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- 저자 : ( Kae Won Cho ) (검색결과 21 건)
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Cho, Kae Won,Cho, Du-Hyong Yeungnam University College of Medicine 2019 Yeungnam University Journal of Medicine Vol.36 No.1
Background: Dysregulation of hepatic glucose production (HGP) contributes to the development of type 2 diabetes mellitus. Telmisartan, an angiotensin II type 1 receptor blocker (ARB), has various ancillary effects in addition to common blood pressure-lowering effects. The effects and mechanism of telmisartan on HGP have not been fully elucidated and, therefore, we investigated these phenomena in hyperglycemic HepG2 cells and high-fat diet (HFD)-fed mice. Methods: Glucose production and glucose uptake were measured in HepG2 cells. Expression levels of phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase ${\alpha}$ ($G6Pase-{\alpha}$), and phosphorylation levels of insulin receptor substrate-1 (IRS-1) and protein kinase C ${\zeta}$ ($PKC{\zeta}$) were assessed by western blot analysis. Animal studies were performed using HFD-fed mice. Results: Telmisartan dose-dependently increased HGP, and PEPCK expression was minimally increased at a $40{\mu}M$ concentration without a change in $G6Pase-{\alpha}$ expression. In contrast, telmisartan increased phosphorylation of IRS-1 at Ser302 ($p-IRS-1-Ser^{302}$) and decreased $p-IRS-1-Tyr^{632}$ dose-dependently. Telmisartan dose-dependently increased $p-PKC{\zeta}-Thr^{410}$ which is known to reduce insulin action by inducing IRS-1 serine phosphorylation. Ectopic expression of dominant-negative $PKC{\zeta}$ significantly attenuated telmisartan-induced HGP and $p-IRS-1-Ser^{302}$ and -inhibited $p-IRS-1-Tyr^{632}$. Among ARBs, including losartan and fimasartan, only telmisartan changed IRS-1 phosphorylation and pretreatment with GW9662, a specific and irreversible peroxisome proliferator-activated receptor ${\gamma}$ ($PPAR{\gamma}$) antagonist, did not alter this effect. Finally, in the livers from HFD-fed mice, telmisartan increased $p-IRS-1-Ser^{302}$ and decreased $p-IRS-1-Tyr^{632}$, which was accompanied by an increase in $p-PKC{\zeta}-Thr^{410}$. Conclusion: These results suggest that telmisartan increases HGP by inducing $p-PKC{\zeta}-Thr^{410}$ that increases $p-IRS-1-Ser^{302}$ and decreases $p-IRS-1-Tyr^{632}$ in a $PPAR{\gamma}$-independent manner
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Genetic Variations Leading to Familial Dilated Cardiomyopathy
Cho, Kae Won,Lee, Jongsung,Kim, Youngjo Korean Society for Molecular and Cellular Biology 2016 Molecules and cells Vol.39 No.10
Cardiomyopathy is a major cause of death worldwide. Based on pathohistological abnormalities and clinical manifestation, cardiomyopathies are categorized into several groups: hypertrophic, dilated, restricted, arrhythmogenic right ventricular, and unclassified. Dilated cardiomyopathy, which is characterized by dilation of the left ventricle and systolic dysfunction, is the most severe and prevalent form of cardiomyopathy and usually requires heart transplantation. Its etiology remains unclear. Recent genetic studies of single gene mutations have provided significant insights into the complex processes of cardiac dysfunction. To date, over 40 genes have been demonstrated to contribute to dilated cardiomyopathy. With advances in genetic screening techniques, novel genes associated with this disease are continuously being identified. The respective gene products can be classified into several functional groups such as sarcomere proteins, structural proteins, ion channels, and nuclear envelope proteins. Nuclear envelope proteins are emerging as potential molecular targets in dilated cardiomyopathy. Because they are not directly associated with contractile force generation and transmission, the molecular pathways through which these proteins cause cardiac muscle disorder remain unclear. However, nuclear envelope proteins are involved in many essential cellular processes. Therefore, integrating apparently distinct cellular processes is of great interest in elucidating the etiology of dilated cardiomyopathy. In this mini review, we summarize the genetic factors associated with dilated cardiomyopathy and discuss their cellular functions.
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Kae Won Cho,조두형 영남대학교 의과대학 2019 Yeungnam University Journal of Medicine Vol.36 No.1
Background: Dysregulation of hepatic glucose production (HGP) contributes to the development of type 2 diabetes mellitus. Telmisartan, an angiotensin II type 1 receptor blocker (ARB), has various ancillary effects in addition to common blood pressure-lowering effects. The effects and mechanism of telmisartan on HGP have not been fully elucidated and, therefore, we investigated these phenomena in hyperglycemic HepG2 cells and high-fat diet (HFD)-fed mice. Methods: Glucose production and glucose uptake were measured in HepG2 cells. Expression levels of phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase α (G6Pase-α), and phosphorylation levels of insulin receptor substrate-1 (IRS-1) and protein kinase C ζ (PKCζ) were assessed by western blot analysis. Animal studies were performed using HFD-fed mice. Results: Telmisartan dose-dependently increased HGP, and PEPCK expression was minimally increased at a 40 μM concentration without a change in G6Pase-α expression. In contrast, telmisartan increased phosphorylation of IRS-1 at Ser302 (p-IRS-1-Ser302) and decreased p-IRS-1-Tyr632 dose-dependently. Telmisartan dose-dependently increased p-PKCζ-Thr410 which is known to reduce insulin action by inducing IRS-1 serine phosphorylation. Ectopic expression of dominant-negative PKCζ significantly attenuated telmisartan-induced HGP and p-IRS-1-Ser302 and -inhibited p-IRS-1-Tyr632. Among ARBs, including losartan and fimasartan, only telmisartan changed IRS-1 phosphorylation and pretreatment with GW9662, a specific and irreversible peroxisome proliferator-activated receptor γ (PPARγ) antagonist, did not alter this effect. Finally, in the livers from HFD-fed mice, telmisartan increased p-IRS-1-Ser302 and decreased p-IRS-1-Tyr632, which was accompanied by an increase in p-PKCζ-Thr410. Conclusion: These results suggest that telmisartan increases HGP by inducing p-PKCζ-Thr410 that increases p-IRS-1-Ser302 and decreases p-IRS-1-Tyr632 in a PPARγ-independent manner.
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Cho, Kae Won,Zamarron, Brian F.,Muir, Lindsey A.,Singer, Kanakadurga,Porsche, Cara E.,DelProposto, Jennifer B.,Geletka, Lynn,Meyer, Kevin A.,O’Rourke, Robert W.,Lumeng, Carey N. American Association of Immunologists 2016 Journal of Immunology Vol. No.
<P>Dynamic changes of adipose tissue leukocytes, including adipose tissue macrophage (ATM) and adipose tissue dendritic cells (ATDCs), contribute to obesity-induced inflammation and metabolic disease. However, clear discrimination between ATDC and ATM in adipose tissue has limited progress in the field of immunometabolism. In this study, we use CD64 to distinguish ATM and ATDC, and investigated the temporal and functional changes in these myeloid populations during obesity. Flow cytometry and immunostaining demonstrated that the definition of ATM as F4/80(+)CD11b(+) cells overlaps with other leukocytes and that CD45(+)CD64(+) is specific for ATM. The expression of core dendritic cell genes was enriched in CD11c(+)CD64(-) cells (ATDC), whereas core macrophage genes were enriched in CD45(+)CD64(+) cells (ATM). CD11c(+)CD64(-) ATDCs expressed MHC class II and costimulatory receptors, and had similar capacity to stimulate CD4(+) T cell proliferation as ATMs. ATDCs were predominantly CD11b(+) conventional dendritic cells and made up the bulk of CD11c(+) cells in adipose tissue with moderate high-fat diet exposure. Mixed chimeric experiments with Ccr2(-/-) mice demonstrated that high-fat diet induced ATM accumulation from monocytes was dependent on CCR2, whereas ATDC accumulation was less CCR2 dependent. ATDC accumulation during obesity was attenuated in Ccr7(-/-) mice and was associated with decreased adipose tissue inflammation and insulin resistance. CD45(+)CD64(+) ATM and CD45(+)CD64(-)CD11c(+) ATDCs were identified in human obese adipose tissue and ATDCs were increased in s.c. adipose tissue compared with omental adipose tissue. These results support a revised strategy for unambiguous delineation of ATM and ATDC, and suggest that ATDCs are independent contributors to adipose tissue inflammation during obesity.</P>
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Choi, Kae Won,Cho, Young Su,Aneta, Young Su,Lee, Ji Wun,Cho, Sung Min,Choi, Jaehyuk Elsevier 2017 Journal of Computer Communications Vol.112 No.-
<P><B>Abstract</B></P> <P>In this paper, we investigate a scheduler for a multipath transmission control protocol (MPTCP) for bandwidth aggregation in heterogeneous wireless environments. The performance of the MPTCP can be degraded due to the head-of-line (HOL) blocking caused by path heterogeneity, when a buffer size is limited. This performance degradation can be overcome by a careful design of a scheduler, which has a role of allocating each data segment to one of subflows. We derive the theoretical limit of the achievable aggregate throughput and show that the optimality is achieved when the load is balanced between subflows. Based on the analysis, we propose the optimal load balancing (OLB) scheduler that approximately achieves the theoretical throughput limit. By simulations and experiments, we show that the proposed OLB scheduler outperforms the default scheduler of the Linux MPTCP implementation.</P>
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Role of adipose tissue in the development of non-alcoholic fatty liver disease
조계원 ( Kae Won Cho ) 대한간학회 2016 간학회 싱글토픽 심포지움 Vol.2016 No.2
Non-alcololic fatty liver disease (NAFLD) is a condition in which excess fat accumulates in the liver of a patient with no history of alcohol abuse or other causes for secondary hepatic steatosis. The prevalence of non-alcholic fatty liver disease (NAFLD) is rapidly increasing, however, the pathogenesis of NAFLD has not been completely elucidated. Visceral adipose tissue has increasingly been recognized as a biologically active organ contributing to the pathogenesis of NAFLD. This paper summarizes findings on the role of visceral adipose tissues in the context of fatty liver and liver fibrosis and their potential mechanisms. A thorough insight into the pathophysiologic mechanisms linking adipose tissue with NAFLD may result in the designing of studies investigating new diagnostic marker of NAFLD and clinical trials targeting the treatment of NAFLD.
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이원우,황계영,김덕하,조경숙 ( Won Woo Lee,Kae Yong Hwang,Duck Ha Kim,Kyeong Sook Cho ) 대한피부과학회 1991 대한피부과학회지 Vol.29 No.4
A Case of Polyarteritis Nodosa, Possibly of Cutaneous Type Won Woo Lee, M.D., Kae Yong Hwnag, M.D., Duck Ha Kim, M.D., Kyeong Sook Cho, M.D.* Departments of Dermatology and Pediatrics*, Maryknoll Hospital Pusan, Korea Cutaneous polyarteritis nodosa, a distinct clinical entity, is a chronic and benign vascular disease in which cutaneous lesions are predominent with no visceral involvement. We report a case of polyarteritis nodosa, possibly of cutaneous type in a 9-year old boy who on the occasions presented with generalized tender cutaneous or subcutaneous nodules and livedo reticularis. Fever, chilling, and arthralgia were also present. Histopathologic examination of the nodular lesions showed panarteritis of small and medium-sized arteries at the dermal-subcutaneous junction with little evidence of panniculitis. The patient was treated with acetyl salicylate and prednisclone with a good clinical response. (Kor J Dermatol 29(4) : 557-561, 1991)
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Genetic Variations Leading to Familial Dilated Cardiomyopathy
김영조,Kae Won Cho,Jongsung Lee 한국분자세포생물학회 2016 Molecules and cells Vol.39 No.10
Cardiomyopathy is a major cause of death worldwide. Based on pathohistological abnormalities and clinical manifestation, cardiomyopathies are categorized into several groups: hypertrophic, dilated, restricted, arrhythmogenic right ventricular, and unclassified. Dilated cardiomyopathy, which is characterized by dilation of the left ventricle and systolic dysfunction, is the most severe and prevalent form of cardiomyopathy and usually requires heart transplantation. Its etiology remains unclear. Recent genetic studies of single gene mutations have provided significant insights into the complex processes of cardiac dysfunction. To date, over 40 genes have been demonstrated to contribute to dilated cardiomyopathy. With advances in genetic screening techniques, novel genes associated with this disease are continuously being identified. The respective gene products can be classified into several functional groups such as sarcomere proteins, structural proteins, ion channels, and nuclear envelope proteins. Nuclear envelope proteins are emerging as potential molecular targets in dilated cardiomyopathy. Because they are not directly associated with contractile force generation and transmission, the molecular pathways through which these proteins cause cardiac muscle disorder remain unclear. However, nuclear envelope proteins are involved in many essential cellular processes. Therefore, integrating apparently distinct cellular processes is of great interest in elucidating the etiology of dilated cardiomyopathy. In this mini review, we summarize the genetic factors associated with dilated cardiomyopathy and discuss their cellular functions.
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