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

Author:

De Lara Luis Vázquez1,Becerril Carina2,Montaño Martha2,Ramos Carlos2,Maldonado Vilma3,Meléndez Jorge3,Phelps David S.4,Pardo Annie5,Selman Moisés2

Affiliation:

1. Universidad Autónoma de Puebla, Puebla, Puebla CP 72190;

2. Instituto Nacional de Enfermedades Respiratorias, México DF, CP 14080;

3. Instituto Nacional de Cancerologı́a, México DF, CP 14000;

4. Department of Pediatrics, Pennsylvania State University College of Medicine, Hershey, Pennsylvania 17033

5. Facultad de Ciencias, Universidad Nacional Autónoma de Mexico, México DF, CP 04510, Mexico; and

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/ml 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 results. 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 intraluminal fibrogenesis by inducing fibroblast apoptosis and decreasing collagen accumulation.

Publisher

American Physiological Society

Subject

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

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