Effect of cigarette smoke and dexamethasone on Hsp72 system of alveolar epithelial cells

• DOI: 10.1007/s12192-010-0249-z
• Publication Date: 2010-12-27T19:58:03Z
• Authors: Krisztina Gál; Áron Cseh; Balázs Szalay; Krisztina Rusai; Ádám Vannay; József Lukácsovits; Uwe Heemann; Attila J. Szabó; György Losonczy; Lilla Tamási; Veronika Müller
• Keywords: Nicotiana; 0303 health sciences; Dose-Response Relationship, Drug; Smoking; Gene Expression; Apoptosis; HSP72 Heat-Shock Proteins; Respiratory Mucosa; Dexamethasone; Cell Line; 3. Good health; Pulmonary Alveoli; Necrosis; 03 medical and health sciences; Cytoprotection; Smoke; Humans; Gene Silencing; RNA, Messenger; RNA, Small Interfering

Smoking is the leading risk factor of chronic obstructive pulmonary disease (COPD) and lung cancer. Corticosteroids are abundantly used in these patients; however, interaction smoking steroid treatment not fully understood. Heat shock proteins (Hsps) play a central role maintenance cell integrity, apoptosis cellular action. To better understand cigarette smoke-steroid interaction, we examined effect smoke extract (CSE) and/or dexamethasone (DEX) on changes intracellular heat protein-72 (Hsp72) cells. Alveolar epithelial cells (A549) were exposed to increasing doses (0; 0.1; 1; 10 μM/μl) DEX medium absence(C) presence CSE. Apoptosis, necrosis, Hsp72 messenger-ribonucleic acid (mRNA) protein expression measured, examined. CSE reduced number viable by significantly apoptotic necrotic dose-dependently decreased ratio when was administered, without change necrosis. − co-treatment increased mRNA expression, with highest level measured + (10) cells, while lower levels noted all respective C groups. Pretreatment silencing RNA confirmed that survival observed following administration CSE-treated mainly mediated via system. decreases inducing increases only resulting protection survival. exerts its protective effects decreasing death system alveolar