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Suppression of PTPN6 exacerbates aluminum oxide nanoparticle-induced COPD-like lesions in mice through activation of STAT pathway
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نویسنده
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li x. ,yang h. ,wu s. ,meng q. ,sun h. ,lu r. ,cui j. ,zheng y. ,chen w. ,zhang r. ,aschner m. ,chen r.
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منبع
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particle and fibre toxicology - 2017 - دوره : 14 - شماره : 1
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چکیده
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Background: inhaled nanoparticles can deposit in the deep lung where they interact with pulmonary cells. despite numerous studies on pulmonary nanotoxicity,detailed molecular mechanisms of specific nanomaterial-induced lung injury have yet to be identified. results: using whole-body dynamic inhalation model,we studied the interactions between aluminum oxide nanoparticles (al2o3 nps) and the pulmonary system in vivo. we found that seven-day-exposure to al2o3 nps resulted in emphysema and small airway remodeling in murine lungs,accompanied by enhanced inflammation and apoptosis. al2o3 nps exposure led to suppression of ptpn6 and phosphorylation of stat3,culminating in increased expression of the apoptotic marker pdcd4. rescue of ptpn6 expression or application of a stat3 inhibitor,effectively protected murine lungs from inflammation and apoptosis,as well as,in part,from the induction of chronic obstructive pulmonary disease (copd)-like effects. conclusion: in summary,our studies show that inhibition of ptpn6 plays a critical role in al2o3 nps-induced copd-like lesions. © 2017 the author(s).
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کلیدواژه
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Aluminum oxide nanoparticles; Experimental COPD; Inflammation; PTPN6
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آدرس
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southeast university,key laboratory of environmental medicine engineering,ministry of education,school of public health,dingjiaqiao 87,nanjing,210009, China, china pharmaceutical university,center for new drug safety evaluation and research,nanjing, China, southeast university,key laboratory of environmental medicine engineering,ministry of education,school of public health,dingjiaqiao 87,nanjing,210009, China, southeast university,key laboratory of environmental medicine engineering,ministry of education,school of public health,dingjiaqiao 87,nanjing,210009, China, southeast university,key laboratory of environmental medicine engineering,ministry of education,school of public health,dingjiaqiao 87,nanjing,210009, China, southeast university,key laboratory of environmental medicine engineering,ministry of education,school of public health,dingjiaqiao 87,nanjing,210009, China, southeast university,key laboratory of environmental medicine engineering,ministry of education,school of public health,dingjiaqiao 87,nanjing,210009, China, school of public health,qingdao university,qingdao,266021, China, sun yat-sen university,guangzhou key laboratory of environmental pollution and health risk assessment,department of toxicology,school of public health,guangzhou,510080, China, hebei medical university,department of toxicology,school of public health,shijiazhuang,050017, China, albert einstein college of medicine,department of molecular pharmacology,bronx,ny 10461, United States, southeast university,key laboratory of environmental medicine engineering,ministry of education,school of public health,dingjiaqiao 87,nanjing,210009,china,guangzhou medical university,institute for chemical carcinogenesis,guangzhou,511436, China
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Authors
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