altered monocyte and fibrocyte phenotype and function in scleroderma interstitial lung disease reversal by caveolin-1 scaffolding domain peptide在硬皮病改变单核细胞和纤维细胞表型和功能间质性肺疾病逆转caveolin-1脚手架域肽.pdfVIP
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altered monocyte and fibrocyte phenotype and function in scleroderma interstitial lung disease reversal by caveolin-1 scaffolding domain peptide在硬皮病改变单核细胞和纤维细胞表型和功能间质性肺疾病逆转caveolin-1脚手架域肽
Tourkina et al. Fibrogenesis Tissue Repair 2011, 4:15
/content/4/1/15
RESEARCH Open Access
Altered monocyte and fibrocyte phenotype and
function in scleroderma interstitial lung disease:
reversal by caveolin-1 scaffolding domain peptide
1* 1 1 1 1 1
Elena Tourkina , Michael Bonner , James Oates , Ann Hofbauer , Mathieu Richard , Sergei Znoyko ,
2 2 1 1 1,2
Richard P Visconti , Jing Zhang , Corey M Hatfield , Richard M Silver and Stanley Hoffman
Abstract
Interstitial lung disease (ILD) is a major cause of morbidity and mortality in scleroderma (systemic sclerosis, or SSc).
Fibrocytes are a monocyte-derived cell population implicated in the pathogenesis of fibrosing disorders. Given the
recently recognized importance of caveolin-1 in regulating function and signaling in SSc monocytes, in the present
study we examined the role of caveolin-1 in the migration and/or trafficking and phenotype of monocytes and
fibrocytes in fibrotic lung disease in human patients and an animal model. These studies fill a gap in our
understanding of how monocytes and fibrocytes contribute to SSc-ILD pathology. We found that C-X-C chemokine
+ + + + + +
receptor type 4-positive (CXCR4 )/collagen I-positive (ColI ), CD34 /ColI and CD45 /ColI cells are present in SSc-
ILD lungs, but not in control lungs, with CXCR4+ cells being most prevalent. Expression of CXCR4 and its ligand,
stromal cell-derived factor 1 (CXCL12), are also highly upregulated in SSc-ILD lung tissue. SSc monocytes, which
lack cave
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