Biomedical subjects

Shu-Er Chow

Publications and source records attributed to Shu-Er Chow.

7 recordsLinked to original sources

PubMed2006

Resveratrol attenuates oxLDL-stimulated NADPH oxidase activity and protects endothelial cells from oxidative functional damages.

trans-Resveratrol (RSV) has been shown to have cardioprotective effect during ischemia-reperfusion through reactive oxygen species (ROS)-scavenging activity. Elevated ROS has been implicated in the initiation and progression of atherosclerosis. The nicotinamide adenine dinucleotide phosphate oxidase (NOX) is a major source of vascular ROS formation. In the present study, we show that exposure of vascular endothelial cells (EC) to oxidized low-density lipoproteins (oxLDL) results in elevations of NOX activity and cellular ROS levels. The oxLDL effects are effectively suppressed by RSV or astringinin (AST), either before or after oxLDL exposure. In this study, we show that RSV or AST treatment appears to suppress NOX activity by reducing the membrane association of gp91(phox) and Rac1, two protein species required for the assembly of active NOX complex. Exposure to RSV or AST protects EC from oxidative functional damages, including antiplatelet activity and mononucleocyte adhesion. In addition, ANG II-induced NOX activation is also attenuated. These results suggest that RSV or AST protects EC from oxLDL-induced oxidative stress by both direct ROS scavenging and inhibition of NOX activity.

Cells, Cultured↗

PubMed2006

Role of exercise intensities in oxidized low-density lipoprotein-mediated redox status of monocyte in men.

Exercise significantly influences the progression of atherosclerosis. Oxidized LDL (ox-LDL), as a stimulator of oxidative stress, facilitates monocyte-related atherogenesis. This study investigates how exercise intensity impacts ox-LDL-mediated redox status of monocytes. Twenty-five sedentary healthy men exercised mildly, moderately, and heavily (i.e., 40, 60, and 80% maximal oxygen consumption, respectively) on a bicycle ergometer. Reactive oxygen species (ROS) production, cytosolic and mitochondrial superoxide dismutase (c-SOD and m-SOD, respectively) activities, and total and reduced-form gamma-glutamylcysteinyl glycine (t-GSH and r-GSH, respectively) contents in monocytes mediated by ox-LDL were measured. This experiment obtained the following findings: 1) ox-LDL increased monocyte ROS production and was accompanied by decreased c-SOD and m-SOD activities, as well as t-GSH and r-GSH contents, whereas treating monocytes with diphenyleneiodonium (DPI) (a NADPH oxidase inhibitor) or rotenone/2-thenoyltrifluoroacetone (TTFA) (mitochondrial complex I/II inhibitors) hindered ox-LDL-induced monocyte ROS production; 2) production of ROS and reduction of m-SOD activity and r-GSH content in monocyte by ox-LDL were enhanced by heavy exercise and depressed by mild and moderate exercise; and 3) heavy exercise augmented the inhibition of ox-LDL-induced monocyte ROS production by DPI and rotenone/TTFA, whereas these DPI- and rotenone/TTFA-mediated monocyte ROS productions were unchanged in response to mild and moderate exercise. We conclude that heavy exercise increases ox-LDL-induced monocyte ROS production, possibly by decreasing m-SOD activity and r-GSH content in monocytes. However, mild and moderate exercise likely protects individuals against suppression of anti-oxidative capacity of monocyte by ox-LDL.

Adult↗

PubMed2006

Dual regulation of the DeltaNp63 transcriptional activity by DeltaNp63 in human nasopharyngeal carcinoma cell.

p63 splicing variants lacking NH(2)-terminal transactivating domain, known as DeltaNp63, are thought to antagonize p53 and p63 functions and are suggested to play roles in keratinocyte differentiation. Here, we show that DeltaNp63 has a dual-regulatory effect on the activity of its own promoter in NPC-076 cell. Down-regulation of the transcriptional activity is observed when DeltaNp63 is present in low levels. In contrast, up-regulation of DeltaNp63 transcriptional activity is observed when DeltaNp63 is expressed at higher levels. The down-regulation effect is abolished when the p53-binding site of the DeltaNp63 promoter is mutated. In sharp contrast, similar mutation does not affect the up-regulation of the DeltaNp63 transcriptional activity under the same experimental conditions. Further study shows that the up-regulation is correlated with the activation of the STAT3, as the blockade of STAT3 nuclear translocation abolishes the up-regulation by DeltaNp63. Thus, DeltaNp63 exerts a bidirectional regulation of the DeltaNp63 transcriptional activity in NPC-076 cell.

Carcinoma↗

PubMed2005

Exercise paradoxically modulates oxidized low density lipoprotein-induced adhesion molecules expression and trans-endothelial migration of monocyte in men.

Physical exercise can affect the risk of cardiovascular disease. Oxidized-low density lipoprotein (ox-LDL) promotes transendothelial migration (TEM) of monocyte, thereby accelerating the pathogenesis of atherosclerosis. This study investigated how exercise intensity affects monocyte/EC interactions under ox-LDL-mediated condition. Light- (LIE), moderate- (MIE) and high- (HIE) intensity exercise (i.e., 40%, 60%, and 80% VO2max, respectively) on a bicycle ergometer in 18 sedentary healthy men were performed on three separate occasions. Before and immediately after exercise, ox-LDL-promoted expressions of monocyte adhesion molecules and TEM of monocyte, as well as oxidation of LDL and amounts of soluble adhesion molecules in plasma were measured. Analytical results showed that (1) ox-LDL furthered monocyte L-selectin shedding and Mac-1 expression, and an attendant increase in TEM of monocyte, while treating the monocyte with Mac-1 antibody inhibited the ox-LDL-promoted TEM of monocyte; (2) under ox-LDL-treated condition, MIE increased monocyte Mac-1 and LFA-1 expressions, enhancing the TEM of monocyte, whereas HIE downregulated monocyte Mac-1 expression, suppressing the TEM of monocyte; (3) LIE decreased basal LFA-1 expression as well as basal and ox-LDL-promoted TEM of monocyte; and (4) MIE and HIE, but not LIE, elevated plasma ox-LDL level, while there were no significant changes in sL-selectin, sE-selectin, sICAM-1, and sVCAM-1 following these exercises. Therefore, we conclude that monocyte activation and subsequent TEM promoted by ox-LDL are changed by short-term exercise in an intensity-dependent manner. These findings provide a new insight into the may aid the development of suitable exercise intensity enable people to prevent early atherogenesis.

Adult↗

PubMed2005

Antioxidants and myocardial ischemia: reperfusion injuries.

Animal studies have demonstrated that restoration of blood flow to severely ischemic myocardium is a prerequisite for myocardial salvage. However, it has been shown that the restoration of blood flow to ischemic myocardium may be associated with deleterious changes of the myocardium, including arrhythmias, enzyme release, and contractile dysfunction. These changes were considered to be additional injuries to the myocardium manifested at the time of reperfusion. The reperfusion was accompanied by a burst of oxygen free radical generation and their role as main mediators of the reperfusion injury have been well accepted. Reactive oxygen species (ROS) and cellular redox status regulate many important cellular activities. The role of antioxidant as a therapy for reperfusion injury has thus been tried with mixed and mostly negative results. Further studies are needed if the antioxidant therapies for ischemia reperfusion injury were to be effective.

Animals↗

PubMed2004

Effects of exercise training and detraining on oxidized low-density lipoprotein-potentiated platelet function in men.

OBJECTIVE: To investigate how exercise training and detraining affect oxidized low-density lipoprotein (Ox-LDL)-potentiated platelet function in men. DESIGN: Cohort study. SETTING: Department of physical medicine and rehabilitation. PARTICIPANTS: Ten sedentary men (mean age +/- standard error of the mean, 21.6+/-0.2 y) who did not engage in any regular physical activity for at least 1 year before the study. INTERVENTIONS: Subjects cycled on an ergometer at about 50% of maximal oxygen consumption for 30 minutes daily, 5 days a week, for 8 weeks, then detrained for 12 weeks. MAIN OUTCOME MEASURES: During the experimental period, blood samples from the subjects were collected before and immediately after a progressive exercise test (ie, strenuous, acute exercise) every 4 weeks. The following measurements were taken when the subjects were at rest and immediately after exercise: plasma lipid profile, plasma Ox-LDL level, and platelet aggregation and intracellular calcium concentration ([Ca2+]i) elevation induced by adenosine disphosphate (ADP) alone or simultaneous ADP and Ox-LDL addition. RESULTS: Analytical results indicated that: (1) plasma total cholesterol and LDL levels were reduced after exercise training from 151+/-7 mg/dL and 58+/-2 mg/dL to 133+/-6 mg/dL and 46+/-2 mg/dL (P<.05), respectively, whereas the plasma Ox-LDL level remained unchanged; (2) platelet aggregation and [Ca2+]i elevation promoted by 100 microg/mL of Ox-LDL were significantly increased from 70%+/-5% and 91%+/-7% of resting level to 108%+/-4% and 125%+/-3% after strenuous, acute exercise (P<.05); (3) exercise training decreased resting and postexercise 100 microg/mL Ox-LDL-potentiated platelet aggregation (ie, 31%+/-4% and 82%+/-4%, respectively; P<.05) and [Ca2+]i elevation (ie, 35%+/-6% and 71%+/-4%, respectively; P<.05); (4) detraining reversed the training effects on lipid profile and platelet function; and (5) treating the platelet with L-arginine-inhibited Ox-LDL-potentiated platelet activation during the experimental period. CONCLUSIONS: Our results suggest that 8 weeks of exercise training decreased the plasma LDL level, but failed to influence production of plasma Ox-LDL. Importantly, resting and exercise-induced Ox-LDL-potentiated platelet activation was decreased by exercise training. However, this was reversed by detraining to the pretraining level.

Adenosine Diphosphate↗

PubMed2002

Exposure to oxidized low-density lipoprotein reduces activable Ras protein in vascular endothelial cells.

Oxidized low-density lipoprotein (ox-LDL) has been shown to alter the migratory and proliferative activities of the vascular endothelial cells (EC) in response to serum and growth factors. The mechanism underlying the antiproliferative effect of ox-LDL on vascular EC has not been fully elucidated. In this report, we show that exposure of vascular EC to ox-LDL results in a marked reduction of the membrane-associated Ras protein. Further study shows that in ox-LDL-treated EC, reduction of the membrane-associated Ras protein is correlated with a reduced amount of active Ras (Ras-guanosine triphosphate), indicating that the Ras signaling pathway is attenuated. The attenuation of the Ras signaling pathway in ox-LDL-treated EC may thus be responsible for the retarded response to the mitogenic stimulation of serum and growth factors.

Cells, Cultured↗