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10.1016/j.tox.2017.03.018 http://scihub22266oqcxt.onion/10.1016/j.tox.2017.03.018 C5470547!5470547!28341147     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28341147&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\28341147.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Toxicology 2017 ; 383 (�): 50-6 Nephropedia Template TP {{tp|p=28341147|t=2017. Cadmium stimulates myofibroblast differentiation and mouse lung fibrosis |pdf=|usr=}}{{28341147}} gab.com Text Cadmium stimulates myofibroblast differentiation and mouse lung fibrosis JO: Toxicology http://www.kidney.de/pget.php?&tw=1&pmid=28341147 #FOAvip Increasing evidence suggests that Cd at levels found in the human diet can cause oxidative stress and activate redox-sensitive transcription factors in inflammatory signaling. Following inflammation, tissue repair often involves activation of redox-sensitive transcription factors in fibroblasts. In lungs, epithelial barrier remodeling is required to restore gas exchange and barrier function, and aberrant myofibroblast differentiation leads to pulmonary fibrosis. Contributions of exogenous exposures, such as dietary Cd, to pulmonary fibrosis remain incompletely defined. In the current study, we tested whether Cd activates fibrotic signaling in human fetal lung fibroblasts (HFLF) at micromolar and submicromolar Cd concentrations that do not cause cell death. Exposure of HFLF to low-dose Cd (?1.0 ?M) caused an increase in stress fibers and increased protein levels of myofibroblast differentiation markers, including ?-smooth muscle actin (?-SMA) and extra-domain-A-containing fibronectin (ED-A-FN). Assay of transcription factor (TF) activity using a 45-TF array showed that Cd increased activity of 12 TF, including SMAD2/3/4 (mothers against decapentaplegic homolog) signaling differentiation and fibrosis. Results were confirmed by real-time PCR and supported by increased expression of target genes of SMAD2/3/4. Immunocytochemistry of lungs of mice exposed to Cd (0.3 and 1.0 mg/L in drinking water) showed increased ?-SMA staining with lung Cd accumulation similar to lung Cd in non-smoking humans. Together, the results show that relatively low Cd exposures stimulate pulmonary fibrotic signaling and myofibroblast differentiation by activating SMAD2/3/4?dependent signaling. The results indicate that dietary Cd intake could be an important variable contributing to pulmonary fibrosis in humans. Twit Text FOAVip Cadmium stimulates myofibroblast differentiation and mouse lung fibrosis ????Toxicology http://www.kidney.de/pget.php?&tw=1&pmid=28341147 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28341147 #FOAvip English Wikipedia <ref>{{Cite pmid|28341147}}</ref> Cadmium stimulates myofibroblast differentiation and mouse lung fibrosis #MMPMID28341147 Hu X; Fernandes J; Jones DP; Go YM Toxicology 2017[May]; 383 (�): 50-6 PMID28341147show ga Increasing evidence suggests that Cd at levels found in the human diet can cause oxidative stress and activate redox-sensitive transcription factors in inflammatory signaling. Following inflammation, tissue repair often involves activation of redox-sensitive transcription factors in fibroblasts. In lungs, epithelial barrier remodeling is required to restore gas exchange and barrier function, and aberrant myofibroblast differentiation leads to pulmonary fibrosis. Contributions of exogenous exposures, such as dietary Cd, to pulmonary fibrosis remain incompletely defined. In the current study, we tested whether Cd activates fibrotic signaling in human fetal lung fibroblasts (HFLF) at micromolar and submicromolar Cd concentrations that do not cause cell death. Exposure of HFLF to low-dose Cd (?1.0 ?M) caused an increase in stress fibers and increased protein levels of myofibroblast differentiation markers, including ?-smooth muscle actin (?-SMA) and extra-domain-A-containing fibronectin (ED-A-FN). Assay of transcription factor (TF) activity using a 45-TF array showed that Cd increased activity of 12 TF, including SMAD2/3/4 (mothers against decapentaplegic homolog) signaling differentiation and fibrosis. Results were confirmed by real-time PCR and supported by increased expression of target genes of SMAD2/3/4. Immunocytochemistry of lungs of mice exposed to Cd (0.3 and 1.0 mg/L in drinking water) showed increased ?-SMA staining with lung Cd accumulation similar to lung Cd in non-smoking humans. Together, the results show that relatively low Cd exposures stimulate pulmonary fibrotic signaling and myofibroblast differentiation by activating SMAD2/3/4?dependent signaling. The results indicate that dietary Cd intake could be an important variable contributing to pulmonary fibrosis in humans. �Cadmium stimulates myofibroblast differentiation and mouse lung fibros(epmc).pdf DeepDyve Pubget Overpricing