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Journal of Environmental Pathology, Toxicology and Oncology
Главный редактор: Qian Peng (open in a new tab)

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ISSN Печать: 0731-8898

ISSN Онлайн: 2162-6537

The Impact Factor measures the average number of citations received in a particular year by papers published in the journal during the two preceding years. 2017 Journal Citation Reports (Clarivate Analytics, 2018) IF: 2.4 To calculate the five year Impact Factor, citations are counted in 2017 to the previous five years and divided by the source items published in the previous five years. 2017 Journal Citation Reports (Clarivate Analytics, 2018) 5-Year IF: 2.8 The Immediacy Index is the average number of times an article is cited in the year it is published. The journal Immediacy Index indicates how quickly articles in a journal are cited. Immediacy Index: 0.5 The Eigenfactor score, developed by Jevin West and Carl Bergstrom at the University of Washington, is a rating of the total importance of a scientific journal. Journals are rated according to the number of incoming citations, with citations from highly ranked journals weighted to make a larger contribution to the eigenfactor than those from poorly ranked journals. Eigenfactor: 0.00049 The Journal Citation Indicator (JCI) is a single measurement of the field-normalized citation impact of journals in the Web of Science Core Collection across disciplines. The key words here are that the metric is normalized and cross-disciplinary. JCI: 0.59 SJR: 0.429 SNIP: 0.507 CiteScore™:: 3.9 H-Index: 49

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Effect of Platelet-Derived Growth Factor on the Development and Persistence of Asbestos-Induced Fibroproliferative Lung Disease

Том 23, Выпуск 4, 2004, 14 pages
DOI: 10.1615/JEnvPathToxOncol.v23.i4.20
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Краткое описание

Platelet-derived growth factor (PDGF) isoforms and PDGF receptor-α are upregulated in fibroproliferative lesions in response to asbestos exposure. To examine the functional role of PDGF in asbestos-induced lung disease, we have evaluated the impact of PDGF-B overexpression in the lung on the development of pulmonary fibrosis induced by asbestos inhalation. Transgenic mice expressing PDGF-B from the surfactant protein C promoter and wild-type C57BL/6 mice were exposed to aerosolized chrysotile asbestos fibers via three different exposure regimens: 3 consecutive days to 9 mg/m3, once a week for 5 weeks to 12 mg/m3, or once a week for 8 weeks to 11 mg/m3. The 3-day exposure did not produce fibroproliferative lesions in SPC-PDGFB or wild-type mice, indicating that PDGF expression did not increase susceptibility to a subthreshold dose of asbestos. Transgenic and wild-type mice subjected to the 5-week exposure protocol exhibited similar fibrogenic lesions histologically 48 hours and 8 weeks postexposure, but lungs from transgenic mice had elevated lung hydroxyproline content 8 weeks postexposure relative to wild-type mice. In addition, SPC-PDGFB transgenic mice developed pronounced thickening of arterioles following the 5-week exposure regimen. Mice exposed to asbestos for 8 weeks and examined 10 months later showed pronounced, diffuse fibrotic lesions of terminal bronchioles and alveolar ducts, but no histological differences between transgenic and nontransgenic mice were observed. These results indicated that PDGF-B overexpression can stimulate increased collagen deposition and vascular smooth muscle hyper-plasia following asbestos inhalation and that a limited exposure (8 times) to chrysotile aerosol can produce long-lasting fibrotic lesions. The 8-week exposure regimen provides an animal model that encompasses an important aspect of human asbestosis—i.e., persistence of fibrosis for long periods after cessation of asbestos exposure.

ЦИТИРОВАНО В
  1. Yin Qian, Nan Haiyan, Yan Linfeng, Huang Xiaofeng, Wang Wei, Cui Guangbin, Wei Jingguo, Alteration of tight junctions in pulmonary microvascular endothelial cells in bleomycin-treated rats, Experimental and Toxicologic Pathology, 64, 1-2, 2012. Crossref

  2. Perkins T.N., Peeters P.M., Wouters E.F.M., Reynaert N.L., Mossman B.T., Pathogenesis and Mechanisms of Asbestosis and Silicosis, in Pathobiology of Human Disease, 2014. Crossref

  3. Brody Arnold, Sullivan Deborah, The Asbestos Model of Interstitial Pulmonary Fibrosis, in Particle Toxicology, 2006. Crossref

  4. Mo Yiqun, Chen Jing, Schlueter Connie F., Hoyle Gary W., Differential susceptibility of inbred mouse strains to chlorine-induced airway fibrosis, American Journal of Physiology-Lung Cellular and Molecular Physiology, 304, 2, 2013. Crossref

  5. Tashiro Jun, Rubio Gustavo A., Limper Andrew H., Williams Kurt, Elliot Sharon J., Ninou Ioanna, Aidinis Vassilis, Tzouvelekis Argyrios, Glassberg Marilyn K., Exploring Animal Models That Resemble Idiopathic Pulmonary Fibrosis, Frontiers in Medicine, 4, 2017. Crossref

  6. Du Jiang, Zhang Lin, Pathway deviation-based biomarker and multi-effect target identification in asbestos-related squamous cell carcinoma of the lung, International Journal of Molecular Medicine, 39, 3, 2017. Crossref

  7. Patete Carissa L., Toonkel R. L., Glassberg Marilyn, Stem Cell Based Therapy for Lung Disease Preclinical evidence for the role of stem/stromal cells Clinical application of stem/stromal cells in lung fibrosis, in Stem Cell-Based Therapy for Lung Disease, 2019. Crossref

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