Yudi Her Oktaviono, Yudi Her
Department Of Cardiology & Vascular Medicine, Faculty Of Medicine, Universitas Airlangga, Dr. Soetomo Hospital, Surabaya

Published : 25 Documents Claim Missing Document
Claim Missing Document
Check
Articles

Found 3 Documents
Search
Journal : The Indonesian Biomedical Journal

Proliferation of Peripheral Blood-derived Endothelial Progenitor Cells from Stable Angina Subjects Yudi Her Oktaviono; Djanggan Sargowo; Mohammad Aris Widodo; Yanni Dirgantara; Angliana Chouw; Ferry Sandra
The Indonesian Biomedical Journal Vol 6, No 2 (2014)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v6i2.34

Abstract

BACKGROUND: A population of circulating Endothelial Progenitor Cells (EPCs) has been reported to play important role in maintaining endothelial function and integrity. Since EPCs culture is crucial and an optimized medium is currently available. Therefore we conducted a study to investigate whether stable angina subjects peripheral blood-derived EPCs could be cultured in this medium. Here, we performed study to detect EPCs characteristics and extracellular signalregulated kinase (Erk)1/2 Mitogen-Activated Protein Kinase (MAPK) pathway as possible underlying pathway for EPCs proliferation.METHODS: Peripheral blood EPCs from 8 stable angina subjects were cultured in an optimized medium with/without addition of supplement for 1 or 3 days. Then, the membrane of cultured EPCs were detected with immunofluorescence method for CD34, Vascular Endothelial Growth Factor Receptor 2 (VEGFR-2) and CD133. Colony forming unit (CFU) enumeration was performed. XTT Cell proliferation assay was performed to assess EPCs growth after 1 and 3-days culture. The western blot analysis was performed to detect possible activation of Erk1/2 MAPK.RESULTS: Number of EPCs and CFU cultured for 3 days were significantly higher than the ones cultured for 1 day (p=0.012). EPCs membrane markers from stable angina subjects were detected as well as CFUs were formed. There were significant increase of EPCs number, CFUs number and phosphorylated-Erk2 amount when the groups with and without supplement were compared (p<0.05). Meanwhile U0126, a MAPK Erk1/2 (MEK1/2) inhibitor, significantly inhibited the supplement-induced EPCs number, CFUs number and phosphorylated-Erk2 amount (p<0.05).CONCLUSION: Our results showed that ERK2 MAPK signaling pathway might play an important role in supplement-induced peripheral blood EPCs proliferation in subjects with stable angina.KEYWORDS: endothelial progenitor cell, EPC, p42, Erk2, proliferation
The Role of Endothelial Progenitor Cells in Coronary Artery Disease: Basic Molecular Mechanisms and Its Clinical Potentials Yudi Her Oktaviono; Suryo Ardi Hutomo; Kevin Luke
The Indonesian Biomedical Journal Vol 13, No 2 (2021)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v13i2.1570

Abstract

BACKGROUND: Coronary artery disease (CAD) remains as the world number one cause of morbidity and mortality. Endothelial progenitor cells (EPCs) are known to be involved in vascular biology. Current review briefly summarizes the basics of EPCs and its clinical use in CAD.CONTENT: EPCs were firstly isolated in 1997 and involved in neovascularization. Further evidence defined EPCs into two distinguishable groups, namely: myeloid angiogenic cells (MACs) and endothelial colony forming cells (ECFCs). Common cardiovascular drugs, statin, angiotensin-converting enzyme (ACE) inhibitor, and their combinations, showed beneficial effects on EPCs. Likewise, the incorporation of EPCs upon CAD intervention management had been recently studied. Intramyocardial EPCs implementation and anti-CD34 antibody-coated stents could provide a promising option for refractory symptoms in CAD.SUMMARY: Association between EPCs and CAD is very dynamic and complex. EPCs could serve as both therapeutic target and agent in CAD patients. Subsequently, a universal definition of EPCs is needed for greater research in the future.KEYWORDS: atherosclerosis, coronary artery disease, endothelial progenitor cells, neovascularization
Quercetin Stabilizes Atherosclerotic Plaques by Reducing Matrix Metalloproteinase-9 Expression and Enhancing M2 Macrophage Activity in Wistar Rats Ermawan, Romi; Pikir, Budi Susetyo; Mulyanto, Mulyanto; Utomo, Budi; Widjiati, Widjiati; Oktaviono, Yudi Her
The Indonesian Biomedical Journal Vol 17, No 5 (2025)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v17i5.3790

Abstract

BACKGROUND: Quercetin has been shown to alleviate and prevent atherosclerosis. However, its role in stabilizing atherosclerotic plaques to prevent plaque rupture remains unclear. Therefore, this study was conducted to investigate the effects of quercetin on stabilizing atherosclerotic plaques.METHODS: Thirty-two Wistar rats were objected to a high-fat diet, along with an endothelial injury procedure conducted during the second week to create atherosclerotic plaque models. After six weeks, the subjects were randomly assigned to five groups consist of two control groups and three treatment groups treated with different quercetin dosages. Following the treatment, all subjects were euthanized to collect the left common carotid artery. The stability of the atherosclerotic plaques was evaluated by measuring the expression of matrix metalloproteinase-9 (MMP-9) using real-time polymerase chain reaction, assessing the activity of M1 and M2 macrophages along with the M1/M2 ratio using an enzyme-linked immunosorbent assay, and determining the maximum intima thickness through histopathological examination.RESULTS: Quercetin significantly reduced the expression of MMP-9, increased the activity of M2 macrophages, and lowered the M1/M2 ratio at doses of 10 and 50 mg/kg. However, there was no effect on M1 macrophage activity or maximum intima thickness. Path analysis indicated that quercetin primarily enhanced atherosclerotic plaque stability by reducing MMP-9 expression (p<0.001) and subsequently enhancing M2 macrophage activity (p=0.002).CONCLUSION: Quercetin administration significantly decreased the expression of MMP-9, enhanced the activity of M2 macrophages, and lowered the M1/M2 ratio at specific doses. These findings emphasize the significance of quercetin in stabilizing atherosclerotic plaques.KEYWORDS: atherosclerotic plaque, quercetin, stability, Wistar rats