Naslov
CIGARETTE SMOKE EXTRACT INDUCES EXPRESSION OF HSP27 AND HSP32 BUT NOT HSP70 IN A549 ALVEOLAR EPITHELIAL CELLS

Autori
Somborac Bacura, Anita ; Rumora, Lada ; Zanic Grubisic, Tihana

Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni

Izvornik
The FEBS Journal / - , 2014, 106-107

Skup
FEBS EMBO 2014 Conference

Mjesto i datum
Pariz, Francuska, 30.08.2014. - 04.09.2014

Vrsta sudjelovanja
Poster

Vrsta recenzije
Međunarodna recenzija

Ključne riječi
chronic obstructive pulmonary disease ; cigarette smoke extract ; heat shock proteins

Sažetak
Abstract: Heat shock proteins (HSPs) are highly conserved proteins involved in folding of native and damaged cell proteins. HSPs participate in cellular responses to stress and can be induced by various stress conditions, including high and low temperatures, reactive oxygen species, hypoxia, infection, inflammation etc. Cigarette smoke is known to contain many different oxidants and reactive oxygen species, thereby causing oxidative stress, chronic inflammation and severe damage to proteins in the lungs of smokers and patients with chronic obstructive pulmonary disease (COPD). The aim of this study was to find out whether exposure of A549 alveolar epithelial cells to increasing concentrations (1.25 ; 2.5 ; 5 ; 10 and 20 %) of cigarette smoke extract (CSE) during 4, 6, 8, 24 and 48 h activates cellular defense mechanisms, including expression of HSP27, HSP32 (also known as heme oxygenase 1) and HSP70 in response to accumulation of damaged proteins. Our study shows that exposure of A549 cells to 20 % CSE for 24 h produced considerable damage to cellular membranes with increased permeability and leakage of LDH into the incubation medium, as compared to untreated cells (P = 0.01). Metabolic activity explored by MTT test was reduced at the same time point (P < 0.01). In addition, AnnexinV - propidium iodide double staining confirmed that 20% CSE during 24 h is causing primarily necrotic cell death (P<0.001). However, cellular defense mechanisms were only partially activated. Expression of HSP32 was induced 8 h after incubation with 20 % CSE (P = 0.029) and 24 h after incubation with 10 % and 20 % CSE (P = 0.019). HSP27 was induced with 20 % CSE only after 48 h (P = 0.012). Unexpectedly, we could not detect significant changes in HSP70 expression (P > 0.05). The unchanged level of HSP70 expression might reflect lack of induction, or increased release of HSP70 from the damaged, necrotic cells. We conclude that CSE-induced stress produces only limited activation of HSPs response indicating disturbed cellular defense mechanisms. It is possible that chronic exposure to CSE leads to the depletion of HSP-related defense mechanisms and contributes to the abnormal inflammatory response observed in lungs of smokers and COPD patients.

Izvorni jezik
Engleski

Znanstvena područja
Temeljne medicinske znanosti, Farmacija

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