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10.3109/01902148.2014.983282 http://scihub22266oqcxt.onion/10.3109/01902148.2014.983282 C4524537!4524537 !25513848     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25513848 &cmd=llinks): Failed to open stream: HTTP request failed! 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Pulmonary preconditioning, injury, and inflammation modulate expression of the candidate tumor suppressor gene ECRG4 in lung |pdf=|usr=}}{{25513848 }} gab.com Text Pulmonary preconditioning, injury, and inflammation modulate expression of the candidate tumor suppressor gene ECRG4 in lung JO: Exp Lung Res http://www.kidney.de/pget.php?&tw=1&pmid=25513848 #FOAvip PURPOSE: The human c2orf40 gene encodes a candidate tumor suppressor called Esophageal Cancer-Related Gene-4 (ECRG4) that is a cytokine-like epigenetically-regulated protein that is characteristically downregulated in cancer, injury, inflammation, and infection. Here, we asked whether ECRG4 gene expression is detectable in lung epithelial cells and if its expression changes with inflammation, infection, and/or protective preconditioning. MATERIALS AND METHODS: We used immunoblotting, PCR, and quantitative PCR to measure ECRG4 and either inhalation anesthesia preconditioning, lipopolysaccharide injection, or laparotomy to modulate lung inflammation. RESULTS: Immunoblotting establishes the presence of the full-length 14 kDa ECRG4 peptide in mouse lung. Immunohistochemistry localizes ECRG4 to type l alveolar epithelial cells. Basal ECRG4 mRNA is greater than TNF-?, IL-1?, and IL-6 but following inflammatory lung injury, TNF-?, IL-1?, IL-6, and IL-10 are upregulated while ECRG4 gene expression is decreased. Similar findings are observed after an intravenous administration of lipopolysaccharide. In contrast, lung preconditioning with isoflurane anesthesia increases lung ECRG4 gene expression. Over-expression of ECRG4 in human lung epithelial cells in vitro decreases cell proliferation implying that a loss of ECRG4 in vivo would be permissive to cell growth. CONCLUSIONS: This study supports the hypothesis that ECRG4 acts as a sentinel growth inhibitor in lung alveolar epithelial cells. Its downregulation by injury, infection, and inflammation and upregulation by preconditioning supports a role for ECRG4 in regulating the alveolar epithelium response to injury and inflammation. By extension, the findings support a functional consequence to its inhibition by promoter hypermethylation (i.e. lung cancer) and suggest potential benefits to its upregulation. Twit Text FOAVip Pulmonary preconditioning, injury, and inflammation modulate expression of the candidate tumor suppressor gene ECRG4 in lung ????Exp Lung Res http://www.kidney.de/pget.php?&tw=1&pmid=25513848 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25513848 #FOAvip English Wikipedia <ref>{{Cite pmid|25513848 }}</ref> Pulmonary preconditioning, injury, and inflammation modulate expression of the candidate tumor suppressor gene ECRG4 in lung #MMPMID25513848 Kao S ; Shaterian A ; Cauvi DM ; Dang X ; Chun HB ; De Maio A ; Costantini TW ; Coimbra R ; Eliceiri BP ; Baird A Exp Lung Res 2015[Apr]; 41 (3 ): 162-72 PMID25513848 show ga PURPOSE: The human c2orf40 gene encodes a candidate tumor suppressor called Esophageal Cancer-Related Gene-4 (ECRG4) that is a cytokine-like epigenetically-regulated protein that is characteristically downregulated in cancer, injury, inflammation, and infection. Here, we asked whether ECRG4 gene expression is detectable in lung epithelial cells and if its expression changes with inflammation, infection, and/or protective preconditioning. MATERIALS AND METHODS: We used immunoblotting, PCR, and quantitative PCR to measure ECRG4 and either inhalation anesthesia preconditioning, lipopolysaccharide injection, or laparotomy to modulate lung inflammation. RESULTS: Immunoblotting establishes the presence of the full-length 14 kDa ECRG4 peptide in mouse lung. Immunohistochemistry localizes ECRG4 to type l alveolar epithelial cells. Basal ECRG4 mRNA is greater than TNF-?, IL-1?, and IL-6 but following inflammatory lung injury, TNF-?, IL-1?, IL-6, and IL-10 are upregulated while ECRG4 gene expression is decreased. Similar findings are observed after an intravenous administration of lipopolysaccharide. In contrast, lung preconditioning with isoflurane anesthesia increases lung ECRG4 gene expression. Over-expression of ECRG4 in human lung epithelial cells in vitro decreases cell proliferation implying that a loss of ECRG4 in vivo would be permissive to cell growth. CONCLUSIONS: This study supports the hypothesis that ECRG4 acts as a sentinel growth inhibitor in lung alveolar epithelial cells. Its downregulation by injury, infection, and inflammation and upregulation by preconditioning supports a role for ECRG4 in regulating the alveolar epithelium response to injury and inflammation. By extension, the findings support a functional consequence to its inhibition by promoter hypermethylation (i.e. lung cancer) and suggest potential benefits to its upregulation. |Animals [MESH] |Cell Proliferation/genetics [MESH] |Down-Regulation/genetics [MESH] |Epithelial Cells/metabolism [MESH] |Female [MESH] |Genes, Tumor Suppressor [MESH] |Humans [MESH] |Interleukins/genetics/metabolism [MESH] |Lung Injury/*genetics/metabolism [MESH] |Lung/metabolism [MESH] |Male [MESH] |Mice [MESH] |Mice, Inbred BALB C [MESH] |Middle Aged [MESH] |Neoplasm Proteins/*genetics/metabolism [MESH] |Pneumonia/*genetics/metabolism [MESH] |Promoter Regions, Genetic/genetics [MESH] |Rats, Sprague-Dawley [MESH] |Tumor Necrosis Factor-alpha/genetics/metabolism [MESH]Pulmonary preconditioning, injury, and inflammation modulate expressio(epmc).pdf DeepDyve Pubget Overpricing