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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]
Park, Sungha,Youn, Jong-Chan,Shin, Dong-Jik,Park, Chan-Mi,Kim, Jung-Sun,Ko, Young-Guk,Choi, Donghoon,Ha, Jong-Won,Jang, Yangsoo,Chung, Namsik Lippincott Williams Wilkins, Inc. 2007 Coronary artery disease Vol.18 No.6
BACKGROUND: Pregnancy-associated plasma protein-A (PAPP-A) is a high-molecular-weight, zinc-binding matrix metalloproteinase that is known to be abundantly expressed in ruptured plaques. Previous studies have shown PAPP-A to be a significant marker of plaque instability and cardiovascular events in patients with acute coronary syndromes. Because the activity of PAPP-A may be modulated by genetic variants in the PAPP-A genes, we tried to determine the association of PAPP-A gene with acute myocardial infarction (AMI). METHODS: We analyzed four single nucleotide polymorphisms (SNPs) of PAPP-A gene variants and seven other polymorphisms of cytokine genes that have been reported to have functional significance (RANTES G-403A, MCP1 G-2518A, CRP A2147G, CRP G-717A, AGER G557A, LTA T26A, IL-6 G-572C) for possible association with AMI in 170 unrelated AMI patients and unrelated age-matched controls, respectively. RESULTS: The average age of the study population was 62.2±11.4 years in AMI patients and 62.6±10.4 years in healthy controls. Multiple logistic regression analysis with risk factors such as age, male sex, smoking, hypertension, diabetes mellitus, and dyslipidemia revealed the PAPP-A IVS6+95 C allele to be associated with an increased risk of AMI (dominancy: odds ratio, 2.13; 95% confidence interval, 1.12–4.07; P=0.022; codominancy: odds ratio, 1.89; 95% confidence interval, 1.14–3.16; P=0.015). CONCLUSIONS: We found, for the first time, that PAPP-A IVS6+95 C allele is an independent risk factor for AMI even after adjustment for traditional risk factors. The determination of such genotype contributing to AMI could provide a new tool for identifying high-risk individuals.
Increased phosphorylation of Ca(2+) handling proteins as a proarrhythmic mechanism in myocarditis.
Park, Hyelim,Park, Hyewon,Lee, Dajeong,Oh, Sujung,Lim, Jisoo,Hwang, Hye Jin,Park, Sungha,Pak, Hui-Nam,Lee, Moon-Hyoung,Joung, Boyoung Japanese Circulation Society 2014 CIRCULATION JOURNAL Vol.78 No.9
<P>Because fatal arrhythmia is an important cause of death in patients with myocarditis, we investigated the proarrhythmic mechanisms of experimental autoimmune myocarditis. METHODS???AND???RESULTS: Myocarditis was induced by injection of 2 mg porcine cardiac myosin into the footpads of adult Lewis rats on days 1 and 8 (Myo, n=15) and the results compared with Control rats (Control, n=15). In an additional 15 rats, 6 mg/kg prednisolone was injected into the gluteus muscle before the injection of porcine cardiac myosin on days 1 and 8 (MyoS, n=15). Hearts with myocarditis had longer action potential duration (APD), slower conduction velocity (CV; P<0.01 vs. Control), higher CV heterogeneity, greater fibrosis, higher levels of immunoblotting of high-mobility group protein B1, interleukin 6 and tumor necrosis factor-관 proteins. Steroid treatment partially reversed the translations for myocarditis, CV heterogeneity, reduced APD at 90% recovery to baseline, increased CV (P<0.01), and reversed fibrosis (P<0.05). Programmed stimulation triggered sustained ventricular tachycardia in Myo rats (n=4/5), but not in controls (n=0/5) or Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) inhibitor (KN93) treated Myo rats (n=0/5, P=0.01). CaMKII autophosphorylation at Thr287 (201%), and RyR2 phosphorylation at Ser2808 (protein kinase A/CaMKII site, 126%) and Ser2814 (CaMKII site, 21%) were increased in rats with myocarditis and reversed by steroid.</P>
Resistant hypertension: consensus document from the Korean society of hypertension
Park Sungha,Shin Jinho,임상현,김광일,Kim Hack-Lyoung,Kim Hyeon Chang,Lee Eun Mi,Lee Jang Hoon,Ahn Shin Young,Cho Eun Joo,Kim Ju Han,Kang Hee-Taik,Lee Hae-Young,Lee Sunki,Kim Woohyeun,Park Jong-Moo 대한고혈압학회 2023 Clinical Hypertension Vol.29 No.-
Although reports vary, the prevalence of true resistant hypertension and apparent treatment-resistant hypertension (aTRH) has been reported to be 10.3% and 14.7%, respectively. As there is a rapid increase in the prevalence of obesity, chronic kidney disease, and diabetes mellitus, factors that are associated with resistant hypertension, the prevalence of resistant hypertension is expected to rise as well. Frequently, patients with aTRH have pseudoresistant hypertension [aTRH due to white-coat uncontrolled hypertension (WUCH), drug underdosing, poor adherence, and inaccurate office blood pressure (BP) measurements]. As the prevalence of WUCH is high among patients with aTRH, the use of out-of-office BP measurements, both ambulatory blood pressure monitoring (ABPM) and home blood pressure monitoring (HBPM), is essential to exclude WUCH. Non-adherence is especially problematic, and methods to assess adherence remain limited and often not clinically feasible. Therefore, the use of HBPM and higher utilization of singlepill fixed-dose combination treatments should be emphasized to improve drug adherence. In addition, primary aldosteronism and symptomatic obstructive sleep apnea are quite common in patients with hypertension and more so in patients with resistant hypertension. Screening for these diseases is essential, as the treatment of these secondary causes may help control BP in patients who are otherwise difficult to treat. Finally, a proper drug regimen combined with lifestyle modifications is essential to control BP in these patients.
Association of central hemodynamics with estimated 24-h urinary sodium in patients with hypertension
Park, Sungha,Park, Jeong B.,Lakatta, Edward G. Lippincott Williams Wilkins, Inc. 2011 Journal of Hypertension Vol.29 No.8
OBJECTIVE: High salt intake is known to be the most pivotal environmental factor in the pathogenesis of hypertension. However, the association of high sodium intake with central hemodynamics in hypertensive individuals has not been well defined. Here, we determined the association of estimated 24-h urine sodium and potassium excretion estimated from a spot urine analysis with parameters of central pulse wave analysis in 515 hypertensive individuals. METHODS: Fasting spot urine samples were obtained in the early morning after the first void, and estimated 24-h urine sodium and potassium excretion were estimated from measurement of urine sodium, potassium and creatinine. Central hemodynamics and arterial stiffness parameters were assessed via pulse wave analysis of the radial artery. RESULTS: The estimated 24-h sodium and potassium excretion values were 150 ± 40 and 49 ± 10 mEq, respectively. There was a step-wise decrease in pulse pressure amplification with increasing estimated 24-h urine sodium excretion. Multiple linear regression analyses revealed that both estimated 24-h urine sodium excretion and sodium/potassium ratio were independently associated with increases in central pulse pressure, augmented aortic pressure and augmentation index and were inversely associated with pulse pressure amplification. CONCLUSION: The estimated 24-h urinary sodium excretion is independently associated with central hemodynamics. This may provide the basis for prospective interventional studies of epidemiologic scale to determine the potential beneficial effects of reduced salt consumption on central hemodynamics.