Association of hsp70-2 (+1267A/G), hsp70-hom (+2437T/C), HMOX-1 (number of GT repeats) and TNF-alpha (+489G/A) polymorphisms with COPD in Croatian population

Matokanović, Mirela; Rumora, Lada; Popović‐Grle, Sanja; Čepelak, Ivana; Čulić, Ognjen; Barišić, Karmela

doi:10.1016/j.clinbiochem.2012.04.003

Cited by 13 publications

(11 citation statements)

References 21 publications

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“…Another study supported the similar conclusion in Croatian population to develop chronic obstructive pulmonary disease where there was no evidence for the association of A1L2437 (Matokanovic et al, 2012).…”

Section: Discussionsupporting

confidence: 70%

Polymorphisms in Heat Shock Proteins A1B and A1L (HOM) as Risk Factors for Oesophageal Carcinoma in Northeast India

Saikia

Barooah²,

Bhattacharyya³

et al. 2016

Asian Pacific Journal of Cancer Prevention

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Section: Discussionsupporting

confidence: 70%

Polymorphisms in Heat Shock Proteins A1B and A1L (HOM) as Risk Factors for Oesophageal Carcinoma in Northeast India

Saikia

Barooah²,

Bhattacharyya³

et al. 2016

Asian Pacific Journal of Cancer Prevention

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“…HO‐1 inducibility is associated with the presence of a microsatellite polymorphism (repetition of GT dinucleotides) in the promoter region of the HO‐1 gene, which was shown to reduce expression of HO‐1, and thus affects the susceptibility of an individual to developing emphysema (Yamada et al., ). However, our group showed there was no correlation of HO‐1 polymorphism with COPD in the Croatian population (Matokanović et al., ). In the same study, we found a correlation of HSP70‐2 (+1267 A/G) gene polymorphism and COPD (the frequency of G allele and GG genotype was higher in patients with COPD than in healthy subjects).…”

Section: Discussionmentioning

confidence: 87%

Differential expression of heat shock proteins and activation of mitogen‐activated protein kinases in A549 alveolar epithelial cells exposed to cigarette smoke extract

Bačura

Rumora

Novak

et al. 2018

Experimental Physiology

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New Findings What is the central question of this study?What is the effect of cigarette smoke on cell death, oxidative damage, expression of heat shock proteins (HSPs) and activation of mitogen‐activated protein kinases (MAPKs) in A549 alveolar epithelial cells? What is the main finding and its importance?Cigarette smoke induces cytotoxicity and oxidative damage to A549 cells, increases expression of different HSPs and activates MAPK signalling pathways. This could be related to inflammatory response and apoptosis observed in lungs of patients with smoking‐related diseases. Abstract Cigarette smoking is one of the main risk factors for development of chronic obstructive pulmonary disease (COPD). We previously reported that cigarette smoke (CS) induces damage to proteins and their ineffective degradation. Here, we hypothesize that CS could induce oxidative stress and cytotoxicity in lung epithelial cells through alterations of heat shock protein (HSP) expression and mitogen‐activated protein kinase (MAPK) signalling pathways. We exposed A549 alveolar epithelial cells to various concentrations of cigarette smoke extract (CSE). Higher concentrations of CSE caused apoptosis of A549 cells after 4 h, while after 24 h cell viability was decreased, and lactate dehydrogenase in cell culture medium was increased as well as the number of necrotic cells. Concentrations of malondialdehyde (MDA) were elevated, while total thiol groups were decreased. Changes in the expression of HSPs (HSP70, HSP32 and HSP27) were time‐dependent. After 6 h, CSE caused an increase in the expression of HSP70 and HSP32, while after 8 h all examined HSPs were up‐regulated and remained increased up to 48 h. Treatment of A549 cells with CSE stimulated phosphorylation of extracellular signal‐regulated kinase and p38 in a dose‐dependent manner, while c‐Jun N‐terminal kinase activation was not detected. By using specific inhibitors, we demonstrated that MAPKs and HSPs interplay in CSE effects. In conclusion, our results show that MAPKs and HSPs are involved in the mechanism underlying CSE‐induced cytotoxicity and oxidative damage to A549 alveolar epithelial cells. These processes could be related to inflammatory response and apoptosis observed in lungs of patients with smoking‐related diseases, such as COPD.

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“…COPD is a complex disease caused by combination of genetic and environmental factors 35. Smoking is one of the most important aetiological factors for the disease, but only 15%–20% of smokers develop COPD 36.…”

Section: Discussionmentioning

confidence: 99%

PON1gene polymorphisms in patients with chronic obstructive pulmonary disease

et al. 2018

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Association of hsp70-2 (+1267A/G), hsp70-hom (+2437T/C), HMOX-1 (number of GT repeats) and TNF-alpha (+489G/A) polymorphisms with COPD in Croatian population

Cited by 13 publications

References 21 publications

Polymorphisms in Heat Shock Proteins A1B and A1L (HOM) as Risk Factors for Oesophageal Carcinoma in Northeast India

Polymorphisms in Heat Shock Proteins A1B and A1L (HOM) as Risk Factors for Oesophageal Carcinoma in Northeast India

Differential expression of heat shock proteins and activation of mitogen‐activated protein kinases in A549 alveolar epithelial cells exposed to cigarette smoke extract

PON1gene polymorphisms in patients with chronic obstructive pulmonary disease

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