2009
DOI: 10.1096/fj.09-140772
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Adenosine and osteopontin contribute to the development of chronic obstructive pulmonary disease

Abstract: Chronic obstructive pulmonary disease (COPD) is a major health concern. Adenosine, a signaling molecule generated in response to cell stress, contributes to the pathogenesis of COPD. An established model of adenosine-mediated lung injury is the adenosine deaminase-deficient (Ada(-/-)) mouse. Osteopontin (OPN) is a chemokine that is produced following injury and is implicated in a variety of human pathologies, but its expression and role in the pathogenesis of COPD have not been examined. To investigate the rol… Show more

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Cited by 47 publications
(54 citation statements)
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“…Because OPN is a chemotactic factor for macrophages and neutrophils (4,35,64,83), which contribute to the pathological effects induced by O 3 in the lungs (16,33,55), we performed a differential analysis of the cells, retrieved from the BALF of wild-type and OPN-deficient mice, to assess the ability of OPN to promote macrophage and neutrophil chemotaxis following acute exposure to O 3 (Fig. 4).…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…Because OPN is a chemotactic factor for macrophages and neutrophils (4,35,64,83), which contribute to the pathological effects induced by O 3 in the lungs (16,33,55), we performed a differential analysis of the cells, retrieved from the BALF of wild-type and OPN-deficient mice, to assess the ability of OPN to promote macrophage and neutrophil chemotaxis following acute exposure to O 3 (Fig. 4).…”
Section: Discussionmentioning
confidence: 99%
“…Indeed, Kim and colleagues (37) previously reported that exposure to O 3 can increase the expression of OPN in the lungs of mice. OPN can initiate several proinflammatory events, which include, but are not limited to, the activation of NF-B and the recruitment of macrophages, neutrophils, and T cells to sites of inflammation (4,35,63,64,83). NF-B, macrophages, neutrophils, and T cells contribute to the development of O 3 -induced pulmonary injury, pulmonary inflammation, and/or AHR (12,22,50,55,56).…”
mentioning
confidence: 99%
“…However, because no data regarding the components of the leukocyte infiltrate were obtained, we cannot analyze whether A 2B AdoR antagonism qualitatively affected the infiltrate. Moreover, A 2B AdoR signaling may additionally affect cardiac remodeling independently of caspase-1: adenosine stimulates macrophages to produce osteopontin (Schneider et al, 2010) and release of interleukin-6, which induces differentiation of fibroblasts into myofibroblasts (Zhong et al, 2005), potentially affecting tissue remodeling and progression toward heart failure. In addition, although unlikely considering the selectivity of the …”
Section: Discussionmentioning
confidence: 99%
“…Spp1 is located within another QTL associated with lung function on mouse chromosome 5 bounded by markers D5Mit20 to D5Mit403 (97.8-106.2 Mbp) (20,21), which is syntenic to human chromosome 4 (81.8-90.2 Mbp). SPP1 has been associated with chronic lung diseases, including pulmonary fibrosis (27) and COPD (28). An approximately 44 kD glycosylated phosphoprotein, SPP1, is commonly found in adhesive bone matrix protein.…”
Section: Introductionmentioning
confidence: 99%