.81
<P>A <I>c</I>-channel formed inside stacked (001) planes in rutile TiO<SUB>2</SUB> exhibits the lowest energy barrier for Li migration. Based on this rationale, we proposed a three-dimensional TiO<SUB>2</SUB> sphere comprised of radially assembled <I>c</I>-channel specialized nanorods in order to maximize Li storage.</P> <P>Graphic Abstract</P><P>Motivated by anisotropic Li mobility inside a rutile crystal, the <I>c</I>-channel specialized nanorods are radially assembled to form a 3D dendritic TiO<SUB>2</SUB> sphere, which facilitate Li movement during the charge/discharge process. <IMG SRC='http://pubs.rsc.org/services/images/RSCpubs.ePlatform.Service.FreeContent.ImageService.svc/ImageService/image/GA?id=c5cc04864h'> </P>
In vitro and in vivo anti-inflammatory activities of Korean Red Ginseng-derived components
Baek, Kwang-Soo,Yi, Young-Su,Son, Young-Jin,Yoo, Sulgi,Sung, Nak Yoon,Kim, Yong,Hong, Sungyoul,Aravinthan, Adithan,Kim, Jong-Hoon,Cho, Jae Youl The Korean Society of Ginseng 2016 Journal of Ginseng Research Vol.40 No.4
Background: Although Korean Red Ginseng (KRG) has been traditionally used for a long time, its anti-inflammatory role and underlying molecular and cellular mechanisms have been poorly understood. In this study, the anti-inflammatory roles of KRG-derived components, namely, water extract (KRG-WE), saponin fraction (KRG-SF), and nonsaponin fraction (KRG-NSF), were investigated. Methods: To check saponin levels in the test fractions, KRG-WE, KRG-NSF, and KRG-SF were analyzed using high-performance liquid chromatography. The anti-inflammatory roles and underlying cellular and molecular mechanisms of these components were investigated using a macrophage-like cell line (RAW264.7 cells) and an acute gastritis model in mice. Results: Of the tested fractions, KGR-SF (but not KRG-NSF and KRG-WE) markedly inhibited the viability of RAW264.7 cells, and splenocytes at more than 500 mg/mL significantly suppressed NO production at $100{\mu}g/mL$, diminished mRNA expression of inflammatory genes such as inducible nitric oxide synthase, cyclooxygenase-2, tumor necrosis factor-${\alpha}$, and interferon-${\beta}$ at $200{\mu}g/mL$, and completely blocked phagocytic uptake by RAW264.7 cells. All three fractions suppressed luciferase activity triggered by interferon regulatory factor 3 (IRF3), but not that triggered by activator protein-1 and nuclear factor-kappa B. Phospho-IRF3 and phospho-TBK1 were simultaneously decreased in KRG-SF. Interestingly, all these fractions, when orally administered, clearly ameliorated the symptoms of gastric ulcer in HCl/ethanol-induced gastritis mice. Conclusion: These results suggest that KRG-WE, KRG-NSF, and KRG-SF might have anti-inflammatory properties, mostly because of the suppression of the IRF3 pathway.
Selective production of 1,3-butadiene using glucose fermentation liquor
Baek, Jayeon,Kim, Tae Yong,Kim, Wooyoung,Lee, Hee Jong,Yi, Jongheop The Royal Society of Chemistry 2014 GREEN CHEMISTRY Vol.16 No.7
<P>The production of 2,3-butanediol from glucose fermentation products and its subsequent esterification and conversion to 1,3-butadiene is reported. The addition of formic acid and acetic acid (C1–C2 acids) to the esterification reaction mixture resulted in yields of the diesters of 70% and 85%, without the loss of C1–C2 acids during the reaction. In the pyrolysis step, a highly selective (94% and 82% for formic acid 2-formyloxy-1-methyl-propyl ester and acetic acid 2-acetoxy-1-methyl-propyl ester, respectively) C–O cleavage to 1,3-butadiene over diesters was achieved without a catalyst. In the case of acetic acid, 100% was recovered, whereas in the case of formic acid, only 20% was recovered. Based on these results, it can be concluded that using glucose fermentation liquor as the starting material with external addition of acetic acid (2,3-butanediol : formic acid : acetic acid = 1 : 0.5 : 2.5), 70% yield of 1,3-butadiene can be achieved where the loss of formic acid is compensated by the acid in the starting material.</P> <P>Graphic Abstract</P><P>An alternative biomass-based route to the petrochemical process for the production of 1,3-butadiene has been developed using glucose fermentation products. <IMG SRC='http://pubs.rsc.org/services/images/RSCpubs.ePlatform.Service.FreeContent.ImageService.svc/ImageService/image/GA?id=c4gc00485j'> </P>