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( Suyeon Jin ),( Chan Joo Lee ),( Gibbeum Lim ),( Sungha Park ),( Sang-hak Lee ),( Ji Hyung Chung ),( Jaewon Oh ),( Seok-min Kang ) 생화학분자생물학회 2023 BMB Reports Vol.56 No.12
C-reactive protein (CRP) is an inflammatory marker and risk factor for atherosclerosis and cardiovascular diseases. However, the mechanism through which CRP induces myocardial damage remains unclear. This study aimed to determine how CRP damages cardiomyocytes via the change of mitochondrial dynamics and whether survivin, an anti-apoptotic protein, exerts a cardioprotective effect in this process. We treated H9c2 cardiomyocytes with CRP and found increased intracellular ROS production and shortened mitochondrial length. CRP treatment phosphorylated ERK1/2 and promoted increased expression, phosphorylation, and translocation of DRP1, a mitochondrial fission-related protein, from the cytoplasm to the mitochondria. The expression of mitophagy proteins PINK1 and PARK2 was also increased by CRP. YAP, a transcriptional regulator of PINK1 and PARK2, was also increased by CRP. Knockdown of YAP prevented CRP-induced increases in DRP1, PINK1, and PARK2. Furthermore, CRP-induced changes in the expression of DRP1 and increases in YAP, PINK1, and PARK2 were inhibited by ERK1/2 inhibition, suggesting that ERK1/2 signaling is involved in CRP-induced mitochondrial fission. We treated H9c2 cardiomyocytes with a recombinant TAT-survivin protein before CRP treatment, which reduced CRP-induced ROS accumulation and reduced mitochondrial fission. CRP-induced activation of ERK1/2 and increases in the expression and activity of YAP and its downstream mitochondrial proteins were inhibited by TAT-survivin. This study shows that mitochondrial fission occurs during CRPinduced cardiomyocyte damage and that the ERK1/2-YAP axis is involved in this process, and identifies that survivin alters these mechanisms to prevent CRP-induced mitochondrial damage. [BMB Reports 2023; 56(12): 663-668]
Chung, Ji-Yun,Park, Hee Ra,Lee, Su-Jin,Lee, Sun-Hye,Kim, Jin Sik,Jung, Youn-Sang,Hwang, Sang Hyun,Ha, Nam-Chul,Seol, Won-Gi,Lee, Jaewon,Park, Bum-Joon United States and Canadian Academy of Pathology [e 2013 Laboratory investigation Vol.93 No.6
<P>Parkinson's disease (PD) is the second leading neurodegenerative disease, and is known to be induced by environmental factors or genetic mutations. Among the verified genetic mutations of PD, Parkin, isolated from the PARK2 locus, shows an autosomal recessive inheritance pattern and is known to be an E3 ligase. However, the physiological target of Parkin and the molecular mechanism of Parkin-deficiency-induced PD have not been clearly demonstrated until now. It has recently been proposed that inflammation, suggesting as a causal factor for PD, is enhanced by Parkin deficiency. Thus, we examined the relationship between inflammation-related factors and Parkin. Here, we provide the evidence that Parkin suppresses inflammation and cytokine-induced cell death by promoting the proteasomal degradation of TRAF2/6 (TNF-α receptor-associated factor 2/6). Overexpression of Parkin can reduce the half-lives of TRAF2 and TRAF6, whereas si-Parkin can extend them. However, mutant Parkins did not alter the expression of TRAF2/6. Thus, loss of Parkin enhances sensitivity to TNF-α- or IL-1β-induced JNK activation and NF-κB activation. Indeed, si-Parkin-induced apoptosis is suppressed by the knockdown of TRAF6 or TRAF2. We also observed elevated expression levels of TRAF6 and a reduction of IκB in an 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced PD mouse model. Moreover, elevated expression levels or aggregation of TRAF6 were detected in approximately half of the human PD tissues (7/15 cases) and 2 cases, respectively. In addition, TRAF6 and Parkin expression levels show a reverse relationship in human PD tissues. Our results strongly suggest that the reduction of Parkin or overexpression of TRAF2/6 by chronic inflammation would be the reason for occurrence of PD.</P>
Systematic Risks in the Options Market: Evidence from S&P 500 Index Options
Jaewon Park,Tong S. Kim 한국재무학회 2009 한국재무학회 학술대회 Vol.2009 No.05
The assumption of dynamic replication in no-arbitrage option pricing models does not hold in practice due to discreteness of trading hours as well as trading costs, which suggests the potential presence of preference-driven risk premiums. In this paper, we empirically show that discretely hedged S&P 500 index option portfolios are exposed to covariance and coskewness risk with the market portfolio. Using the three-moment CAPM of Kraus and Litzenberger (1976), we find that the rate of return of the portfolio significantly loads on the two risk factors, and their risk premiums are significantly positive. The equilibrium model complements the prevailing approach of the no-arbitrage framework, and reveals that the volatility smile is linked to investors’ preference on the unhedged market risks.
Optimum Morphology of Mixed-Olivine Mesocrystals for a Li-Ion Battery
Park, Kimin,Kim, Jaewon,Wi, Sungun,Lee, Sangheon,Hwang, Taehyun,Kim, Jaewook,Kang, Joonhyeon,Choi, Joon-Phil,Nam, Seunghoon,Park, Byungwoo American Chemical Society 2018 Inorganic Chemistry Vol.57 No.10
<P>In this present work, we report on the synthesis of micron-sized LiMn<SUB>0.8</SUB>Fe<SUB>0.2</SUB>PO<SUB>4</SUB> (LMFP) mesocrystals via a solvothermal method with varying pH and precursor ratios. The morphologies of resultant LMFP secondary particles are classified into two major classes, flakes and ellipsoids, both of which are featured by the mesocrystalline aggregates where the primary particles constituting LMFP secondary particles are crystallographically aligned. Assessment of the battery performance reveals that the flake-shaped LMFP mesocrystals exhibit a specific capacity and rate capability superior to those of other mesocrystals. The origin of the enhanced electrochemical performance is investigated in terms of primary particle size, pore structure, antisite-defect concentration, and secondary particle shape. It is shown that the shape of the secondary particle has just as much of a significant effect on the battery performance as the crystallite size and antisite defects do. We believe that this work provides a rule of design for electrochemically favorable meso/nanostructures, which is of great potential for improving battery performance by tuning the morphology of particles on multilength scales.</P><P>Micron-sized LiMn<SUB>0.8</SUB>Fe<SUB>0.2</SUB>PO<SUB>4</SUB> mesocrystals having various morphologies were facilely synthesized via a solvothermal method. The origin of the different electrochemical performances of the mesocrystals was investigated in terms of primary particle size, pore structure, antisite-defect concentration, and secondary particle shape. We believe that this work can provide a rule of design for the electrochemically favorable meso/nanostructures, which is of great potential for improving battery performance.</P> [FIG OMISSION]</BR>