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RISS 인기검색어
- 검색키워드
- 저자 : Jun-ichi Abe (검색결과 5 건)
- 무료
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Role for SUMOylation in Disturbed Flow-induced Atherosclerotic Plaque Formation
Jun-ichi Abe,Nhat-Tu Le,허경선 대한의용생체공학회 2015 Biomedical Engineering Letters (BMEL) Vol.5 No.3
Although atherosclerosis is a multi-factorial disease, thefocalization of atherosclerotic plaques on the vessel wallsuggests that local factors such as patterns of local bloodflow are critical in the progression of atherosclerosis. Bloodflow creates various types of forces onto the surface ofvascular endothelial cells (ECs). Among those various typesof forces, fluid shear stress has a major influence on thestructure and function of ECs. At the branch points and thelesser curvature of the aortic arch, blood flow is disturbed (dflow)and atherosclerotic plaques are frequently detected. Atthe straight parts of the arterial tree and the greater curvatureof aortic arch, blood flow is steady (s-flow, high shear stress)and atherosclerotic plaques are rare. These two patterns ofblood flow (d-flow and s-flow) affects EC structure andfunction differently. However, molecular mechanisms underlinethe difference remains unclear. To provide insights into thisquestion, studies have suggested a number of theories withmultiple proposed signaling pathways, and the role ofpost-translational modifications has emerged. Particularly,SUMOylation is highlighted based on its potentiality toregulate a wide range of cellular functions. EC dysfunctioninduced by SUMOylation is proposed to accelerate d-flowinducedatherosclerosis. In this review, we focus onSUMOylation and its role in regulating transcriptional networksand propose a mechanistic link between d-flow and ECdysfunction. Since a strong correlation exists between d-flowand atherosclerotic plaque formation, understanding themechanism of d-flow-induced SUMOylation events mayreveal new paths towards therapeutic interventions againstEC dysfunction and atherosclerosis.
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Shear Stress and Atherosclerosis
허경선,Keigi Fujiwara,Jun-ichi Abe 한국분자세포생물학회 2014 Molecules and cells Vol.37 No.6
Hemodynamic shear stress, the frictional force acting on vascular endothelial cells, is crucial for endothelial homeostasis under normal physiological conditions. When discussing blood flow effects on various forms of endothelial (dys)function, one considers two flow patterns: steady laminar flow and disturbed flow because endothelial cells respond differently to these flow types both in vivo and in vitro. Laminar flow which exerts steady laminar shear stress is atheroprotective while disturbed flow creates an atheroprone environment. Emerging evidence has provided new insights into the cellular mechanisms of flow-dependent regulation of vascular function that leads to cardiovascular events such as atherosclerosis, atherothrombosis, and myocardial infarction. In order to study effects of shear stress and different types of flow, various models have been used. In this review, we will summarize our current views on how disturbed flow-mediated signaling pathways are involved in the development of atherosclerosis.
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Shear Stress and Atherosclerosis
Heo, Kyung-Sun,Fujiwara, Keigi,Abe, Jun-Ichi Korean Society for Molecular and Cellular Biology 2014 Molecules and cells Vol.37 No.6
Hemodynamic shear stress, the frictional force acting on vascular endothelial cells, is crucial for endothelial homeostasis under normal physiological conditions. When discussing blood flow effects on various forms of endothelial (dys)function, one considers two flow patterns: steady laminar flow and disturbed flow because endothelial cells respond differently to these flow types both in vivo and in vitro. Laminar flow which exerts steady laminar shear stress is atheroprotective while disturbed flow creates an atheroprone environment. Emerging evidence has provided new insights into the cellular mechanisms of flowdependent regulation of vascular function that leads to cardiovascular events such as atherosclerosis, atherothrombosis, and myocardial infarction. In order to study effects of shear stress and different types of flow, various models have been used. In this review, we will summarize our current views on how disturbed flow-mediated signaling pathways are involved in the development of atherosclerosis.
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Xie, Shaozhen,Lee, Yi-Fen,Kim, Eungseok,Chen, Lu-Min,Ni, Jing,Fang, Lei-Ya,Liu, Su,Lin, Shin-Jen,Abe, Jun-Ichi,Berk, Bradford,Ho, Feng-Ming,Chang, Chawnshang National Academy of Sciences 2009 PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF Vol.106 No.32
<P>Testicular orphan nuclear receptor 4 (TR4) is an orphan member of the nuclear receptor superfamily with diverse physiological functions. Using TR4 knockout (TR4(-/-)) mice to study its function in cardiovascular diseases, we found reduced cluster of differentiation (CD)36 expression with reduced foam cell formation in TR4(-/-) mice. Mechanistic dissection suggests that TR4 induces CD36 protein and mRNA expression via a transcriptional regulation. Interestingly, we found this TR4-mediated CD36 transactivation can be further enhanced by polyunsaturated fatty acids (PUFAs), such as omega-3 and -6 fatty acids, and their metabolites such as 15-hydroxyeico-satetraonic acid (15-HETE) and 13-hydroxy octa-deca dieonic acid (13-HODE) and thiazolidinedione (TZD)-rosiglitazone. Both electrophoretic mobility shift assays (EMSA) and chromatin immunoprecipitation (ChIP) assays demonstrate that TR4 binds to the TR4 response element located on the CD36 5'-promoter region for the induction of CD36 expression. Stably transfected TR4-siRNA or functional TR4 cDNA in the RAW264.7 macrophage cells resulted in either decreased or increased CD36 expression with decreased or increased foam cell formation. Restoring functional CD36 cDNA in the TR4 knockdown macrophage cells reversed the decreased foam cell formation. Together, these results reveal an important signaling pathway controlling CD36-mediated foam cell formation/cardiovascular diseases, and findings that TR4 transactivation can be activated via its ligands/activators, such as PUFA metabolites and TZD, may provide a platform to screen new drug(s) to battle the metabolism syndrome, diabetes, and cardiovascular diseases.</P>
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