Surfactant components modulate fibroblast apoptosis and type I collagen and collagenase-1 expression

Luis Vázquez De Lara, Carina Becerril, Martha Montaño, Carlos Ramos, Vilma Maldonado, Jorge Meléndez, David S. Phelps, Annie Pardo, Moisés Selman

Research output: Contribution to journalArticlepeer-review

36 Scopus citations

Abstract

During lung injury, fibroblasts migrate into the alveolar spaces where they can be exposed to pulmonary surfactant. We examined the effects of Survanta and surfactant protein A (SP-A) on fibroblast growth and apoptosis and on type I collagen, collagenase-1, and tissue inhibitor of metalloproteinase (TIMP)-1 expression. Lung fibroblasts were treated with 100, 500, and 1,000 μg/ml of Survanta; 10, 50, and 100 μg/rnl of SP-A; and 500 μg/ml of Survanta plus 50 μg/ml of SP-A. Growth rate was evaluated by a formazan-based chromogenic assay, apoptosis was evaluated by DNA end labeling and ELISA, and collagen, collagenase-1, and TIMP-1 were evaluated by Northern blotting. Survanta provoked fibroblast apoptosis, induced collagenase-1 expression, and decreased type I collagen affecting mRNA stability ~10-fold as assessed with the use of actinomycin D. Collagen synthesis and collagenase activity paralleled the gene expression resuits. SP-A increased collagen expression ~2-fold and had no effect on collagenase-1, TIMP-1, or growth rate. When fibroblasts were exposed to a combination of Survanta plus SP-A, the effects of Survanta were partially reversed. These findings suggest that surfactant lipids may protect against intralunfinal fibrogenesis by inducing fibroblast apoptosis and decreasing collagen accumulation.

Original languageEnglish (US)
Pages (from-to)L950-L957
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Volume279
Issue number5 23-5
DOIs
StatePublished - 2000

All Science Journal Classification (ASJC) codes

  • Physiology
  • Pulmonary and Respiratory Medicine
  • Physiology (medical)
  • Cell Biology

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