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Ambient PM2.5 Exposure Promotes Angiogenesis and Inflammation of Lung Cancer Mediated by Macrophage
Description
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A7076 - Ambient PM2.5 Exposure Promotes Angiogenesis and Inflammation of Lung Cancer Mediated by Macrophage
Author Block: R. Li1, R. Zhou*1, J. Zhang*2; 1Department of Respiratory Medicine, the Second Xiangya Hospital, Central South University, Changsha, China, 2Innovation Research Institute of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
RATIONALE:
The close association between ambient PM2.5 exposure and the increment of morbidity and mortality of lung cancer has been verified in previous studies. Macrophage exerts a multifunctional role in the alteration of the microenvironment of lung cancer. However, less attention is focused on the role of PM2.5 in macrophage-mediated alteration of the microenvironment of lung cancer.
METHODS:
MTT assays were performed to explore the cytotoxicity of PM2.5. Quantitative RT-PCR assays were used to detect the mRNA expressions of inflammatory cytokines and angiogenetic factors in LLC cells, which were short-term exposed to ambient PM2.5 or RAW264.7 supernatant interacting with PM2.5 extract. Protein levels of VEGF in LLC cells exposed to RAW264.7 supernatant were tested by adopting enzyme-linked immunosorbent assays (ELISA). We also conducted sponge implantation model and tumor bearing model in mice to explore whether ambient PM2.5 can enhance angiogenesis and inflammation in lung cancer mediated by macrophage in vivo models.
RESULTS:
We detected the overexpressions of inflammatory cytokines (e.g., α-TNF, β-TGF and IL-1β) and angiogenetic factors (e.g., VEGF-A, MMP-9, PDGF, bFGF) in LLC cells which were exposed to RAW264.7 supertanant interacting with PM2.5 extract. In contrast, exposed to ambient PM2.5 directly can not significantly elevate the expressions of these cytokines in LLC cells. The upregulation expressions of CD47 and its specific receptor Sirp-α were also found respectively in PM2.5-mediated LLC cells and RAW264.7 cells by adopting quantitative RT-PCR. Protein levels of VEGF significantly enhanced in supernatant-mediated LLC cells. Increased mRNA expresssions of inflammatory cytokines (e,g., VEGF-A, bFGF, CD47), elevation of macrophage count, mirovessel density and exacerbation of hypoxia were also detected in vivo models, such as sponge implantation model, tumor bearing model.
CONCLUSIONS
Ambient PM2.5 can enhance angiogenesis and inflammation of lung cancer mediated by macrophage, and the underlying mechanisms possibly include promoting the release of inflammatory and angiogenetic cytokines of macrophage and activating CD47/Sirp-α pathway, which may provide new ideas for the phathogenesis of lung cancer PM2.5 involved in.
Author Block: R. Li1, R. Zhou*1, J. Zhang*2; 1Department of Respiratory Medicine, the Second Xiangya Hospital, Central South University, Changsha, China, 2Innovation Research Institute of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
RATIONALE:
The close association between ambient PM2.5 exposure and the increment of morbidity and mortality of lung cancer has been verified in previous studies. Macrophage exerts a multifunctional role in the alteration of the microenvironment of lung cancer. However, less attention is focused on the role of PM2.5 in macrophage-mediated alteration of the microenvironment of lung cancer.
METHODS:
MTT assays were performed to explore the cytotoxicity of PM2.5. Quantitative RT-PCR assays were used to detect the mRNA expressions of inflammatory cytokines and angiogenetic factors in LLC cells, which were short-term exposed to ambient PM2.5 or RAW264.7 supernatant interacting with PM2.5 extract. Protein levels of VEGF in LLC cells exposed to RAW264.7 supernatant were tested by adopting enzyme-linked immunosorbent assays (ELISA). We also conducted sponge implantation model and tumor bearing model in mice to explore whether ambient PM2.5 can enhance angiogenesis and inflammation in lung cancer mediated by macrophage in vivo models.
RESULTS:
We detected the overexpressions of inflammatory cytokines (e.g., α-TNF, β-TGF and IL-1β) and angiogenetic factors (e.g., VEGF-A, MMP-9, PDGF, bFGF) in LLC cells which were exposed to RAW264.7 supertanant interacting with PM2.5 extract. In contrast, exposed to ambient PM2.5 directly can not significantly elevate the expressions of these cytokines in LLC cells. The upregulation expressions of CD47 and its specific receptor Sirp-α were also found respectively in PM2.5-mediated LLC cells and RAW264.7 cells by adopting quantitative RT-PCR. Protein levels of VEGF significantly enhanced in supernatant-mediated LLC cells. Increased mRNA expresssions of inflammatory cytokines (e,g., VEGF-A, bFGF, CD47), elevation of macrophage count, mirovessel density and exacerbation of hypoxia were also detected in vivo models, such as sponge implantation model, tumor bearing model.
CONCLUSIONS
Ambient PM2.5 can enhance angiogenesis and inflammation of lung cancer mediated by macrophage, and the underlying mechanisms possibly include promoting the release of inflammatory and angiogenetic cytokines of macrophage and activating CD47/Sirp-α pathway, which may provide new ideas for the phathogenesis of lung cancer PM2.5 involved in.
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