Nicotine enhances expression of the neutrophil elastase gene and protein in a human myeloblast/promyelocyte cell line

Linda W. Armstrong, William N. Rom, Frank T. Martiniuk, David Hart, Jaishree Jagirdar, Morton Galdston

Research output: Contribution to journalArticle

14 Scopus citations

Abstract

The pathogenesis of emphysema is considered to be an imbalance of protease and antiprotease activity in the lower respiratory tract leading to uninhibited degradation of lung interstitium by elastolytic enzymes. An increased amount of the serine protease neutrophil elastase (NE) is though to play a major role in this degradation. Because the expression of NE is limited to neutrophil precursors in the bone marrow, we hypothesized that nicotine, which is readily absorbed from lung and distributed to tissue, including bone marrow, would increase expression of the NE gene and protein. HL-60 cells, a myeloblast/promyelocyte cell line, were cultured in the presence or absence of 0.06 and 0.8 μM nicotine for 5 d. Both concentrations of nicotine caused a 2.4- to 3.3-fold increase, respectively, in NE gene expression over unstimulated cells, and NE protein increased 4.8- to 3.4- fold over unstimulated cells, respectively, similar to our positive control DMSO. Nicotine did not induce upregulation of the NE gene by initiating cell differentiation. Both low and high nicotine concentrations upregulate the NE gene in HL-60 cells leading to increased NE protein concentration per cell suggesting a pathophysiologic mechanism for emphysema.

Original languageEnglish (US)
Pages (from-to)1520-1524
Number of pages5
JournalAmerican Journal of Respiratory and Critical Care Medicine
Volume154
Issue number5
DOIs
StatePublished - 1996

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine
  • Critical Care and Intensive Care Medicine

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