Cigarette smoke alters cell cycle and induces inflammation in lung fibroblasts (Articolo in rivista)

Type
Label
  • Cigarette smoke alters cell cycle and induces inflammation in lung fibroblasts (Articolo in rivista) (literal)
Anno
  • 2015-01-01T00:00:00+01:00 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
  • 10.1016/j.lfs.2015.01.017. (literal)
Alternative label
  • D'ANNA C., CIGNA D., COSTANZO G., FERRARO M., SIENA L., VITULO P., GJOMARKAJ M., PACE E (2015)
    Cigarette smoke alters cell cycle and induces inflammation in lung fibroblasts
    in Life sciences (1973)
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • D'ANNA C., CIGNA D., COSTANZO G., FERRARO M., SIENA L., VITULO P., GJOMARKAJ M., PACE E (literal)
Rivista
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • IBIM CNR (literal)
Titolo
  • Cigarette smoke alters cell cycle and induces inflammation in lung fibroblasts (literal)
Abstract
  • BACKGROUND: Lung fibroblasts are crucial for the integrity of alveolar structure. Cigarette smoking, the major risk factor for chronic obstructive pulmonary disease, impairs the repair functions of lung fibroblasts. AIMS:The study simultaneously assessed for the first time cell cycle, p53, p21, p38, ERK 1/2 and IL-8. MAIN METHODS:Primary foetal lung fibroblasts (HFL-1) and primary lung fibroblasts from former (n=5) and current (n=5) smokers with/without cigarette smoke extracts (CSEs) and inhibitors of p38 and ERK1/2 were studied for cell cycle events and for marker expression by flow-cytometry, western-blot analysis and ELISA. KEY FINDINGS:CSE exposure did not induce caspase 3 cleavage or DNA laddering but reduced S phase, and increased G1 and G2/M in HFL-1. Furthermore CSE increased: p53 and p21 expression; p38 and ERK 1/2 pathway activation; and IL-8 release. Inhibitors of p38 and ERK 1/2 reversed the effects of CSE on cell cycle and on IL-8 release. ERK 1/2 inhibitor was able to reverse the effects of CSE on p21 expression. Primary lung fibroblasts from current smokers had higher ERK 1/2 activation in comparison to normal primary fibroblasts and higher percentage of cells in G1 phase and lower percentage of cells in S phase in comparison to former smoker fibroblasts. SIGNIFICANCE:Cigarette smoke may affect the reparative potential of lung fibroblasts altering the expression of p53 and p21 and the progression of the cell cycle to S phase. All these events are promoted by the activation of pro-inflammatory pathways. (literal)
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