Abstract
Surfactant protein-B (SP-B) is a small, hydrophobic pcptide that plays a critical role in pulmonary function and surfactant homeostasis. To determine whether SP-B protects mice from oxygen-induced injury, heterozygous SP-B+/- gene-targeted mice and wild-type SP-B+/+ littermates were exposed to hyperoxia (95% oxygen for 3 d) or room air. Although specific lung compliance in room air in SP-B+/- mice was slightly reduced as compared with that in SP-B+/+ mice, it was reduced more markedly during hyperoxia (46% versus 25% decrease, respectively). The larger decrease in lung compliance in SP-B+/- mice was associated with increased severity of pulmonary edema, hemorrhage and inflammation, lung permeability and protein leakage into the alveolar space. Hyperoxia increased SP-B messenger RNA (mRNA) and total protein concentrations by 2-fold in SP-B+/+ and SP-B+/- mice, but decreased the abundance of SP-B protein in lavage fluid relative to total protein only in SP-B+/- mice. Hyperoxia increased SP-B expression, but apparently not enough to maintain SP-B function and lung compliance in the presence of increased protein leakage in SP-B+/- mice. Increased alveolar-capillary leakage and relative deficiency of SP-B may therefore contribute to oxygen-induced pulmonary dysfunction in SP-B+/- mice. These data support the concept that SP-B plays an important protective role in the lung.
| Original language | English |
|---|---|
| Pages (from-to) | 463-472 |
| Number of pages | 10 |
| Journal | American Journal of Respiratory Cell and Molecular Biology |
| Volume | 21 |
| Issue number | 4 |
| Publication status | Published - 1999 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Cell Biology
- Molecular Biology
- Pulmonary and Respiratory Medicine
Cite this
Surfactant protein-B-deficient mice are susceptible to hyperoxic lung injury. / Tokieda, Keisuke; Iwamoto, Harriet S.; Bachurski, Cindy; Wert, Susan E.; Hull, William M.; Ikeda, Kazushige; Whitsett, Jeffrey A.
In: American Journal of Respiratory Cell and Molecular Biology, Vol. 21, No. 4, 1999, p. 463-472.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Surfactant protein-B-deficient mice are susceptible to hyperoxic lung injury
AU - Tokieda, Keisuke
AU - Iwamoto, Harriet S.
AU - Bachurski, Cindy
AU - Wert, Susan E.
AU - Hull, William M.
AU - Ikeda, Kazushige
AU - Whitsett, Jeffrey A.
PY - 1999
Y1 - 1999
N2 - Surfactant protein-B (SP-B) is a small, hydrophobic pcptide that plays a critical role in pulmonary function and surfactant homeostasis. To determine whether SP-B protects mice from oxygen-induced injury, heterozygous SP-B+/- gene-targeted mice and wild-type SP-B+/+ littermates were exposed to hyperoxia (95% oxygen for 3 d) or room air. Although specific lung compliance in room air in SP-B+/- mice was slightly reduced as compared with that in SP-B+/+ mice, it was reduced more markedly during hyperoxia (46% versus 25% decrease, respectively). The larger decrease in lung compliance in SP-B+/- mice was associated with increased severity of pulmonary edema, hemorrhage and inflammation, lung permeability and protein leakage into the alveolar space. Hyperoxia increased SP-B messenger RNA (mRNA) and total protein concentrations by 2-fold in SP-B+/+ and SP-B+/- mice, but decreased the abundance of SP-B protein in lavage fluid relative to total protein only in SP-B+/- mice. Hyperoxia increased SP-B expression, but apparently not enough to maintain SP-B function and lung compliance in the presence of increased protein leakage in SP-B+/- mice. Increased alveolar-capillary leakage and relative deficiency of SP-B may therefore contribute to oxygen-induced pulmonary dysfunction in SP-B+/- mice. These data support the concept that SP-B plays an important protective role in the lung.
AB - Surfactant protein-B (SP-B) is a small, hydrophobic pcptide that plays a critical role in pulmonary function and surfactant homeostasis. To determine whether SP-B protects mice from oxygen-induced injury, heterozygous SP-B+/- gene-targeted mice and wild-type SP-B+/+ littermates were exposed to hyperoxia (95% oxygen for 3 d) or room air. Although specific lung compliance in room air in SP-B+/- mice was slightly reduced as compared with that in SP-B+/+ mice, it was reduced more markedly during hyperoxia (46% versus 25% decrease, respectively). The larger decrease in lung compliance in SP-B+/- mice was associated with increased severity of pulmonary edema, hemorrhage and inflammation, lung permeability and protein leakage into the alveolar space. Hyperoxia increased SP-B messenger RNA (mRNA) and total protein concentrations by 2-fold in SP-B+/+ and SP-B+/- mice, but decreased the abundance of SP-B protein in lavage fluid relative to total protein only in SP-B+/- mice. Hyperoxia increased SP-B expression, but apparently not enough to maintain SP-B function and lung compliance in the presence of increased protein leakage in SP-B+/- mice. Increased alveolar-capillary leakage and relative deficiency of SP-B may therefore contribute to oxygen-induced pulmonary dysfunction in SP-B+/- mice. These data support the concept that SP-B plays an important protective role in the lung.
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UR - http://www.scopus.com/inward/citedby.url?scp=0033210850&partnerID=8YFLogxK
M3 - Article
C2 - 10502556
AN - SCOPUS:0033210850
VL - 21
SP - 463
EP - 472
JO - American Journal of Respiratory Cell and Molecular Biology
JF - American Journal of Respiratory Cell and Molecular Biology
SN - 1044-1549
IS - 4
ER -