The Experts below are selected from a list of 132 Experts worldwide ranked by ideXlab platform
Toshisuke Morita - One of the best experts on this subject based on the ideXlab platform.
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indoxyl sulfate stimulates monocyte chemoattractant protein 1 expression in human umbilical vein endothelial cells by inducing oxidative stress through activation of the nadph oxidase nuclear factor κb pathway
Circulation, 2010Co-Authors: Natsumi Masai, Junko Tatebe, Gen Yoshino, Toshisuke MoritaAbstract:Background: Chronic kidney disease (CKD) is recognized as a common condition that elevates the risk of atherosclerotic cardiovascular disease (CVD). Evidence suggests that increased oxidative stress is an emerging key Mechanism of Atherosclerosis in CKD. One recent study reported that indoxyl sulfate (IS), a uremic toxin derived from dietary protein, could cause vascular disorder, however, little is known about the Mechanism involved. The present study examined the signaling pathway that is activated by IS to induce monocyte chemoattractant protein-1 (MCP-1), which plays an important role in the development of Atherosclerosis, in cultured human umbilical vein endothelial cells (HUVEC). Methods and Results: We show that IS enhanced reactive oxygen species (ROS) production, assessed by dihydroethidium staining, by HUVEC. IS also induced the expression of MCP-1, which was measured by enzyme-linked immunosorbent assay and real-time reverse transcription-polymerase chain reaction. These changes were suppressed by apocynin, a specific inhibitor of NADPH oxidase. Furthermore, IS induced the expression of NADPH oxidase 4 (Nox4) mRNA. IS-induced stimulation of ERK1/2 and p38 phosphorylation, detected by immunoblotting, was inhibited by apocynin. Finally, IS activated NF-κB, which was suppressed by inhibiting ERK1/2 and p38, resulting in reduced MCP-1 expression. These results suggest that IS increases NADPH oxidase-derived ROS, which in turn, activates the MAPK/NF-κB pathway and leads to induction of MCP-1 expression in HUVEC. Conclusions: These findings raise the possibility that IS plays an important pathophysiological role in the development of CVD in individuals with CKD. (Circ J 2010; 74: 2216-2224)
Natsumi Masai - One of the best experts on this subject based on the ideXlab platform.
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indoxyl sulfate stimulates monocyte chemoattractant protein 1 expression in human umbilical vein endothelial cells by inducing oxidative stress through activation of the nadph oxidase nuclear factor κb pathway
Circulation, 2010Co-Authors: Natsumi Masai, Junko Tatebe, Gen Yoshino, Toshisuke MoritaAbstract:Background: Chronic kidney disease (CKD) is recognized as a common condition that elevates the risk of atherosclerotic cardiovascular disease (CVD). Evidence suggests that increased oxidative stress is an emerging key Mechanism of Atherosclerosis in CKD. One recent study reported that indoxyl sulfate (IS), a uremic toxin derived from dietary protein, could cause vascular disorder, however, little is known about the Mechanism involved. The present study examined the signaling pathway that is activated by IS to induce monocyte chemoattractant protein-1 (MCP-1), which plays an important role in the development of Atherosclerosis, in cultured human umbilical vein endothelial cells (HUVEC). Methods and Results: We show that IS enhanced reactive oxygen species (ROS) production, assessed by dihydroethidium staining, by HUVEC. IS also induced the expression of MCP-1, which was measured by enzyme-linked immunosorbent assay and real-time reverse transcription-polymerase chain reaction. These changes were suppressed by apocynin, a specific inhibitor of NADPH oxidase. Furthermore, IS induced the expression of NADPH oxidase 4 (Nox4) mRNA. IS-induced stimulation of ERK1/2 and p38 phosphorylation, detected by immunoblotting, was inhibited by apocynin. Finally, IS activated NF-κB, which was suppressed by inhibiting ERK1/2 and p38, resulting in reduced MCP-1 expression. These results suggest that IS increases NADPH oxidase-derived ROS, which in turn, activates the MAPK/NF-κB pathway and leads to induction of MCP-1 expression in HUVEC. Conclusions: These findings raise the possibility that IS plays an important pathophysiological role in the development of CVD in individuals with CKD. (Circ J 2010; 74: 2216-2224)
Gen Yoshino - One of the best experts on this subject based on the ideXlab platform.
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indoxyl sulfate stimulates monocyte chemoattractant protein 1 expression in human umbilical vein endothelial cells by inducing oxidative stress through activation of the nadph oxidase nuclear factor κb pathway
Circulation, 2010Co-Authors: Natsumi Masai, Junko Tatebe, Gen Yoshino, Toshisuke MoritaAbstract:Background: Chronic kidney disease (CKD) is recognized as a common condition that elevates the risk of atherosclerotic cardiovascular disease (CVD). Evidence suggests that increased oxidative stress is an emerging key Mechanism of Atherosclerosis in CKD. One recent study reported that indoxyl sulfate (IS), a uremic toxin derived from dietary protein, could cause vascular disorder, however, little is known about the Mechanism involved. The present study examined the signaling pathway that is activated by IS to induce monocyte chemoattractant protein-1 (MCP-1), which plays an important role in the development of Atherosclerosis, in cultured human umbilical vein endothelial cells (HUVEC). Methods and Results: We show that IS enhanced reactive oxygen species (ROS) production, assessed by dihydroethidium staining, by HUVEC. IS also induced the expression of MCP-1, which was measured by enzyme-linked immunosorbent assay and real-time reverse transcription-polymerase chain reaction. These changes were suppressed by apocynin, a specific inhibitor of NADPH oxidase. Furthermore, IS induced the expression of NADPH oxidase 4 (Nox4) mRNA. IS-induced stimulation of ERK1/2 and p38 phosphorylation, detected by immunoblotting, was inhibited by apocynin. Finally, IS activated NF-κB, which was suppressed by inhibiting ERK1/2 and p38, resulting in reduced MCP-1 expression. These results suggest that IS increases NADPH oxidase-derived ROS, which in turn, activates the MAPK/NF-κB pathway and leads to induction of MCP-1 expression in HUVEC. Conclusions: These findings raise the possibility that IS plays an important pathophysiological role in the development of CVD in individuals with CKD. (Circ J 2010; 74: 2216-2224)
Junko Tatebe - One of the best experts on this subject based on the ideXlab platform.
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indoxyl sulfate stimulates monocyte chemoattractant protein 1 expression in human umbilical vein endothelial cells by inducing oxidative stress through activation of the nadph oxidase nuclear factor κb pathway
Circulation, 2010Co-Authors: Natsumi Masai, Junko Tatebe, Gen Yoshino, Toshisuke MoritaAbstract:Background: Chronic kidney disease (CKD) is recognized as a common condition that elevates the risk of atherosclerotic cardiovascular disease (CVD). Evidence suggests that increased oxidative stress is an emerging key Mechanism of Atherosclerosis in CKD. One recent study reported that indoxyl sulfate (IS), a uremic toxin derived from dietary protein, could cause vascular disorder, however, little is known about the Mechanism involved. The present study examined the signaling pathway that is activated by IS to induce monocyte chemoattractant protein-1 (MCP-1), which plays an important role in the development of Atherosclerosis, in cultured human umbilical vein endothelial cells (HUVEC). Methods and Results: We show that IS enhanced reactive oxygen species (ROS) production, assessed by dihydroethidium staining, by HUVEC. IS also induced the expression of MCP-1, which was measured by enzyme-linked immunosorbent assay and real-time reverse transcription-polymerase chain reaction. These changes were suppressed by apocynin, a specific inhibitor of NADPH oxidase. Furthermore, IS induced the expression of NADPH oxidase 4 (Nox4) mRNA. IS-induced stimulation of ERK1/2 and p38 phosphorylation, detected by immunoblotting, was inhibited by apocynin. Finally, IS activated NF-κB, which was suppressed by inhibiting ERK1/2 and p38, resulting in reduced MCP-1 expression. These results suggest that IS increases NADPH oxidase-derived ROS, which in turn, activates the MAPK/NF-κB pathway and leads to induction of MCP-1 expression in HUVEC. Conclusions: These findings raise the possibility that IS plays an important pathophysiological role in the development of CVD in individuals with CKD. (Circ J 2010; 74: 2216-2224)
Yanzhe Wang - One of the best experts on this subject based on the ideXlab platform.
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association of g protein coupled purinergic receptor p2y2 with ischemic stroke in a han chinese population of north china
Neural Regeneration Research, 2019Co-Authors: Liying Yuan, Yanzhe WangAbstract:The G-protein-coupled purinergic receptor P2Y2 (P2RY2) plays an important role in the Mechanism of Atherosclerosis, which is relevant to ischemic stroke. This retrospective case-control study aimed to assess the relationship between P2RY2 gene polymorphisms and ischemic stroke risk in the northern Han Chinese population. In this study, clinical data and peripheral blood specimens were collected from 378 ischemic stroke patients and 344 controls. The ischemic stroke participants were recruited from the First Affiliated Hospital of China Medical University and the First Affiliated Hospital of Liaoning Medical University. The controls were recruited from the Health Check Center at the First Affiliated Hospital of China Medical University. Ischemic stroke patients were divided into two subgroups according to the Trial of ORG 10172 in Acute Stroke Treatment (TOAST) classification: large-artery Atherosclerosis (n = 178) and small-artery occlusion (n = 200) strokes. All subjects were genotyped for three single nucleotide polymorphisms (rs4944831, rs1783596, and rs4944832) in the P2RY2 gene using peripheral venous blood samples. The distribution of the dominant rs4944832 phenotype (GG vs. GA+AA) differed significantly between small-artery occlusion patients and control subjects (odds ratio (OR) = 1.720, 95% confidence interval (CI): 1.203–2.458, P
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Association of G-protein coupled purinergic receptor P2Y2 with ischemic stroke in a Han Chinese population of North China
Medknow Publications, 2019Co-Authors: Liying Yuan, Yanzhe WangAbstract:The G-protein-coupled purinergic receptor P2Y2 (P2RY2) plays an important role in the Mechanism of Atherosclerosis, which is relevant to ischemic stroke. This retrospective case-control study aimed to assess the relationship between P2RY2 gene polymorphisms and ischemic stroke risk in the northern Han Chinese population. In this study, clinical data and peripheral blood specimens were collected from 378 ischemic stroke patients and 344 controls. The ischemic stroke participants were recruited from the First Affiliated Hospital of China Medical University and the First Affiliated Hospital of Liaoning Medical University. The controls were recruited from the Health Check Center at the First Affiliated Hospital of China Medical University. Ischemic stroke patients were divided into two subgroups according to the Trial of ORG 10172 in Acute Stroke Treatment (TOAST) classification: large-artery Atherosclerosis (n = 178) and small-artery occlusion (n = 200) strokes. All subjects were genotyped for three single nucleotide polymorphisms (rs4944831, rs1783596, and rs4944832) in the P2RY2 gene using peripheral venous blood samples. The distribution of the dominant rs4944832 phenotype (GG vs. GA+AA) differed significantly between small-artery occlusion patients and control subjects (odds ratio (OR) = 1.720, 95% confidence interval (CI): 1.203–2.458, P < 0.01). Multivariable logistic regression analysis revealed that the GG genotype of rs4944832 was significantly more prevalent in small-artery occlusion patients than in control subjects (OR = 1.807, 95% CI: 1.215–2.687, P < 0.01). The overall distribution of the haplotype established by rs4944831-rs1783596-rs4944832 was significantly different between ischemic stroke patients and controls (P < 0.01). In ischemic stroke patients, the frequency of the G-C-G haplotype was significantly higher than in control subjects (P = 0.028), whereas the frequency of the T-C-A haplotype was lower than in control subjects (P = 0.047). These results indicate that the G-C-G haplotype of P2RY2 is a susceptibility haplotype for ischemic stroke. In addition, the GG genotype of rs4944832 may be associated with the development of small-artery occlusion in the northern Han Chinese population. The study protocol was approved by the Ethics Committee of the First Affiliated Hospital of China Medical University on February 20, 2012 (No. 2012-38-1) and the First Affiliated Hospital of Liaoning Medical University, China, on March 1, 2013 (No. 2013-03-1). All participants gave their informed consent. This trial was registered with the ISRCTN Registry (ISRCTN11439124) on October 24, 2018. Protocol version (1.0)