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Article ; Online: Corrigendum.

Shyu, Kou-Gi

European journal of clinical investigation

2019 Volume 49, Issue 1, Page(s) e13046

Language	English
Publishing date	2019-01-29
Publishing country	England
Document type	Journal Article ; Published Erratum
ZDB-ID	186196-7
ISSN	1365-2362 ; 0014-2972 ; 0960-135X
ISSN (online)	1365-2362
ISSN	0014-2972 ; 0960-135X
DOI	10.1111/eci.13046
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Article ; Online: Exosomal MALAT1 from macrophages treated with high levels of glucose upregulates LC3B expression via miR-204-5p downregulation.

Kou-Gi, Shyu / Wang, Bao-Wei / Pan, Chun-Ming / Fang, Wei-Jen / Lin, Chiu-Mei

Journal of the Chinese Medical Association : JCMA

2024

Abstract: Background: Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) plays a critical role in the pathophysiology of diabetes-related complications. However, whether macrophage-derived MALAT1 affects autophagic activity under hyperglycemic ... ...

Abstract	Background: Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) plays a critical role in the pathophysiology of diabetes-related complications. However, whether macrophage-derived MALAT1 affects autophagic activity under hyperglycemic conditions is unclear. Therefore, we investigated the molecular regulatory mechanisms of macrophage-derived MALAT1 and autophagy under hyperglycemic conditions. Methods: Hyperglycemia was induced by culturing macrophages in 25 mM glucose for 1 h. Exosomes were extracted from the culture media. A rat model of carotid artery balloon injury was established to assess the effect of MALAT1 on vascular injury. Reverse transcription, real-time quantitative polymerase chain reaction, western blotting, immunohistochemical staining, and luciferase activity assays were performed. Results: Stimulation with high levels of glucose significantly enhanced MALAT1 expression in macrophage-derived exosomes. MALAT1 inhibited miR-204-5p expression in macrophage-derived exosomes under hyperglycemic conditions. siRNA-induced silencing of MALAT1 significantly reversed macrophage-derived exosome-induced miR-204-5p expression. Hyperglycemic treatment caused a significant, exosome-induced increase in the expression of the autophagy marker LC3B in macrophages. Silencing MALAT1 and overexpression of miR-204-5p significantly decreased LC3B expression induced by macrophage-derived exosomes. Overexpression of miR-204-5p significantly reduced LC3B luciferase activity induced by macrophage-derived exosomes. Balloon injury to the carotid artery in rats significantly enhanced MALAT1 and LC3B expression, and significantly reduced miR-204-5p expression in carotid artery tissue. Silencing MALAT1 significantly reversed miR-204-5p expression in carotid artery tissue after balloon injury. MALAT1 silencing or miR-204-5p overexpression significantly reduced LC3B expression after balloon injury. Conclusion: This study demonstrated that hyperglycemia upregulates MALAT1. MALAT1 suppresses miR-204-5p expression and counteracts the inhibitory effect of miR-204-5p on LC3B expression in macrophages to promote vascular disease.
Language	English
Publishing date	2024-04-23
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2107283-8
ISSN	1728-7731 ; 1726-4901
ISSN (online)	1728-7731
ISSN	1726-4901
DOI	10.1097/JCMA.0000000000001098
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Zs.A 2699: Show issues

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Article: Statement of the Chairman of the Publication Committee of Acta Cardiologica Sinica.

Shyu, Kou-Gi

Acta Cardiologica Sinica

2016 Volume 29, Issue 2, Page(s) 113–114

Language	English
Publishing date	2016-04-28
Publishing country	China (Republic : 1949- )
Document type	Journal Article
ZDB-ID	1051394-2
ISSN	1011-6842
ISSN	1011-6842
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Zs.A 3059: Show issues

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Article: The Role of Endoglin in Myocardial Fibrosis.

Shyu, Kou-Gi

Acta Cardiologica Sinica

2017 Volume 33, Issue 5, Page(s) 461–467

Abstract: Myocardial fibrosis is closely associated with heart failure because myocardial fibrosis may cause the loss of normal cardiac function. Endoglin is a homeodimeric membrane glycoprotein, a co-receptor of transforming growth factor-β1 (TGF-β1) and β3. ... ...

Abstract	Myocardial fibrosis is closely associated with heart failure because myocardial fibrosis may cause the loss of normal cardiac function. Endoglin is a homeodimeric membrane glycoprotein, a co-receptor of transforming growth factor-β1 (TGF-β1) and β3. Endoglin is a potent mediator of profibrotic effects of angiotensin II on cardiac fibroblasts and can modulate the effect of TGF-β1 on extracellular matrix synthesis. These data indicate that endoglin plays an important role in fibrogenesis in cardiac remodeling. Endoglin induced by TGF-β1 is largely through PI-3 kinase, Akt, Smad3/4 and endoglin promoter pathways. Endoglin was upregulated in pressure- overload, volume-overload heart failure and acute myocardial infarction and was associated with myocardial fibrosis. Silencing endoglin expression could attenuate myocardial fibrosis and improve survival in animal study. Endoglin expression was increased in failing left ventricle before use of left ventricle assist device, and reduced back to control levels after use of left ventricle assist device. Targeting endoglin may provide a potentially unique and novel therapeutic approach for reducing myocardial fibrosis in patients with heart failure.
Language	English
Publishing date	2017-08-31
Publishing country	China (Republic : 1949- )
Document type	Journal Article ; Review
ZDB-ID	1051394-2
ISSN	1011-6842
ISSN	1011-6842
DOI	10.6515/acs20170221b
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Article ; Online: Reply to the letter to the Editor "ECs-derived exosomes: A novel therapeutic target for myocardial ischemia-reperfusion injury".

Shyu, Kou-Gi / Wang, Bao-Wei / Lin, Chiu-Mei

International journal of cardiology

2021 Volume 332, Page(s) 39

MeSH term(s)	Exosomes ; Humans ; Hyperbaric Oxygenation ; MicroRNAs ; Myocardial Reperfusion Injury/drug therapy ; RNA, Long Noncoding
Chemical Substances	MicroRNAs ; RNA, Long Noncoding
Language	English
Publishing date	2021-03-20
Publishing country	Netherlands
Document type	Letter ; Comment
ZDB-ID	779519-1
ISSN	1874-1754 ; 0167-5273
ISSN (online)	1874-1754
ISSN	0167-5273
DOI	10.1016/j.ijcard.2021.03.044
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Article: Association of Heart Rate Trajectory Patterns with the Risk of Adverse Outcomes for Acute Heart Failure in a Heart Failure Cohort in Taiwan.

Wei, Cheng-Chun / Shyu, Kou-Gi / Chien, Kuo-Liong

Acta Cardiologica Sinica

2020 Volume 36, Issue 5, Page(s) 439–447

Abstract: Background: Heart rate trajectory with multiple heart rate measurements is considered to be a more sensitive predictor of outcomes than single heart rate measurements. The association of heart rate trajectory patterns with acute heart failure outcomes ... ...

Abstract	Background: Heart rate trajectory with multiple heart rate measurements is considered to be a more sensitive predictor of outcomes than single heart rate measurements. The association of heart rate trajectory patterns with acute heart failure outcomes has not been well studied. We examined the association of heart rate trajectory patterns with post-discharge outcomes. Methods: This prospective cohort study was based on an acute heart failure registry in Taiwan. A total of 1509 patients were enrolled in the Taiwan Society of Cardiology - Heart Failure with Reduced Ejection Fraction Registry from May 2013 to October 2015. The outcomes were post-discharge all-cause mortality and heart failure re-admission. Results: Two heart trajectory patterns were identified in group-based trajectory analysis. One started with a higher heart rate and had an increasing trend over 6 months then a subsequent decline (high-increasing-decreasing group; n = 352; 23.9%). The other started with a lower heart rate and had a relatively stable pattern (low-stable group; n = 1121; 76.1%). Compared with those in the low-stable group, patients in the high-increasing-decreasing group had a higher risk of events (all-cause mortality: hazard ratio 3.10 and 95% confidence interval 1.24-7.77; heart failure re-admission: hazard ratio 1.13 and 95% confidence interval 0.55-2.32). Conclusions: Patients with a high-increasing-decreasing heart rate trajectory pattern had a higher risk of all-cause mortality than those with a low-stable pattern.
Language	English
Publishing date	2020-09-14
Publishing country	China (Republic : 1949- )
Document type	Journal Article
ZDB-ID	1051394-2
ISSN	1011-6842
ISSN	1011-6842
DOI	10.6515/ACS.202009_36(5).20200519A
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Article ; Online: Exosomal MALAT1 Derived from High Glucose-Treated Macrophages Up-Regulates Resistin Expression via miR-150-5p Downregulation.

Shyu, Kou-Gi / Wang, Bao-Wei / Fang, Wei-Jen / Pan, Chun-Ming / Lin, Chiu-Mei

International journal of molecular sciences

2022 Volume 23, Issue 3

Abstract: Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) plays a crucial role in the pathophysiological process associated with diabetes-related complications. The effect of high glucose levels on macrophage-derived exosomal MALAT1 is unknown. ... ...

Abstract	Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) plays a crucial role in the pathophysiological process associated with diabetes-related complications. The effect of high glucose levels on macrophage-derived exosomal MALAT1 is unknown. Therefore, we investigated the molecular regulatory mechanisms controlling exosomal MALAT1 in macrophages under high glucose treatment and the therapeutic target of macrophage-derived exosomal MALAT1 using a balloon injury model of vascular disease in diabetic rats. High glucose (25 mM) significantly increased MALAT1 expression in macrophage-derived exosomes. MALAT1 suppressed miR-150-5p expression in macrophage-derived exosomes under high-glucose conditions. Silencing MALAT1 using MALAT1 siRNA significantly reversed miR-150-5p expression induced by macrophage-derived exosomes. Macrophage-derived exosomes under high-glucose treatment significantly increased resistin expression in macrophages. Silencing MALAT1 and overexpression of miR-150-5p significantly decreased resistin expression induced by macrophage-derived exosomes. Overexpression of miR-150-5p significantly decreased resistin luciferase activity induced by macrophage-derived exosomes. Macrophage-derived exosome significantly decreased glucose uptake in macrophages and silencing MALAT1, resistin or overexpression of miR-150-5p significantly reversed glucose uptake. Balloon injury to the carotid artery significantly increased MALAT1 and resistin expression and significantly decreased miR-150-5p expression in arterial tissue. Silencing MALAT1 significantly reversed miR-150-5p expression in arterial tissue after balloon injury. Silencing MALAT1 or overexpression of miR-150-5p significantly reduced resistin expression after balloon injury. In conclusion, high glucose up-regulates MALAT1 to suppress miR-150-5p expression and counteracts the inhibitory effect of miR-150-5p on resistin expression in macrophages to promote vascular disease. Macrophage-derived exosomes containing MALAT1 may serve as a novel cell-free approach for the treatment of vascular disease in diabetes mellitus.
MeSH term(s)	Animals ; Carotid Artery Diseases/etiology ; Carotid Artery Diseases/metabolism ; Carotid Artery Diseases/pathology ; Diabetes Mellitus, Experimental/complications ; Disease Models, Animal ; Exosomes/genetics ; Exosomes/metabolism ; Gene Expression Regulation ; Glucose/toxicity ; Hyperglycemia/chemically induced ; Hyperglycemia/pathology ; Macrophages/metabolism ; Macrophages/pathology ; Male ; Mice ; MicroRNAs/antagonists & inhibitors ; RNA, Long Noncoding/genetics ; RNA, Long Noncoding/metabolism ; Rats ; Rats, Wistar ; Resistin/genetics ; Resistin/metabolism ; Sweetening Agents/toxicity
Chemical Substances	Malat1 long non-coding RNA, mouse ; MicroRNAs ; Mirn150 microRNA, mouse ; RNA, Long Noncoding ; Resistin ; Sweetening Agents ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2022-01-20
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms23031095
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Article ; Online: Hyperbaric oxygen activates visfatin expression and angiogenesis via angiotensin II and JNK pathway in hypoxic human coronary artery endothelial cells.

Chiu, Chiung-Zuan / Wang, Bao-Wei / Yu, Ying-Ju / Shyu, Kou-Gi

Journal of cellular and molecular medicine

2020 Volume 24, Issue 4, Page(s) 2434–2443

Abstract: Visfatin is an adipocytokine with important roles in endothelial angiogenesis. Hyperbaric oxygen (HBO) has been widely used to treat various medical illness with enhanced angiogenesis. The molecular effects of HBO on visfatin under hypoxia are poorly ... ...

Abstract	Visfatin is an adipocytokine with important roles in endothelial angiogenesis. Hyperbaric oxygen (HBO) has been widely used to treat various medical illness with enhanced angiogenesis. The molecular effects of HBO on visfatin under hypoxia are poorly understood. This study aimed to investigate the effect of HBO on visfatin in hypoxic human coronary arterial endothelial cells (HCAECs). HCAECs under chemical hypoxia (antimycin A, 0.01 mmol/L) were exposed to HBO (2.5 atmosphere absolute; ATA) for 2-4 hours. Western blot, real-time polymerase chain reaction, electrophoretic mobility shift assay, luciferase promoter activity, migration and tube formation assay, and in vitro glucose uptake were measured. Visfatin protein expression increased in hypoxic HCAECs with earlier angiotensin II (AngII) secretion and c-Jun N-terminal kinase (JNK) phosphorylation, which could be effectively suppressed by the JNK inhibitor (SP600125), AngII antibody or AngII receptor blocker (losartan). In hypoxic HCAECs, HBO further induced earlier expression of visfatin and AngII. Hypoxia significantly increased DNA-protein binding activity of hypoxia-inducible factor-1α (HIF-1α) and visfatin. Hypoxia, hypoxia with HBO and exogenous addition of AngII also increased promoter transcription to visfatin; SP600125 and losartan blocked this activity. In HCAECs, glucose uptake, migration and tube formation were increased in the presence of hypoxia with HBO, but were inhibited by visfatin small interfering RNA, SP600125 and losartan. In conclusion, HBO activates visfatin expression and angiogenesis in hypoxic HCAECs, an effect mediated by AngII, mainly through the JNK pathway.
MeSH term(s)	Angiotensin II/metabolism ; Anthracenes/pharmacology ; Cell Movement/drug effects ; Cell Movement/genetics ; Cells, Cultured ; Coronary Vessels/drug effects ; Coronary Vessels/metabolism ; Cytokines/metabolism ; Endothelial Cells/drug effects ; Endothelial Cells/metabolism ; Glucose/metabolism ; Humans ; Hyperbaric Oxygenation/methods ; Hypoxia/metabolism ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; JNK Mitogen-Activated Protein Kinases/metabolism ; Losartan/pharmacology ; Neovascularization, Pathologic/metabolism ; Nicotinamide Phosphoribosyltransferase/metabolism ; Oxygen/metabolism ; Promoter Regions, Genetic/drug effects ; Promoter Regions, Genetic/genetics ; RNA, Small Interfering/genetics ; Signal Transduction/drug effects ; Signal Transduction/physiology
Chemical Substances	Anthracenes ; Cytokines ; Hypoxia-Inducible Factor 1, alpha Subunit ; RNA, Small Interfering ; Angiotensin II (11128-99-7) ; pyrazolanthrone (1TW30Y2766) ; Nicotinamide Phosphoribosyltransferase (EC 2.4.2.12) ; nicotinamide phosphoribosyltransferase, human (EC 2.4.2.12) ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Glucose (IY9XDZ35W2) ; Losartan (JMS50MPO89) ; Oxygen (S88TT14065)
Language	English
Publishing date	2020-01-19
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2074559-X
ISSN	1582-4934 ; 1582-4934 ; 1582-1838
ISSN (online)	1582-4934
ISSN	1582-4934 ; 1582-1838
DOI	10.1111/jcmm.14926
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Zs.A 5752: Show issues

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Article ; Online: Exosomal MALAT1 Derived from High Glucose-Treated Macrophages Up-Regulates Resistin Expression via miR-150-5p Downregulation

Kou-Gi Shyu / Bao-Wei Wang / Wei-Jen Fang / Chun-Ming Pan / Chiu-Mei Lin

International Journal of Molecular Sciences, Vol 23, Iss 1095, p

2022 Volume 1095

Abstract	Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) plays a crucial role in the pathophysiological process associated with diabetes-related complications. The effect of high glucose levels on macrophage-derived exosomal MALAT1 is unknown. Therefore, we investigated the molecular regulatory mechanisms controlling exosomal MALAT1 in macrophages under high glucose treatment and the therapeutic target of macrophage-derived exosomal MALAT1 using a balloon injury model of vascular disease in diabetic rats. High glucose (25 mM) significantly increased MALAT1 expression in macrophage-derived exosomes. MALAT1 suppressed miR-150-5p expression in macrophage-derived exosomes under high-glucose conditions. Silencing MALAT1 using MALAT1 siRNA significantly reversed miR-150-5p expression induced by macrophage-derived exosomes. Macrophage-derived exosomes under high-glucose treatment significantly increased resistin expression in macrophages. Silencing MALAT1 and overexpression of miR-150-5p significantly decreased resistin expression induced by macrophage-derived exosomes. Overexpression of miR-150-5p significantly decreased resistin luciferase activity induced by macrophage-derived exosomes. Macrophage-derived exosome significantly decreased glucose uptake in macrophages and silencing MALAT1, resistin or overexpression of miR-150-5p significantly reversed glucose uptake. Balloon injury to the carotid artery significantly increased MALAT1 and resistin expression and significantly decreased miR-150-5p expression in arterial tissue. Silencing MALAT1 significantly reversed miR-150-5p expression in arterial tissue after balloon injury. Silencing MALAT1 or overexpression of miR-150-5p significantly reduced resistin expression after balloon injury. In conclusion, high glucose up-regulates MALAT1 to suppress miR-150-5p expression and counteracts the inhibitory effect of miR-150-5p on resistin expression in macrophages to promote vascular disease. Macrophage-derived exosomes containing MALAT1 may serve as a novel cell-free approach for the treatment of vascular disease in diabetes mellitus.
Keywords	high glucose ; macrophage ; MALAT1 ; exosome ; miR-1505p ; resistin ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Language	English
Publishing date	2022-01-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article ; Online: Enhancement of bicycle exercise capacity in patients with chronotropic incompetence through closed-loop stimulation: a randomized crossover trial.

Chua, Su-Kiat / Chen, Wen-Ling / Chen, Lung-Ching / Shyu, Kou-Gi / Hung, Huei-Fong / Lee, Shih-Huang / Wang, Tzu-Lin / Lai, Wei-Ting / Chen, Kuan-Jen / Liao, Zhen-Yu / Chuang, Cheng-Yen / Chou, Ching-Yao

Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology

2023 Volume 25, Issue 12

Abstract: Aims: This study aimed to investigate the effectiveness of closed-loop stimulation (CLS) pacing compared with the traditional DDD mode in patients with chronotropic incompetence (CI) using bicycle-based cardiopulmonary exercise testing (CPET).: ... ...

Abstract	Aims: This study aimed to investigate the effectiveness of closed-loop stimulation (CLS) pacing compared with the traditional DDD mode in patients with chronotropic incompetence (CI) using bicycle-based cardiopulmonary exercise testing (CPET). Methods and results: This single-centre, randomized crossover trial involved 40 patients with CI. Patients were randomized to receive either DDD-CLS or DDD mode pacing for 2 months, followed by a crossover to the alternative mode for an additional 2 months. Bicycling-based CPET was conducted at the 3- and 5-month follow-up visits to assess exercise capacity. Other cardiopulmonary exercise outcome measures and health-related quality of life (QoL) were also assessed. DDD-CLS mode pacing significantly improved exercise capacity, resulting in a peak oxygen uptake (14.8 ± 4.0 vs. 12.0 ± 3.6 mL/kg/min, P < 0.001) and oxygen uptake at the ventilatory threshold (10.0 ± 2.2 vs. 8.7 ± 1.8 mL/kg/min, P < 0.001) higher than those of the DDD mode. However, there were no significant differences in other cardiopulmonary exercise outcome measures such as ventilatory efficiency of carbon dioxide production slope, oxygen uptake efficiency slope, and end-tidal carbon dioxide between the two modes. Patients in the DDD-CLS group reported a better QoL, and 97.5% expressed a preference for the DDD-CLS mode. Conclusion: DDD-CLS mode pacing demonstrated improved exercise capacity and QoL in patients with CI, highlighting its potential as an effective pacing strategy for this patient population.
MeSH term(s)	Humans ; Quality of Life ; Cardiac Pacing, Artificial/methods ; Carbon Dioxide ; Bicycling ; Exercise Tolerance ; Cross-Over Studies ; Exercise Test ; Oxygen ; Heart Rate/physiology
Chemical Substances	Carbon Dioxide (142M471B3J) ; Oxygen (S88TT14065)
Language	English
Publishing date	2023-11-21
Publishing country	England
Document type	Randomized Controlled Trial ; Journal Article
ZDB-ID	1449879-0
ISSN	1532-2092 ; 1099-5129
ISSN (online)	1532-2092
ISSN	1099-5129
DOI	10.1093/europace/euad358
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