Acid Sphingomyelinase Deficiency Attenuates Bleomycin-Induced Lung Inflammation and Fibrosis in Mice | Zendy

Rajwinder Dhami | Zendy; Xingxuan He | Zendy; Edward H. Schuchman | Zendy

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Acid Sphingomyelinase Deficiency Attenuates Bleomycin-Induced Lung Inflammation and Fibrosis in Mice

Author(s) -

Rajwinder Dhami,

Xingxuan He,

Edward H. Schuchman

Publication year - 2010

Publication title -

cellular physiology and biochemistry

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.486

H-Index - 87

eISSN - 1421-9778

pISSN - 1015-8987

DOI - 10.1159/000322342

Subject(s) - bleomycin , acid sphingomyelinase , sphingomyelin phosphodiesterase , pulmonary fibrosis , ceramide , inflammation , fibrosis , myofibroblast , lipid signaling , pathogenesis , cancer research , sphingolipid , sphingosine , sphingomyelin , idiopathic pulmonary fibrosis , lung , chemistry , apoptosis , medicine , immunology , biology , endocrinology , microbiology and biotechnology , pathology , biochemistry , receptor , chemotherapy , cholesterol

The sphingomyelin/ceramide signaling pathway is an important component of many cellular processes implicated in the pathogenesis of lung disease. Acid sphingomyelinase (ASM) is a key mediator of this pathway, but its specific role in pulmonary fibrosis has not been previously investigated. Here we used the bleomycin model of pulmonary fibrosis to investigate fibrotic responses in normal and ASM knockout (ASM(-/-)) mice, and in NIH3T3 fibroblasts with and without ASM siRNA treatment.

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