Chronic Obstructive Airway Disease
|
0.600 |
Biomarker
|
disease |
BEFREE |
The PLA-MnPD/DOTAP/pHDAC2 system proposed offers a new therapeutic approach for COPD based on the synergism of ROS elimination and HDAC2 expression.
|
31809610 |
2019 |
Chronic Obstructive Airway Disease
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
Briefly, COPD model rats showed an increased basal release of inflammatory cytokines (lung TNF-α: 45.7 ± 6.1 vs. 20.1 ± 3.8 pg/mL, P < 0.01; serum TNF-α: 8.9 ± 1.2 vs. 6.7 ± 0.5 pg/mL, P = 0.01; lung TGF-β: 122.4 ± 20.8 vs. 81.9 ± 10.8 pg/mL, P < 0.01; serum TGF-β: 38.9 ± 8.5 vs. 20.6 ± 2.3 pg/mL, P < 0.01) and COPD related lung tissue histopathological changes, as well as corticosteroid resistance molecular profile characterized by an increase in phosphoinositide 3-kinase (PI3K)/Akt (0.5 ± 0.1 fold of control vs. 0.2 ± 0.1 fold of control, P = 0.04) and a decrease in HDAC2 expression and activity (expression: 13.1 ± 0.4 μmol/μg vs. 17.4 ± 1.1 μmol/μg, P < 0.01; activity: 1.1 ± 0.1 unit vs. 1.4 ± 0.1 unit, P < 0.01), compared with control group.
|
30741829 |
2019 |
Chronic Obstructive Airway Disease
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
In the Jinwei Tang + budesonide and theophylline + budesonide groups, IL-8 and TNF-α expression was significantly decreased (P<0.05) and the HDAC2 level increased (P<0.05) compared with that in the COPD group.
|
29456664 |
2018 |
Chronic Obstructive Airway Disease
|
0.600 |
Biomarker
|
disease |
BEFREE |
Our study reveals that HDAC2 is a key player regulating CS-induced DNA damage, inflammatory response, and cellular senescence leading to COPD/emphysema.-Sundar, I. K., Rashid, K., Gerloff, J., Rangel-Moreno, J., Li, D., Rahman, I.
|
29630406 |
2018 |
Chronic Obstructive Airway Disease
|
0.600 |
Biomarker
|
disease |
BEFREE |
In patients with chronic obstructive pulmonary disease (COPD) the inflammatory response is often steroid-resistant, likely since oxidative stress and cigarette smoking impair histone deacetylase 2 (HDAC2) activity.
|
29782855 |
2018 |
Chronic Obstructive Airway Disease
|
0.600 |
Biomarker
|
disease |
BEFREE |
Nuclear factor-kappa B (NF-κB) DNA binding activity in muscle biopsies of COPD patients (10.1 ± 7.4) was significantly higher than that in SM (3.9 ± 7.3, p = 0.020) and NS (1.0 ± 1.2, p = 0.004and significantly correlated with HDAC2 decrease (r<sub>s</sub> = -0.59, p = 0.003) and HDAC5 (r<sub>s</sub> = 0.050, p = 0.012).
|
28526090 |
2017 |
Chronic Obstructive Airway Disease
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
These data indicated that cigarette smoke inhibited HDAC2 expression and its interaction with NF-κBp65 to stimulate inflammation, contributing to the pathogenesis of COPD-related skeletal muscle atrophy in mice.
|
28915625 |
2017 |
Chronic Obstructive Airway Disease
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
Levels of miR-223 are induced by interleukin-1β and tumor necrosis factor-α. miR-223 controls the expression of fractalkine by targeting histone deacetylase 2. miR-223 levels are increased in COPD mouse models. miR-223 levels inversely correlate with HDAC2 expression in COPD patients.
|
26864305 |
2016 |
Chronic Obstructive Airway Disease
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
In the lungs of patients who smoke and have chronic obstructive pulmonary disease (COPD) or asthma, glucocorticoids are not effective enough to suppress airway inflammation, which is so called "glucocorticoid resistance", due to decreased HDAC2 level caused by cigarette smoke.
|
26617781 |
2015 |
Chronic Obstructive Airway Disease
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
Data identify novel molecular targets for therapeutic strategies aimed at dampening inflammation in pathologies such as chronic obstructive pulmonary disease, in which reduced intracellular HDAC2 levels have been described.
|
26044852 |
2015 |
Chronic Obstructive Airway Disease
|
0.600 |
Biomarker
|
disease |
BEFREE |
CSE also down-regulated and post-translationally inhibited the glucocorticoid receptor (GR-α) and histone deacetylase 2 (HDAC2), a corepressor important for glucocorticoid action and whose down-regulation is thought to cause glucocorticoid insensitivity in COPD.
|
24368768 |
2014 |
Chronic Obstructive Airway Disease
|
0.600 |
Therapeutic
|
disease |
RGD |
In conclusion, Quanzhenyiqitang is capable of inducing apoptosis of AMs, which are the primary inflammatory cells in COPD, and modulating the expression of the important inflammatory factor HDAC2, producing an overall anti-inflammatory effect.
|
24940433 |
2014 |
Chronic Obstructive Airway Disease
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
We found that among the three HDAC proteins, the mRNA and protein levels of HDAC2, but not HDAC3 and HDAC5, in the tissues or cultured cells from patients have a significant correlation with development and prognosis of COPD.
|
23275209 |
2013 |
Chronic Obstructive Airway Disease
|
0.600 |
Biomarker
|
disease |
BEFREE |
HDAC2 appears to mediate the action of steroids to switch off activated inflammatory genes, but in patients with COPD, patients with severe asthma, and smokers with asthma, HDAC2 activity and expression are reduced by oxidative stress through activation of phosphoinositide 3-kinase δ.
|
23360759 |
2013 |
Chronic Obstructive Airway Disease
|
0.600 |
Biomarker
|
disease |
RGD |
Characteristic comparison of three rat models induced by cigarette smoke or combined with LPS: to establish a suitable model for study of airway mucus hypersecretion in chronic obstructive pulmonary disease.
|
22732689 |
2012 |
Chronic Obstructive Airway Disease
|
0.600 |
Biomarker
|
disease |
BEFREE |
In this perspective, we have discussed the role of HDAC2 posttranslational modifications and its role in regulation of inflammation, histone/DNA epigenetic modifications, DNA damage response, and cellular senescence, particularly in inflammaging, and during the development of COPD.
|
22842217 |
2012 |
Chronic Obstructive Airway Disease
|
0.600 |
Biomarker
|
disease |
BEFREE |
Treatment with sulforaphane, a small-molecule activator of the transcription factor nuclear factor erythroid 2-related factor 2 (NRF2), was also able to denitrosylate HDAC2, restoring dexamethasone sensitivity in alveolar macrophages from patients with COPD.
|
22005302 |
2011 |
Chronic Obstructive Airway Disease
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
Thus, reduced HDAC2 activity in COPD may account for increased Nrf2 acetylation, reduced Nrf2 stability and impaired anti oxidant defences.
|
21320471 |
2011 |
Chronic Obstructive Airway Disease
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
In addition, cigarette smoke/oxidants can reduce glucocorticoid sensitivity by attenuating HDAC2 activity and expression, which may account for the glucocorticoid insensitivity in patients with COPD.
|
18220485 |
2008 |
Chronic Obstructive Airway Disease
|
0.600 |
Biomarker
|
disease |
CTD_human |
Histone deacetylase-2 (HDAC2), a critical component of the corticosteroid anti-inflammatory action, is impaired in lungs of patients with COPD and correlates with disease severity.
|
18421014 |
2008 |
Chronic Obstructive Airway Disease
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
In conclusion, we show that overexpression of HDAC2 in glucocorticoid-insensitive alveolar macrophages from patients with COPD is able to restore glucocorticoid sensitivity.
|
16380507 |
2006 |
Chronic Obstructive Airway Disease
|
0.600 |
Biomarker
|
disease |
BEFREE |
In chronic obstructive pulmonary disease (COPD) patients and asthmatic patients who smoke HDAC2 is markedly impaired as a result of oxidative and nitrative stress so that inflammation is resistant to the anti-inflammatory effects of corticosteroids.
|
16436275 |
2006 |
Chronic Obstructive Airway Disease
|
0.600 |
Biomarker
|
disease |
CTD_human |
Theophylline restores histone deacetylase activity and steroid responses in COPD macrophages.
|
15337792 |
2004 |