27 research outputs found
Flow cytometric analysis of apoptosis and autophagy in CD4 lymphocyte (Day 0).
<p>Graph showing the flow cytometric analysis of high intensity-interval (HIT) (<b>A</b>) and moderate intensity-continuous (MCT) (<b>B</b>) exercise training effects on main biomarkers of apoptosis and autophagy [i.e., LAMP-2, active caspase -3, and annexin V staining (phosphotidylserine exposure)] in untreated CD4 lymphocytes (Day 0). <b>Pre</b>, pre-intervention; <b>Post</b>, post-intervention; <b>Rest</b>, resting; <b>HE</b>, hypoxic (12%O<sub>2</sub>) exercise test<b>; Basal</b>, untreated CD4 lymphocytes (<b>Day 0</b>).</p
Effects of various interventions on levels of active caspase 9 and caspase 3 in CD4 lymphocytes.
<p>(<b>A</b>-<b>C</b>) caspase 9; (<b>D</b>-<b>F</b>) caspase 3; <b>HIT</b>, high-intensity interval training group (<b>A</b>, <b>D</b>); <b>MCT</b>, moderate continuous training group (<b>B</b>, <b>E</b>) ; <b>CTL</b>, control group (<b>C</b>, <b>F</b>)<b>; Pre</b>, pre-intervention; <b>Post</b>, post-intervention; <b>Rest</b>, resting; <b>HE</b>, hypoxic (12%O<sub>2</sub>) exercise test<b>; Basal</b>, untreated CD4 lymphocytes (<b>Day 0</b>); <b>Vehicle</b> and <b>Rap</b>, CD4 lymphocytes treated in the absence and presence of rapamycin (500nM) for 24 h (<b>Day 1</b>), respectively. *P<0.05, <b>Rest</b> vs. <b>HE</b>; +P<0.05, <b>Pre</b> vs. <b>Post</b>; ‡P<0.05, <b>HIT</b> or <b>MCT</b> vs. <b>CTL</b>. Values were mean±SE. n=10 in each group.</p
Possible mechanisms of improved aerobic capacity and modulated CD4 lymphocyte autophagic and apoptotic responses to hypoxic stress by various exercise regimens.
<p>High-intensity interval training (HIT) is more effective for enhancing aerobic capacity (VO<sub>2max</sub>) by increasing cardiac output response to exercise, compared to moderate continuous training (MCT) does. A bout of 12%O<sub>2</sub> exercise (HE) suppresses the initiation, elongation, maturation, and fusion of autophagy by decreased beclin-1, Atg-1, LC3-II, Atg-12, and LAMP-2 expressions, and simultaneously enhances the initiation and execution of apoptosis by increased phospho-Bcl-2 and active caspase-9/-3 levels in CD4 lymphocytes. However, five weeks of HIT and MCT attenuate the extents of declined autophagy and potentiated apoptosis in CD4 lymphocyte caused by HE, possibly by (1) down-regulating mTOR expression, (2) lowering Th2 cytokine (indicated by a decrease in interleukin-4, IL-4) production, and (3) depressing elevation of oxidative stress by HE. Besides, HIT, but not MCT, further depresses resting myeloperoxidase (MPO) and IL-4 levels in plasma.</p
Flow cytometric analysis of apoptosis and autophagy in CD4 lymphocyte (Day 1).
<p>Graph showing the flow cytometric analysis of high intensity-interval (HIT) (<b>A</b>) and moderate intensity-continuous (MCT) (<b>B</b>) exercise training effects on main biomarkers of apoptosis and autophagy [i.e., LAMP-2, active caspase -3, and annexin V staining (phosphotidylserine exposure)] in rapamycin-treated CD4 lymphocytes (Day 1). <b>Pre</b>, pre-intervention; <b>Post</b>, post-intervention; <b>Rest</b>, resting; <b>HE</b>, hypoxic (12%O<sub>2</sub>) exercise test<b>; Basal</b>, untreated CD4 lymphocytes (<b>Day 0</b>).</p
Effects of various interventions on levels of acridine orange (AO)-labeled and phosphatidylserine (PS)-exposed in CD4 lymphocytes.
<p>(<b>A</b>-<b>C</b>) <b>AO</b>-labeled; (<b>D</b>-<b>F</b>) <b>PS</b>-exposed; <b>HIT</b>, high-intensity interval training group (<b>A</b>, <b>D</b>); <b>MCT</b>, moderate continuous training group (<b>B</b>, <b>E</b>) ; <b>CTL</b>, control group (<b>C</b>, <b>F</b>)<b>; Pre</b>, pre-intervention; <b>Post</b>, post-intervention; <b>Rest</b>, resting; <b>HE</b>, hypoxic (12%O<sub>2</sub>) exercise test<b>; Basal</b>, untreated CD4 lymphocytes (<b>Day 0</b>); <b>Vehicle</b> and <b>Rap</b>, CD4 lymphocytes treated in the absence and presence of rapamycin (500nM) for 24 h (<b>Day 1</b>), respectively. *P<0.05, <b>Rest</b> vs. <b>HE</b>; +P<0.05, <b>Pre</b> vs. <b>Post</b>; ‡P<0.05, <b>HIT</b> or <b>MCT</b> vs. <b>CTL</b>. Values were mean±SE. n=10 in each group.</p
Effects of various interventions on levels of Atg-12, LC3-II, and LAMP-2 in CD4 lymphocytes.
<p>(<b>A</b>-<b>C</b>) Atg-12; (<b>D</b>-<b>F</b>) LC3-II; (<b>G</b>-<b>I</b>) LAMP-2; <b>HIT</b>, high-intensity interval training group (<b>A</b>, <b>D</b>, <b>G</b>); <b>MCT</b>, moderate continuous training group (<b>B</b>, <b>E</b>, <b>H</b>)<b>; CTL</b>, control group (<b>C</b>, <b>F</b>, <b>I</b>)<b>; Pre</b>, pre-intervention; <b>Post</b>, post-intervention; <b>Rest</b>, resting; <b>HE</b>, hypoxic (12%O<sub>2</sub>) exercise test<b>; Basal</b>, untreated CD4 lymphocytes (<b>Day 0</b>); <b>Vehicle</b> and <b>Rap</b>, CD4 lymphocytes treated in the absence and presence of rapamycin (500nM) for 24 h (<b>Day 1</b>), respectively. *P<0.05, <b>Rest</b> vs. <b>HE</b>; +P<0.05, <b>Pre</b> vs. <b>Post</b>; ‡P<0.05, <b>HIT</b> or <b>MCT</b> vs. <b>CTL</b>. Values were mean±SE. n=10 in each group.</p
Effects of various interventions on levels of Atg-1 and Beclin-1 in CD4 lymphocytes.
<p>(<b>A</b>-<b>C</b>) Atg-1; (<b>D</b>-<b>F</b>) Beclin-1; <b>HIT</b>, high-intensity interval training group (<b>A</b>, <b>D</b>); <b>MCT</b>, moderate continuous training group (<b>B</b>, <b>E</b>) ; <b>CTL</b>, control group (<b>C</b>, <b>F</b>)<b>; Pre</b>, pre-intervention; <b>Post</b>, post-intervention; <b>Rest</b>, resting; <b>HE</b>, hypoxic (12%O<sub>2</sub>) exercise test<b>; Basal</b>, untreated CD4 lymphocytes (<b>Day 0</b>); <b>Vehicle</b> and <b>Rap</b>, CD4 lymphocytes treated in the absence and presence of rapamycin (500nM) for 24 h (<b>Day 1</b>), respectively. *P<0.05, <b>Rest</b> vs. <b>HE</b>; +P<0.05, <b>Pre</b> vs. <b>Post</b>; ‡P<0.05, <b>HIT</b> or <b>MCT</b> vs. <b>CTL</b>. Values were mean±SE. n=10 in each group.</p
Effects of various interventions on levels of interleukin-6 (IL-6) and myeloperoxidase (MPO) in plasma.
<p>(<b>A</b>) IL-6; (<b>B</b>) MPO; <b>HIT</b>, high-intensity interval training group; <b>MCT</b>, moderate continuous training group; <b>CTL</b>, control group; <b>Pre</b>, pre-intervention; <b>Post</b>, post-intervention; <b>Rest</b>, resting; <b>HE</b>, hypoxic (12%O<sub>2</sub>) exercise test. *P<0.05, <b>Rest</b> vs. <b>HE</b>; +P<0.05, <b>Pre</b> vs. <b>Post</b>. Values were mean±SE. n=10 in each group.</p
Additional file 1: Figure S1. of Interplay of N-Cadherin and matrix metalloproteinase 9 enhances human nasopharyngeal carcinoma cell invasion
The expression of the precursor and active form of ADAM10 after PMA treatment. NPC cells were treated with PMA (100 nM) for the indicated times. Cell lysates underwent western blot analysis to detect levels of the precursor and active form of ADAM10. In response to PMA treatment, the expression of ADAM10 was not significantly changed in NPC cells. (TIF 645 kb
Additional file 1: Figure S1. of Interplay of N-Cadherin and matrix metalloproteinase 9 enhances human nasopharyngeal carcinoma cell invasion
The expression of the precursor and active form of ADAM10 after PMA treatment. NPC cells were treated with PMA (100 nM) for the indicated times. Cell lysates underwent western blot analysis to detect levels of the precursor and active form of ADAM10. In response to PMA treatment, the expression of ADAM10 was not significantly changed in NPC cells. (TIF 645 kb