Bleomycin-induced pulmonary injury in mice deficient in SPARC

Rashmin C. Savani, Zhao Zhou, Evguenia Arguiri, Sunny Wang, Dinh Vu, Chin C. Howe, Horace M. DeLisser

Research output: Contribution to journalArticle

42 Citations (Scopus)

Abstract

SPARC (secreted protein, acidic and rich in cysteine) is a component of the matrix that appears to regulate tissue remodeling. There is evidence that it accumulates in the lung in the setting of pulmonary injury and fibrosis, but direct evidence of its involvement is only now emerging. We therefore investigated the development of pulmonary fibrosis induced by bleomycin administered either intratracheally or intraperitoneally in mice deficient in SPARC. Bleomycin (0.15 U/mouse) given intratracheally induced significantly more pulmonary fibrosis in mice deficient in SPARC compared with that in wild-type control mice, with the mutant mice demonstrating greater neutrophil accumulation in the lung. However, in wild-type and SPARC-deficient mice given intraperitoneal bleomycin (0.8 U/injection x 5 injections over 14 days), the pattern and severity of pulmonary fibrosis, as well as the levels of leukocyte recruitment, were similar in both strains of mice. These findings suggest that the involvement of SPARC in pulmonary injury is likely to be complex, dependent on several factors including the type, duration, and intensity of the insult. Furthermore, increased neutrophil accumulation in the peritoneal cavity was also observed in SPARC-null mice after acute chemical peritonitis. Together, these data suggest a possible role for SPARC in the recruitment of neutrophils to sites of acute inflammation.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Volume279
Issue number4 23-4
StatePublished - 2000

Fingerprint

Bleomycin
Lung Injury
Cysteine
Pulmonary Fibrosis
Proteins
Neutrophils
Lung
Injections
Neutrophil Infiltration
Peritoneal Cavity
Peritonitis
Leukocytes
Inflammation

Keywords

  • Acidic and rich in cysteine
  • Inflammation
  • Lung fibrosis
  • Neurophils
  • Secreted protein

ASJC Scopus subject areas

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

Cite this

Savani, R. C., Zhou, Z., Arguiri, E., Wang, S., Vu, D., Howe, C. C., & DeLisser, H. M. (2000). Bleomycin-induced pulmonary injury in mice deficient in SPARC. American Journal of Physiology - Lung Cellular and Molecular Physiology, 279(4 23-4).

Bleomycin-induced pulmonary injury in mice deficient in SPARC. / Savani, Rashmin C.; Zhou, Zhao; Arguiri, Evguenia; Wang, Sunny; Vu, Dinh; Howe, Chin C.; DeLisser, Horace M.

In: American Journal of Physiology - Lung Cellular and Molecular Physiology, Vol. 279, No. 4 23-4, 2000.

Research output: Contribution to journalArticle

Savani, RC, Zhou, Z, Arguiri, E, Wang, S, Vu, D, Howe, CC & DeLisser, HM 2000, 'Bleomycin-induced pulmonary injury in mice deficient in SPARC', American Journal of Physiology - Lung Cellular and Molecular Physiology, vol. 279, no. 4 23-4.
Savani, Rashmin C. ; Zhou, Zhao ; Arguiri, Evguenia ; Wang, Sunny ; Vu, Dinh ; Howe, Chin C. ; DeLisser, Horace M. / Bleomycin-induced pulmonary injury in mice deficient in SPARC. In: American Journal of Physiology - Lung Cellular and Molecular Physiology. 2000 ; Vol. 279, No. 4 23-4.
@article{5fe7efe004994abb88150b241ef1e4be,
title = "Bleomycin-induced pulmonary injury in mice deficient in SPARC",
abstract = "SPARC (secreted protein, acidic and rich in cysteine) is a component of the matrix that appears to regulate tissue remodeling. There is evidence that it accumulates in the lung in the setting of pulmonary injury and fibrosis, but direct evidence of its involvement is only now emerging. We therefore investigated the development of pulmonary fibrosis induced by bleomycin administered either intratracheally or intraperitoneally in mice deficient in SPARC. Bleomycin (0.15 U/mouse) given intratracheally induced significantly more pulmonary fibrosis in mice deficient in SPARC compared with that in wild-type control mice, with the mutant mice demonstrating greater neutrophil accumulation in the lung. However, in wild-type and SPARC-deficient mice given intraperitoneal bleomycin (0.8 U/injection x 5 injections over 14 days), the pattern and severity of pulmonary fibrosis, as well as the levels of leukocyte recruitment, were similar in both strains of mice. These findings suggest that the involvement of SPARC in pulmonary injury is likely to be complex, dependent on several factors including the type, duration, and intensity of the insult. Furthermore, increased neutrophil accumulation in the peritoneal cavity was also observed in SPARC-null mice after acute chemical peritonitis. Together, these data suggest a possible role for SPARC in the recruitment of neutrophils to sites of acute inflammation.",
keywords = "Acidic and rich in cysteine, Inflammation, Lung fibrosis, Neurophils, Secreted protein",
author = "Savani, {Rashmin C.} and Zhao Zhou and Evguenia Arguiri and Sunny Wang and Dinh Vu and Howe, {Chin C.} and DeLisser, {Horace M.}",
year = "2000",
language = "English (US)",
volume = "279",
journal = "American Journal of Physiology - Heart and Circulatory Physiology",
issn = "0363-6135",
publisher = "American Physiological Society",
number = "4 23-4",

}

TY - JOUR

T1 - Bleomycin-induced pulmonary injury in mice deficient in SPARC

AU - Savani, Rashmin C.

AU - Zhou, Zhao

AU - Arguiri, Evguenia

AU - Wang, Sunny

AU - Vu, Dinh

AU - Howe, Chin C.

AU - DeLisser, Horace M.

PY - 2000

Y1 - 2000

N2 - SPARC (secreted protein, acidic and rich in cysteine) is a component of the matrix that appears to regulate tissue remodeling. There is evidence that it accumulates in the lung in the setting of pulmonary injury and fibrosis, but direct evidence of its involvement is only now emerging. We therefore investigated the development of pulmonary fibrosis induced by bleomycin administered either intratracheally or intraperitoneally in mice deficient in SPARC. Bleomycin (0.15 U/mouse) given intratracheally induced significantly more pulmonary fibrosis in mice deficient in SPARC compared with that in wild-type control mice, with the mutant mice demonstrating greater neutrophil accumulation in the lung. However, in wild-type and SPARC-deficient mice given intraperitoneal bleomycin (0.8 U/injection x 5 injections over 14 days), the pattern and severity of pulmonary fibrosis, as well as the levels of leukocyte recruitment, were similar in both strains of mice. These findings suggest that the involvement of SPARC in pulmonary injury is likely to be complex, dependent on several factors including the type, duration, and intensity of the insult. Furthermore, increased neutrophil accumulation in the peritoneal cavity was also observed in SPARC-null mice after acute chemical peritonitis. Together, these data suggest a possible role for SPARC in the recruitment of neutrophils to sites of acute inflammation.

AB - SPARC (secreted protein, acidic and rich in cysteine) is a component of the matrix that appears to regulate tissue remodeling. There is evidence that it accumulates in the lung in the setting of pulmonary injury and fibrosis, but direct evidence of its involvement is only now emerging. We therefore investigated the development of pulmonary fibrosis induced by bleomycin administered either intratracheally or intraperitoneally in mice deficient in SPARC. Bleomycin (0.15 U/mouse) given intratracheally induced significantly more pulmonary fibrosis in mice deficient in SPARC compared with that in wild-type control mice, with the mutant mice demonstrating greater neutrophil accumulation in the lung. However, in wild-type and SPARC-deficient mice given intraperitoneal bleomycin (0.8 U/injection x 5 injections over 14 days), the pattern and severity of pulmonary fibrosis, as well as the levels of leukocyte recruitment, were similar in both strains of mice. These findings suggest that the involvement of SPARC in pulmonary injury is likely to be complex, dependent on several factors including the type, duration, and intensity of the insult. Furthermore, increased neutrophil accumulation in the peritoneal cavity was also observed in SPARC-null mice after acute chemical peritonitis. Together, these data suggest a possible role for SPARC in the recruitment of neutrophils to sites of acute inflammation.

KW - Acidic and rich in cysteine

KW - Inflammation

KW - Lung fibrosis

KW - Neurophils

KW - Secreted protein

UR - http://www.scopus.com/inward/record.url?scp=0033680476&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0033680476&partnerID=8YFLogxK

M3 - Article

C2 - 11000135

AN - SCOPUS:0033680476

VL - 279

JO - American Journal of Physiology - Heart and Circulatory Physiology

JF - American Journal of Physiology - Heart and Circulatory Physiology

SN - 0363-6135

IS - 4 23-4

ER -