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Enhanced generation of free radicals from phagocytes induced by mineral dusts. Pulmonary chemokine and mutagenic responses in rats after subchronic inhalation of 265005 and crystalline silica.
Excessive mucus production, as implicated by significant overexpression of the pendrin coding gene, SLC26A4was identified as a potential novel mechanism for silica-induced pulmonary toxicity.
Results of these analyses can be found in our recent publication Sellamuthu et al. Risk of silicosis in a Colorado mining community.
An oey role has been attributed to lipoxins mainly because of their ability to inhibit chemotaxis, adhere and transmigrate neutrophils and antagonize the pro-inflammatory effects of leukotriens Colgan et al. J Radiat Res Tokyo ; The time-course of enrichment of acute phase response and complement system in the silica-exposed rat lungs during the post-exposure time intervals are oey as representative canonical pathways enriched by silica exposure in the rats Fig.
2650 hybridizations, washing, Cy3-streptavidin staining and scanning of the chips on the Beadstation platform Illumina Inc. Interlaboratory evaluation of genomic signatures for predicting carcinogenicity in the rat. The significant overexpression of the profibrotic chemokines such as CCl2 Mercer et al. Supporting information can be found in the online version of this article. Bioinformatics analysis of the significantly differentially expressed genes in the silica exposed rat lungs was done using IPA software.
Author manuscript; available in PMC Dec Lipoxin A4 modulates transmigration of human neutrophils across intestinal epithelial le.
The findings of the present transcriptomics study also provided novel insights into the mechanisms potentially underlying the progression of silica-induced pulmonary toxicity related to upper airway diseases. Since a definite relationship is known to exist between unresolved pulmonary inflammation and fibrosis Reynolds,it is reasonable to assume that the significant overexpression of the several pro-inflammatory genes presented in Table 3 and described above and the resulting unresolved pulmonary inflammation observed in the rat lungs might be of significance in the context of silica-induced pulmonary fibrosis.
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Therefore, it is reasonable to assume that, in addition to the significant overexpression of the multiple pro-inflammatory genes, the significant down-regulation of Alox gene expression might have contributed to the establishment of unresolved pulmonary inflammation noticed in the silica-exposed rats. It was placed on the National Register of Historical Places in It is estimated that at least 1.
The findings and conclusions in this report are those of the authors and do not necessarily represent the views of the NIOSH. The gene expression data, in addition, may be useful to generate novel hypotheses regarding the molecular mechanisms underlying the toxicity of the agent being investigated.
Reid Engine Video Virtual Tour-mill. International Agency for Research on Cancer; In addition to confirming the central role played by unresolved inflammation in the pulmonary effects of silica exposure, our transcriptomics data provided insights into the molecular mechanisms, including novel ones, potentially underlying the pulmonary effects of silica exposure.
Respiratory tract mucin genes and mucin glycoproteins in health and disease. Murine models of pulmonary fibrosis. The present study is part of an on-going research project aiming to identify the molecular targets and mechanisms underlying silica-induced pulmonary toxicity.
Lipoxins play an important role in the resolution of pulmonary inflammation Chan and Moore,and the involvement of lipoxins, if any, in pey pulmonary inflammation has not been investigated to date. Presently, the lung samples obtained from these rats were analyzed by microarray to determine a global gene expression profile in order to identify the molecular targets as well as to elucidate the molecular mechanisms underlying the progression of silica-induced pulmonary toxicity.
Some of the genes are listed under more than one category since lley analysis identified their involvement in multiple categories. Osteopontin, one of the key components of extracellular matrix, mediates the migration, adhesion and proliferation leey fibroblasts culminating in pulmonary fibrosis Takahashi et al.
Protective effect of metallothionein on oxidative stress-induced DNA damage. S calcium 226505 protein A8 SA8. Generation of reactive oxygen species directly from silica particles Vallyathan et al.
The involvement of both these canonical pathways, as evidenced by their IPA P -values, in the pulmonary response of the silica-exposed rat lungs also exhibited a steady increase during the post-exposure time intervals analyzed.
Datasets – CKAN
Pulmonary epithelium is a prominent source of proteinase-activated receptorinducible CCL2 in pulmonary fibrosis. To do this, the Society conducts four 62505 meetings each year with programs involving historical subjects.
Bioinformatics analysis of the SDEGs supported the induction and progression of pulmonary inflammation and toxicity noticed in the silica-exposed rats. The profibrotic gene SPP1which codes osteopontin protein, was significantly overexpressed in the silica-exposed rat lungs with increased overexpression at late post-exposure time intervals of 8 and 16 weeks Table 3. In the past, microarray-based transcriptomics studies have been successfully employed to gain insights into the molecular mechanisms underlying the toxicity of chemicals Waring et al.
Potential role of free radicals. A proper understanding of the molecular targets and mechanisms underlying the initiation and progression of silica-induced pulmonary toxicity is required to develop strategies potentially to prevent the various diseases associated with silica exposure.
Genes involved in oxidative stress, inflammation, respiratory diseases, cancer, and tissue remodeling and fibrosis were significantly differentially expressed in the rat lungs; however, unresolved inflammation was the single most significant biological response to pulmonary exposure to silica. Gene expression profiling and bioinformatics analysis of the SDEGs also provided insights into the molecular mechanisms underlying the progression of silica-induced pulmonary lye and toxicity in the rats.
Microarray analysis of the global gene expression profile identified the genes whose expressions were significantly affected by silica exposure in the lungs of rats Supporting Information, tables 1 — 5.
The complement system A and acute phase response signaling B are presented as representative IPA canonical pathways enriched in the silica exposed rat lungs.