Hyoung Chul Choi

ORCID: 0000-0002-1367-0797
Publications
Citations
Views
---
Saved
---
About
Contact & Profiles
Research Areas
  • Metabolism, Diabetes, and Cancer
  • Nitric Oxide and Endothelin Effects
  • Autophagy in Disease and Therapy
  • Sirtuins and Resveratrol in Medicine
  • Protein Kinase Regulation and GTPase Signaling
  • Pancreatic function and diabetes
  • Heme Oxygenase-1 and Carbon Monoxide
  • PI3K/AKT/mTOR signaling in cancer
  • Telomeres, Telomerase, and Senescence
  • Eicosanoids and Hypertension Pharmacology
  • Neuroscience and Neuropharmacology Research
  • Cardiac Ischemia and Reperfusion
  • melanin and skin pigmentation
  • Peroxisome Proliferator-Activated Receptors
  • Antioxidant Activity and Oxidative Stress
  • Endoplasmic Reticulum Stress and Disease
  • Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Mitochondrial Function and Pathology
  • Cancer, Hypoxia, and Metabolism
  • Calcium signaling and nucleotide metabolism
  • Radio Frequency Integrated Circuit Design
  • Advanced Glycation End Products research
  • Neurotransmitter Receptor Influence on Behavior
  • Analytical Chemistry and Sensors
  • Hemoglobin structure and function

Yeungnam University
2014-2024

Daegu Health College
2023

Yeungnam University College
2012-2020

Chungbuk National University
2019

Human Resources Development Institute
2017

Kyungpook National University
2014

Chonnam National University
2014

Chonnam National University Hospital
2014

Korea Research Institute of Bioscience and Biotechnology
2014

University of Oklahoma
2010

Background— Aberrant endoplasmic reticulum (ER) stress is associated with several cardiovascular diseases, including atherosclerosis. The mechanism by which aberrant ER develops poorly understood. This study investigated whether dysfunction of AMP-activated protein kinase (AMPK) causes and atherosclerosis in vivo. Methods Results— Human umbilical vein endothelial cells mouse aortic from AMPK-deficient mice were used to assess the level Western blotting. Reduction AMPKα2 expression...

10.1161/circulationaha.109.900928 article EN Circulation 2010-02-02

OBJECTIVE The oxidation of LDLs is considered a key step in the development atherosclerosis. How LDL contributes to atherosclerosis remains poorly defined. Here we report that oxidized and glycated (HOG-LDL) causes aberrant endoplasmic reticulum (ER) stress AMP-activated protein kinase (AMPK) suppressed HOG-LDL–triggered ER vivo. RESEARCH DESIGN AND METHODS markers, sarcoplasmic/endoplasmic Ca2+ ATPase (SERCA) activity oxidation, AMPK were monitored cultured bovine aortic endothelial cells...

10.2337/db09-1637 article EN cc-by-nc-nd Diabetes 2010-03-18

10.1016/j.bbrc.2012.07.165 article EN Biochemical and Biophysical Research Communications 2012-08-07

GTP cyclohydrolase 1 (GTPCH1) is the rate-limiting enzyme in de novo synthesis of tetrahydrobiopterin (BH4), an essential cofactor for endothelial NO synthase (eNOS) dictating, at least partly, balance and superoxide produced by this enzyme. The aim study was to determine effect acute inhibition GTPCH1 on BH4, eNOS function, blood pressure (BP) vivo. Exposure bovine or mouse aortic cells inhibitors (2,4-diamino-6-hydroxypyrimidine N-acetyl-serotonin) small-interference RNA (siRNA)...

10.1161/hypertensionaha.108.112094 article EN Hypertension 2008-07-22

The AMP-activated protein kinase (AMPK) is reported to mediate the beneficial effects of statin on vascular functions, but biochemical mechanisms are incompletely understood. aim study was determine how activates AMPK. Exposure confluent bovine aortic endothelial cells simvastatin (statin) dose-dependently increased phosphorylation AMPK at Thr172 and activities AMPK, which in parallel with detection both LKB1 Ser428 nuclear export. Furthermore, treatment shown increase C (PKC)-ζ activity...

10.1074/jbc.m803020200 article EN cc-by Journal of Biological Chemistry 2008-05-12

Laminar flow protects from atherosclerosis in endothelium.Laminar induces Nrf2 activation dependent on ERK5 activation, leading to up-regulation of downstream genes Nrf2.ERK5 requires exert cytoprotective effect HUVEC. inhibitor BIX02189 regulates vivo.Identifying as a molecular target for regulating flow-mediating Nrf2-dependent gene expression may have significant therapeutic potential treating atherosclerosis. Atherosclerosis is often observed areas where disturbed formed, whereas...

10.1074/jbc.m112.381509 article EN cc-by Journal of Biological Chemistry 2012-10-06

The vascular tone plays an important role in blood pressure and flow. It is influenced by the contraction of smooth muscle cells (VSMCs), which turn regulated balance between myosin light chain kinase (MLCK) phosphorylated (p-MLC). Quercetin a common flavonoid found many fruits red wine. Although quercetin has been widely reported to be involved cell proliferation, migration, apoptosis VSMCs, it not yet demonstrated whether related vasocontraction, function AMP-activated protein (AMPK)...

10.1089/jmf.2017.4052 article EN Journal of Medicinal Food 2017-10-16

This study was conducted to elucidate the molecular mechanisms of thromboxane A2 receptor (TP)-induced insulin resistance in endothelial cells. Exposure human umbilical vein cells (HUVECs) or mouse aortic either IBOP U46619, two structurally related A(2) mimetics, significantly reduced insulin-stimulated phosphorylation nitric-oxide synthase (eNOS) at Ser(1177) and Akt Ser(473). These effects were abolished by pharmacological genetic inhibitors TP. TP-induced suppression both eNOS...

10.1074/jbc.m109.012583 article EN cc-by Journal of Biological Chemistry 2009-04-30

Aging is one of the risk factors for development cardiovascular diseases. During progression cellular senescence, cells enter a state irreversible growth arrest and display resistance to apoptosis. As flavonoid, quercetin induces apoptosis in various cells. Accordingly, we investigated relationship between quercetin-induced inhibition determined mechanism oxidative stress-induced vascular smooth muscle cell (VSMC) senescence. In cultured VSMCs, hydrogen peroxide (H2O2) dose-dependently...

10.4196/kjpp.2020.24.1.69 article EN Korean Journal of Physiology and Pharmacology 2020-01-01

Abstract Telomere dysfunction is a well-known molecular trigger of senescence and has been associated with various age-related diseases, including atherosclerosis. However, the mechanisms involved have not yet elucidated, extent to which telomeres contribute atherosclerosis unknown. Therefore, we investigated mechanism metformin-induced telomere stabilization ability metformin inhibit vascular smooth muscle cell (VSMC) caused by advanced The present study revealed that inhibited phenotypes...

10.1038/s12276-024-01297-w article EN cc-by Experimental & Molecular Medicine 2024-09-02

Losartan is a selective angiotensin II (Ang II) type 1 (AT1) receptor antagonist which inhibits vascular smooth muscle cells (VSMCs) contraction and proliferation. We hypothesized that losartan may prevent cell proliferation by activating AMP-activated protein kinase (AMPK) in VSMCs. VSMCs were treated with various concentrations of losartan. AMPK activation was measured Western blot analysis MTT assay flowcytometry. dose- time-dependently increased the phosphorylation its downstream target,...

10.4196/kjpp.2010.14.5.299 article EN cc-by-nc Korean Journal of Physiology and Pharmacology 2010-01-01

Cellular senescence is associated with inflammation and the senescence-associated secretory phenotype (SASP) of secreted proteins. Vascular smooth muscle cell (VSMC) expressing SASP contributes to chronic vascular inflammation, loss function, developments age-related diseases. Although VSMC well recognized, mechanism has not been established. In this study, we aimed determine whether prednisolone (PD) attenuates adriamycin (ADR)-induced through SIRT1-AMPK signaling pathway. We found that PD...

10.1371/journal.pone.0239976 article EN cc-by PLoS ONE 2020-09-30

It has been suggested that methylglyoxal (MGO), a glycolytic metabolite, more detrimental effects on endothelial dysfunction than glucose itself. Recent reports showed high and MGO induced endoplasmic reticulum (ER) stress myocyte apoptosis in ischemic heart disease was inhibited by apelin. The goal of the study is to investigate molecular mechanism which induces via regulation ER cells, examine whether apelin-13, cytoprotective polypeptide ligand, protects MGO-induced aortic dysfunction....

10.3390/ijms21114069 article EN International Journal of Molecular Sciences 2020-06-06
Coming Soon ...