Ellagic acid inhibits oxidized LDL-mediated LOX-1 expression, ROS generation, and inflammation in human endothelial cells Wen-Jane Lee, PhD, Hsiu-Chung.

Slides:

Advertisements

Similar presentations

Fig. 1. Impact of AA on ROS generation by human spermatozoa

Advertisements

Metformin prevents glucotoxicity by alleviating oxidative and ER stress–induced CD36 expression in pancreatic beta cells Jun Sung Moon, Udayakumar Karunakaran,

The chemokine CCL2 activates p38 mitogen-activated protein kinase pathway in cultured rat hippocampal cells Jungsook Cho, Donna L. Gruol Journal of.

Β-Glucan attenuates inflammatory responses in oxidized LDL-induced THP-1 cells via the p38 MAPK pathway S. Wang, H. Zhou, T. Feng, R. Wu, X. Sun, N.

Differential effects of GLP-1 receptor agonist on foam cell formation in monocytes between non-obese and obese subjects Masashi Tanaka, Yoshiyuki Matsuo,

Glucocorticoids Augment the Chemically Induced Production and Gene Expression of Interleukin-1α through NF-κB and AP-1 Activation in Murine Epidermal.

Volume 55, Issue 4, Pages (April 1999)

Chrysin restores PDGF-induced inhibition on protein tyrosine phosphatase and reduces PDGF signaling in cultured VSMCs Huey-Ming Lo, Min-Wen Wu, Shiow-Lin.

Oxidized low-density lipoprotein (ox-LDL) binding to lectin-like ox-LDL receptor-1 (LOX- 1) in cultured bovine articular chondrocytes increases production.

MicroRNA-558 regulates the expression of cyclooxygenase-2 and IL-1β-induced catabolic effects in human articular chondrocytes S.J. Park, E.J. Cheon,

Volume 62, Issue 6, Pages (December 2002)

Ellagic acid inhibits oxidized LDL-mediated LOX-1 expression, ROS generation, and inflammation in human endothelial cells Wen-Jane Lee, PhD, Hsiu-Chung.

Crude extracts of Solanum lyratum protect endothelial cells against oxidized low-density lipoprotein-induced injury by direct antioxidant action Wei-Wen.

Regulation of vascular smooth muscle cell expression and function of matrix metalloproteinases is mediated by estrogen and progesterone exposure Oscar.

Reduced hind limb ischemia-reperfusion injury in Toll-like receptor-4 mutant mice is associated with decreased neutrophil extracellular traps Rahmi Oklu,

Ginkgo biloba extract inhibits oxidized low-density lipoprotein (oxLDL)-induced matrix metalloproteinase activation by the modulation of the lectin-like.

Sandhya K. Balaram, MD, Devendra K. Agrawal, PhD, R

Adult Aortic Valve Interstitial Cells Have Greater Responses to Toll-Like Receptor 4 Stimulation Xin-Sheng Deng, MD, Xianzhong Meng, MD, PhD, QingChun.

Regulation of mesenchymal stem cell chondrogenesis by glucose through protein kinase C/transforming growth factor signaling T.-L. Tsai, P.A. Manner,

Role of reactive oxygen species in inhibition of endothelial cell migration by oxidized low-density lipoprotein John A. van Aalst, MD, Dong-Mei Zhang,

Crude extracts of Solanum lyratum protect endothelial cells against oxidized low-density lipoprotein-induced injury by direct antioxidant action Wei-Wen.

M. -H. Moon, J. -K. Jeong, Y. -J. Lee, J. -W. Seol, C. J. Jackson, S

Hyperphosphatemia induces protective autophagy in endothelial cells through the inhibition of Akt/mTOR signaling Yu-Juei Hsu, MD, PhD, Shih-Che Hsu,

Bertrand Poussier, MD, Alfredo C

Peroxynitrite-modified collagen-II induces p38/ERK and NF-κB-dependent synthesis of prostaglandin E2 and nitric oxide in chondrogenically differentiated.

Signal transduction pathways triggered by the FcϵRIIb receptor (CD23) in human monocytes lead to nuclear factor-κB activation Rosa M. Ten, MD, PhDa,

Sun A. Ham, Eun S. Kang, Hanna Lee, Jung S. Hwang, Taesik Yoo, Kyung S

Cytokine-inducible CD40 expression in human endothelial cells is mediated by interferon regulatory factor-1 by Andreas H. Wagner, Matthias Gebauer, Beatrix.

Hyperphosphatemia induces protective autophagy in endothelial cells through the inhibition of Akt/mTOR signaling Yu-Juei Hsu, MD, PhD, Shih-Che Hsu,

MicroRNA-558 regulates the expression of cyclooxygenase-2 and IL-1β-induced catabolic effects in human articular chondrocytes S.J. Park, E.J. Cheon,

Aspirin prevents resistin-induced endothelial dysfunction by modulating AMPK, ROS, and Akt/eNOS signaling Hsiu-Chung Ou, PhD, Wen-Jane Lee, PhD, Ching-Mei.

Histone deacetylase inhibitors suppress interleukin-1β-induced nitric oxide and prostaglandin E2 production in human chondrocytes N. Chabane, M.Sc.,

Transforming growth factor-β increases vascular smooth muscle cell proliferation through the Smad3 and extracellular signal-regulated kinase mitogen-activated.

Sandhya K. Balaram, MD, Devendra K. Agrawal, PhD, R

Dysregulation of LDL receptor under the influence of inflammatory cytokines: A new pathway for foam cell formation1 Dr Xiong Z. Ruan, Zac Varghese, Stephen.

Volume 68, Issue 6, Pages (December 2005)

Indomethacin Sensitizes TRAIL-Resistant Melanoma Cells to TRAIL-Induced Apoptosis through ROS-Mediated Upregulation of Death Receptor 5 and Downregulation.

Volume 124, Issue 5, Pages (May 2003)

Translocation of protein kinase C isoforms is involved in propofol-induced endothelial nitric oxide synthase activation L. Wang, B. Wu, Y. Sun, T. Xu,

Daniel J. Wong, MD, Daniel Y. Lu, MD, Clinton D

Toll-like receptor 9 suppression in plasmacytoid dendritic cells after IgE-dependent activation is mediated by autocrine TNF-α John T. Schroeder, PhD,

Sphingosine-1-phosphate–induced oxygen free radical generation in smooth muscle cell migration requires Gα12/13 protein-mediated phospholipase C activation

Ambient pressure upregulates nitric oxide synthase in a phosphorylated-extracellular regulated kinase– and protein kinase C–dependent manner Angela G.

Simvastatin Protects Human Melanocytes from H2O2-Induced Oxidative Stress by Activating Nrf2 Yuqian Chang, Shuli Li, Weinan Guo, Yuqi Yang, Weigang Zhang,

Interleukin-1β and interleukin-6 disturb the antioxidant enzyme system in bovine chondrocytes: a possible explanation for oxidative stress generation

Akio Horiguchi, Mototsugu Oya, Ken Marumo, Masaru Murai

AT-101, a Pan-Bcl-2 Inhibitor, Leads to Radiosensitization of Non-small Cell Lung Cancer Luigi Moretti, MD, Bo Li, MD, Kwang Woon Kim, PhD, Heidi Chen,

Oxidized low-density lipoprotein (ox-LDL) binding to lectin-like ox-LDL receptor-1 (LOX- 1) in cultured bovine articular chondrocytes increases production.

Evidence for two distinct pathways in TNFα-induced membrane and soluble forms of ICAM-1 in human osteoblast-like cells isolated from osteoarthritic patients

Evidence for low-density lipoprotein–induced expression of connective tissue growth factor in mesangial cells Mimi Sohn, Yan Tan, Richard L. Klein, Ayad.

Lovastatin Sensitizes Lung Cancer Cells to Ionizing Radiation: Modulation of Molecular Pathways of Radioresistance and Tumor Suppression Toran Sanli,

Volume 133, Issue 5, Pages (November 2007)

Selenomethionine inhibits IL-1β inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX2) expression in primary human chondrocytes A.W.M. Cheng,

Endothelial expression of intercellular adhesion molecule 1 and vascular cell adhesion molecule 1 is suppressed by postbypass plasma containing increased.

Sang-Wahn Koo, Katherine A. Casper, Kristen B. Otto, Amy K

Estrogen receptor β agonist diarylpropionitrile inhibits lipopolysaccharide-induced regulated on activation normal T cell expressed and secreted (RANTES)

Secretory Phospholipase A2 Inhibition Attenuates Intercellular Adhesion Molecule-1 Expression in Human Esophageal Adenocarcinoma Cells Miral R. Sadaria,

P38 Mitogen-activated Protein Kinase and Extracellular Signal-regulated Kinases Play Distinct Roles in the Activation of Dendritic Cells by Two Representative.

The effects of ginsenoside Rb1 on endothelial damage and ghrelin expression induced by hyperhomocysteine Zhiwei Xu, PhD, Taohua Lan, MD, Weikang Wu,

Ketoconazole Suppresses Prostaglandin E2-Induced Cyclooxygenase-2 Expression in Human Epidermoid Carcinoma A-431 Cells Naoko Kanda, Dr., Shinichi Watanabe

All-Trans-Retinoic Acid Induces Interleukin-8 via the Nuclear Factor-κB and p38 Mitogen-Activated Protein Kinase Pathways in Normal Human Keratinocytes

Volume 138, Issue 7, Pages e1 (June 2010)

P38 Mitogen-Activated Protein Kinase Mediates Dual Role of Ultraviolet B Radiation in Induction of Maturation and Apoptosis of Monocyte-Derived Dendritic.

Volume 55, Issue 4, Pages (April 1999)

Activation and Translocation of p38 Mitogen-Activated Protein Kinase After Stimulation of Monocytes With Contact Sensitizers Pia Brand, Sibylle Plochmann,

Volume 65, Issue 5, Pages (May 2004)

SIRT1, a Class III Histone Deacetylase, Regulates LPS-Induced Inflammation in Human Keratinocytes and Mediates the Anti-Inflammatory Effects of Hinokitiol

Glucocorticoid-induced surface expression of annexin 1 blocks β2-integrin adhesion of human eosinophils to intercellular adhesion molecule 1 surrogate.

Prasun K. Datta, Elias A. Lianos Kidney International

IGF-1 regulation of type II collagen and MMP-13 expression in rat endplate chondrocytes via distinct signaling pathways M. Zhang, Ph.D., Q. Zhou, M.D.,

Presentation transcript:

Ellagic acid inhibits oxidized LDL-mediated LOX-1 expression, ROS generation, and inflammation in human endothelial cells Wen-Jane Lee, PhD, Hsiu-Chung Ou, PhD, Wen-Cheng Hsu, MD, Min-Min Chou, MD, Jenn-Jhy Tseng, MD, PhD, Shih-Lan Hsu, PhD, Kun-Ling Tsai, MS, Wayne Huey-Herng Sheu, MD, PhD Journal of Vascular Surgery Volume 52, Issue 5, Pages 1290-1300 (November 2010) DOI: 10.1016/j.jvs.2010.04.085 Copyright © 2010 Society for Vascular Surgery Terms and Conditions

Fig 1 Inhibitory effect of ellagic acid on oxidized low-density lipoprotein (oxLDL)-induced endothelial LOX-1 protein expression. Human umbilical vein endothelial cells (HUVECs) were pretreated with ellagic acid (5-20 μM) or DPI (5 μM) for 2 hours followed by exposure to oxLDL (150 μg/mL) for a further 24-hour period. At the end of the incubation period, cells were lysed and proteins were analyzed by Western blot. Protein levels of LOX-1 were normalized to the level of β-actin. Data illustrated on the graph bars represent the mean ± SEM of three different experiments. *P < .05 compared with oxLDL-stimulated HUVECs. Journal of Vascular Surgery 2010 52, 1290-1300DOI: (10.1016/j.jvs.2010.04.085) Copyright © 2010 Society for Vascular Surgery Terms and Conditions

Fig 2 Inhibitory effects of ellagic acid on oxidized low-density lipoprotein (oxLDL)-induced reactive oxygen species (ROS) production in human umbilical vein endothelial cells (HUVECs). After pre-incubation for 2 hours with the indicated concentrations of ellagic acid (5-20 μM), cells were treated with 150 μg/mL oxLDL for 2 hours followed by a 1-hour incubation with superoxide-sensitive fluorescent probe DHE (10 μM). (A) Fluorescence images show the ROS level in control cells (left) and HUVECs stimulated with oxLDL alone (middle) and in the presence of 10 μM ellagic acid (right). (B) Fluorescence intensity of cells was measured with a fluorescence microplate reader. Fluorescence distribution of DHE oxidation is expressed as a percentage of increased intensity. (C, D) Representative Western blots of Cu, Zn-SOD (SOD-1), and Mn-SOD (SOD-2) protein levels in HUVECs pretreated with ellagic acid for 2 hours followed by stimulation with 150 μg/mL oxLDL for 24 hours. Data are expressed as the mean ± SEM of three independent analyses. *P < .05 compared with oxLDL-stimulated HUVECs. Journal of Vascular Surgery 2010 52, 1290-1300DOI: (10.1016/j.jvs.2010.04.085) Copyright © 2010 Society for Vascular Surgery Terms and Conditions

Fig 3 Ellagic acid attenuated the level of NADPH oxidase membrane assembly. Human umbilical vein endothelial cells (HUVECs) were pretreated for 2 hours with the indicated concentrations of ellagic acid followed by stimulation with oxidized low-density lipoprotein (oxLDL) (150 μg/mL) for 1 hour (A-C) or 24 hours (D-F). Preparation of membrane and cytosolic proteins is described in the Material and Methods section. The levels of cytosolic protein and membrane protein were normalized to the levels of β-actin and flotillin-1, respectively. Representative Western blots and summary data showed that ellagic acid protected against oxLDL-induced p47phox and Rac-1 translocation to the plasma membrane, and gp91 as well as p22phox expression. The values represent means ± SEM from three separate experiments. *P < .05 vs oxLDL treatment. Journal of Vascular Surgery 2010 52, 1290-1300DOI: (10.1016/j.jvs.2010.04.085) Copyright © 2010 Society for Vascular Surgery Terms and Conditions

Fig 4 Ellagic acid ameliorated the oxidized low-density lipoprotein (oxLDL)-down-regulated eNOS and up-regulated iNOS protein expression (A-C), oxLDL-enhanced NO release (D), and nitration of tyrosine residues (E, F). In addition, ellagic acid attenuated the oxLDL-enhanced secretion of ET-1 (G). Human umbilical vein endothelial cells (HUVECs) were pretreated for 2 hours with the indicated concentrations of ellagic acid followed by stimulation with oxLDL (150 μg/mL) for 24 hours. At the end of the incubation period, level of eNOS, iNOS, and nitrotyrosine protein (normalized to the levels of β-actin) were determined by immunoblotting; content of NO was assayed using Gries reagent; ET-1 secretion was measured by ELISA. The values represent means ± SEM from three separate experiments. *P < .05 vs oxLDL treatment. Journal of Vascular Surgery 2010 52, 1290-1300DOI: (10.1016/j.jvs.2010.04.085) Copyright © 2010 Society for Vascular Surgery Terms and Conditions

Fig 5 Ellagic acid inhibits oxidized low-density lipoprotein (oxLDL)-induced p38MAPK protein phosphorylation (p-p38MAPK). Human umbilical vein endothelial cells (HUVECs) were pretreated for 2 hours with the indicated concentrations of ellagic acid followed by stimulation with oxLDL (150 μg/mL) for 1 hour. Expression of p38MAPK was analyzed by Western blotting and quantified by densitometry. Treatment with 10 μM SB203580, a specific inhibitor of p38 MAPK, suppressed the oxLDL-induced phosphorylation of the p38MAPK protein. The values represent means ± SEM from three separate experiments. *P < .05 vs oxLDL treatment. Journal of Vascular Surgery 2010 52, 1290-1300DOI: (10.1016/j.jvs.2010.04.085) Copyright © 2010 Society for Vascular Surgery Terms and Conditions

Fig 6 Effects of ellagic acid on oxidized low-density lipoprotein (oxLDL)-induced NF-κB activation. Human umbilical vein endothelial cells (HUVECs) were pretreated for 2 hours with the indicated concentrations of ellagic acid followed by stimulation with oxLDL (150 μg/mL) for 1 hour. Preparation of cytosolic and nuclear proteins is described in the Material and Methods section. The expression levels of the indicated proteins were analyzed by Western blotting and quantified by densitometry (A). The levels of cytosolic protein and nuclear protein were normalized to the levels of β-actin and proliferating cell nuclear antigen, respectively (B, C). The values represent means ± SEM from three separate experiments. *P < .05 vs oxLDL treatment. Journal of Vascular Surgery 2010 52, 1290-1300DOI: (10.1016/j.jvs.2010.04.085) Copyright © 2010 Society for Vascular Surgery Terms and Conditions

Fig 7 Effects of ellagic acid on oxidized low-density lipoprotein (oxLDL)-induced release of inflammatory cytokines, expression of adhesion molecules, and adhesiveness of THP-1 monocytic cells to human umbilical vein endothelial cells (HUVECs). Cells were incubated with indicated concentrations of ellagic acid for 2 hours and then incubated with ox-LDL for an additional 24 hours. ELISA measurements showing IL-6 (A) and IL-8 (B) protein levels in HUVECs treated with oxLDL in the absence or presence of indicated concentrations of ellagic acid. (C) HUVECs were incubated with oxLDL (150 μg/mL) in the absence (light gray) or presence (dark gray) of 20 μM ellagic acid for 24 hours. The histograms of cell surface expression of ICAM-1, VCAM-1, and E-selectin were generated by flow cytometry. (D) Representative fields of monocytes adhering to HUVECs with representative treatments as indicated. (E) Dose-dependent effect of ellagic acid (5-20 μM) on oxLDL (150 μg/mL)-induced adhesiveness of THP-1 to HUVECs was measured as described in the Materials and Methods section. The values represent mean ± SEM of three independent analyses. *P < .05 vs. oxLDL treatment. Journal of Vascular Surgery 2010 52, 1290-1300DOI: (10.1016/j.jvs.2010.04.085) Copyright © 2010 Society for Vascular Surgery Terms and Conditions

Fig 8 Schematic diagram showing cytoprotective signaling of ellagic acid in oxidized low-density lipoprotein (oxLDL)-induced endothelial dysfunction. As depicted, ellagic acid inhibits the LOX-1-mediated signaling cascades initiated by oxLDL-generated reactive oxygen species (ROS). The → indicates activation or induction, and ⊣ indicates inhibition or blockade. Journal of Vascular Surgery 2010 52, 1290-1300DOI: (10.1016/j.jvs.2010.04.085) Copyright © 2010 Society for Vascular Surgery Terms and Conditions