Pulmonary function, oxidative stress and inflammatory markers in severe COPD exacerbation

Stanojkovic, Ivana; Kotur‐Stevuljević, Jelena; Milenković, Branislava; Spasić, Slavica; Vujić, Tatjana; Stefanović, Aleksandra; llic, Aleksandra; Ivanišević, Jasmina

doi:10.1016/s0954-6111(11)70008-7

Cited by 78 publications

(76 citation statements)

References 28 publications

(36 reference statements)

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“…Treatment of mice with the chemical chaperone 4-PBA improved MCC following CS exposure. Our data highlight the benefits of using chemical chaperones as therapeutics to preserve the function of critical proteins in response to noxious cellular stresses such as CS (79)(80)(81). The preservation of proteins required for cilia formation and/or ciliated cell integrity may reduce autophagic substrates and enhance MCC in smokers.…”

Section: Figure 10mentioning

confidence: 79%

Histone deacetylase 6–mediated selective autophagy regulates COPD-associated cilia dysfunction

et al. 2013

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Chronic obstructive pulmonary disease (COPD) involves aberrant airway inflammatory responses to cigarette smoke (CS) that are associated with epithelial cell dysfunction, cilia shortening, and mucociliary clearance disruption. Exposure to CS reduced cilia length and induced autophagy in vivo and in differentiated mouse tracheal epithelial cells (MTECs). Autophagy-impaired (Becn1 +/-or Map1lc3B -/-) mice and MTECs resisted CS-induced cilia shortening. Furthermore, CS increased the autophagic turnover of ciliary proteins, indicating that autophagy may regulate cilia homeostasis. We identified cytosolic deacetylase HDAC6 as a critical regulator of autophagy-mediated cilia shortening during CS exposure. Mice bearing an X chromosome deletion of Hdac6 (Hdac6 -/Y ) and MTECs from these mice had reduced autophagy and were protected from CS-induced cilia shortening. Autophagy-impaired Becn1 -/-, Map1lc3B -/-, and Hdac6 -/Y mice or mice injected with an HDAC6 inhibitor were protected from CS-induced mucociliary clearance (MCC) disruption. MCC was preserved in mice given the chemical chaperone 4-phenylbutyric acid, but was disrupted in mice lacking the transcription factor NRF2, suggesting that oxidative stress and altered proteostasis contribute to the disruption of MCC. Analysis of human COPD specimens revealed epigenetic deregulation of HDAC6 by hypomethylation and increased protein expression in the airways. We conclude that an autophagy-dependent pathway regulates cilia length during CS exposure and has potential as a therapeutic target for COPD.

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Section: Figure 10mentioning

confidence: 79%

Histone deacetylase 6–mediated selective autophagy regulates COPD-associated cilia dysfunction

et al. 2013

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“…In COPD, systemic (226) and local (219, 220) oxidative stress have been reported. Acute bouts of exercise (224,226) as well as acute exacerbation (329,337) increase the level of oxidative stress. Direct oxidative stress exposure (338) or indirect production of ROS through inflammatory response (339,340) induces proteolysis and increases expression of UbP components.…”

Section: Mechanisms Of Limb Muscle Dysfunction In Copdmentioning

confidence: 99%

An Official American Thoracic Society/European Respiratory Society Statement: Update on Limb Muscle Dysfunction in Chronic Obstructive Pulmonary Disease

Maltais¹,

Decramer²,

Casaburi³

et al. 2014

Am J Respir Crit Care Med

885

1,033

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“…It has been reported that enzyme activity is altered as a result of these polymorphisms. [2,5,6] In the present study, we aimed to investigate the association of COPD, in which oxidative stress is involved in pathogenesis, and PON1, which has antioxidant properties, with Q192R and L55M polymorphisms.…”

Section: Introductionmentioning

confidence: 99%

Paraoxonase-1 gene in patients with chronic obstructive pulmonary disease investigation Q192R and L55M polymorphisms

Gürbüz¹,

Yıldız²,

Kara³

et al. 2015

World Journal of Emergency Medicine

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BACKGROUND:The effect of increased oxidative stress on the development of chronic obstructive pulmonary disease (COPD) is well known. One of the antioxidative systems against oxidative stress in human body is paraoxonase (PON) enzyme that protects low density lipoproteins (LDL) against oxidation. This study aimed to explore the polymorphisms on PON1, Q192R, L55M genes of patients with COPD.METHODS: DNAs extraction was obtained from blood samples of 50 patients diagnosed with COPD and 50 patients as a control group who were presented to emergency clinic. Genotypes were obtained with polymerase chain reaction (PCR) and AIw I and Hsp92II restriction enzymes were used for Q192R and L55M polymorphisms, respectively. Analysis of data was done with the Chi-square test and Fisher's exact test. RESULTS:A statistically significant difference in Q192R polymorphism was found between the COPD patients and the control group (P=0.05). There was no statistically signifi cant difference in L55M polymorphisms between the patient and control groups (P>0.05). Q192R polymorphism was signifi cantly correlated with the PON1 gene and cigarette smoking; however other risk factors did not show any significant correlation with this polymorphism. Though L55M polymorphism was signifi cantly correlated with family history and tuberculosis, there was no signifi cant correlation with other risk factors. CONCLUSION:We believe that more studies are needed to study the correlation of L55M polymorphism with other factors.

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Pulmonary function, oxidative stress and inflammatory markers in severe COPD exacerbation

Cited by 78 publications

References 28 publications

Histone deacetylase 6–mediated selective autophagy regulates COPD-associated cilia dysfunction

Histone deacetylase 6–mediated selective autophagy regulates COPD-associated cilia dysfunction

An Official American Thoracic Society/European Respiratory Society Statement: Update on Limb Muscle Dysfunction in Chronic Obstructive Pulmonary Disease

Paraoxonase-1 gene in patients with chronic obstructive pulmonary disease investigation Q192R and L55M polymorphisms

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