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Function of Angiostatin in Acute Lung Inflammation
Author(s) -
Aulakh Gurpreet Kaur,
Liu Lixin,
Suri Sarabjeet Singh,
Singh Baljit
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.111.4
Subject(s) - angiostatin , bronchoalveolar lavage , inflammation , lung , chemokine , lipopolysaccharide , immunology , medicine , angiogenesis , chemistry , cancer research
ALI is characterized by the migration of activated neutrophils into lungs and causes significant mortality. Although necessary, activated neutrophils also cause significant tissue damage. The mechanisms of neutrophils migration and pathogenesis of ALI are not fully understood. Angiostatin binds to ATP synthase and integrins, and inhibits angiogenesis. We investigated effect of subcutaneous administration of angiostatin in a mouse model of E. coli lipopolysaccharide (LPS) induced ALI. Immunohistochemistry showed higher expression of angiostatin/plasminogen in the airways and blood vessels in the inflamed lungs. Angiostatin expression was increased in inflamed lung extracts as well as bronchoalveolar lavage (BAL) supernatant (P<0.007). Angiostatin treatment of the LPS‐treated mice decreased total cell counts and protein concentration (P<0.05) but increased (P<0.05) apoptotic neutrophils in BAL and decreased (P<0.05) myeloperoxide in lung extracts. The protein and mRNA expression of cytokines and chemokines (IL‐1β, KC, MCP‐1 and MIP‐1α) was not altered in LPS+angiostatin mice. We conclude that angiostatin expression is increased in inflamed lungs and angiostatin treatment inhibits neutrophil migration into the inflamed lungs and lung inflammation. (Funding NSERC Discovery Grant) Grant Funding Source : NSERC Discovery Grant