DocumentCode
3343636
Title
Notice of Retraction
Up-Regulation of the NGF-mRNA in Macrophage Cell Induced by Formaldehyde and DEHP
Author
Mingdi Jiang ; Xiaoling Xiang ; Wenhao Yao ; Xu Yang ; Ping Ma
Author_Institution
Hubei Key Lab. of Genetic Regul. & Integrative Biol., Huazhong Normal Univ., Wuhan, China
fYear
2011
fDate
10-12 May 2011
Firstpage
1
Lastpage
4
Abstract
Notice of Retraction
After careful and considered review of the content of this paper by a duly constituted expert committee, this paper has been found to be in violation of IEEE´s Publication Principles.
We hereby retract the content of this paper. Reasonable effort should be made to remove all past references to this paper.
The presenting author of this paper has the option to appeal this decision by contacting TPII@ieee.org.
Formaldehyde (FA) was one of the most important and serious indoor air pollutants while di-(2-ethylhexyl) phthalate (DEHP) was widely used in the plastic industry and distributed in the environment. Many reports have shown that both FA and DEHP exposures could increase the risk of asthma but it was still unclear for its molecular mechanism. Recently, some researches indicated that NGF played a key role in bronchial hyperresponsiveness, airway inflammation and bronchial remodeling, which were the main features of asthma. In order to explore whether FA and DEHP can induce asthma through the NGF way, this study took the macrophage cells of mice as experiment material, applied RT-PCR to assess NGF mRNA expression levels after FA (0, 1, 5, 25, 125 μmol·L-1) and DEHP (0, 25, 50, 100, 200 mg·L-1) exposure in vitro respectively. With the increase of FA and DEHP concentrations, we observed that the experssion of NGF rose at first and then dropped as followed. The result suggested that FA and DEHP can induce NGF-mRNA up-regulation of macrophage cell thus it could be a possible mechanism that FA and DEHP induced asthma.
After careful and considered review of the content of this paper by a duly constituted expert committee, this paper has been found to be in violation of IEEE´s Publication Principles.
We hereby retract the content of this paper. Reasonable effort should be made to remove all past references to this paper.
The presenting author of this paper has the option to appeal this decision by contacting TPII@ieee.org.
Formaldehyde (FA) was one of the most important and serious indoor air pollutants while di-(2-ethylhexyl) phthalate (DEHP) was widely used in the plastic industry and distributed in the environment. Many reports have shown that both FA and DEHP exposures could increase the risk of asthma but it was still unclear for its molecular mechanism. Recently, some researches indicated that NGF played a key role in bronchial hyperresponsiveness, airway inflammation and bronchial remodeling, which were the main features of asthma. In order to explore whether FA and DEHP can induce asthma through the NGF way, this study took the macrophage cells of mice as experiment material, applied RT-PCR to assess NGF mRNA expression levels after FA (0, 1, 5, 25, 125 μmol·L-1) and DEHP (0, 25, 50, 100, 200 mg·L-1) exposure in vitro respectively. With the increase of FA and DEHP concentrations, we observed that the experssion of NGF rose at first and then dropped as followed. The result suggested that FA and DEHP can induce NGF-mRNA up-regulation of macrophage cell thus it could be a possible mechanism that FA and DEHP induced asthma.
Keywords
health hazards; occupational health; occupational safety; plastics industry; DEHP concentrations; FA concentrations; NGF-mRNA expression levels; RT-PCR; airway inflammation; asthma; bronchial hyperresponsiveness; bronchial remodeling; di-(2-ethylhexyl) phthalate; formaldehyde; indoor air pollutants; macrophage cell; mice; molecular mechanism; plastic industry; upregulation; DNA; Humans; In vitro; Lungs; Mice; Plastics;
fLanguage
English
Publisher
ieee
Conference_Titel
Bioinformatics and Biomedical Engineering, (iCBBE) 2011 5th International Conference on
Conference_Location
Wuhan
ISSN
2151-7614
Print_ISBN
978-1-4244-5088-6
Type
conf
DOI
10.1109/icbbe.2011.5781415
Filename
5781415
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