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10.18632/oncotarget.17840 http://scihub22266oqcxt.onion/10.18632/oncotarget.17840 C5663532!5663532 !29137360     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29137360 &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 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 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\29137360 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Oncotarget 2017 ; 8 (48 ): 83509-83522 Nephropedia Template TP {{tp|p=29137360 |t=2017. Novel mechanisms for crotonaldehyde-induced lung edema |pdf=|usr=}}{{29137360 }} gab.com Text Novel mechanisms for crotonaldehyde-induced lung edema JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=29137360 #FOAvip BACKGROUND: Crotonaldehyde is a highly noxious ?,?-unsaturated aldehyde in cigarette smoke that causes edematous acute lung injury. OBJECTIVE: To understand how crotonaldehyde impairs lung function, we examined its effects on human epithelial sodium channels (ENaC), which are major contributors to alveolar fluid clearance. METHODS: We studied alveolar fluid clearance in C57 mice and ENaC activity was examined in H441 cells. Expression of ?- and ?-ENaC was measured at protein and mRNA levels by western blot and real-time PCR, respectively. Intracellular ROS levels were detected by the dichlorofluorescein assay. Heterologous ???-ENaC activity was observed in an oocyte model. RESULTS: Our results showed that crotonaldehyde reduced transalveolar fluid clearance in mice. Furthermore, ENaC activity in H441 cells was inhibited by crotonaldehyde dose-dependently. Expression of ?- and ?-subunits of ENaC was decreased at the protein and mRNA level in H441 cells exposed to crotonaldehyde, which was probably mediated by the increase in phosphorylated extracellular signal-regulated protein kinases 1 and 2. ROS levels increased time-dependently in cells exposed to crotonaldehyde. Heterologous ???-ENaC activity was rapidly eliminated by crotonaldehyde. CONCLUSION: Our findings suggest that crotonaldehyde causes edematous acute lung injury by eliminating ENaC activity at least partly via facilitating the phosphorylation of extracellular signal-regulated protein kinases 1 and 2 signal molecules. Long-term exposure may decrease the expression of ENaC subunits and damage the cell membrane integrity, as well as increase the levels of cellular ROS products. Twit Text FOAVip Novel mechanisms for crotonaldehyde-induced lung edema ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=29137360 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29137360 #FOAvip English Wikipedia <ref>{{Cite pmid|29137360 }}</ref> Novel mechanisms for crotonaldehyde-induced lung edema #MMPMID29137360 Li Y ; Chang J ; Cui Y ; Zhao R ; Ding Y ; Hou Y ; Zhou Z ; Ji HL ; Nie H Oncotarget 2017[Oct]; 8 (48 ): 83509-83522 PMID29137360 show ga BACKGROUND: Crotonaldehyde is a highly noxious ?,?-unsaturated aldehyde in cigarette smoke that causes edematous acute lung injury. OBJECTIVE: To understand how crotonaldehyde impairs lung function, we examined its effects on human epithelial sodium channels (ENaC), which are major contributors to alveolar fluid clearance. METHODS: We studied alveolar fluid clearance in C57 mice and ENaC activity was examined in H441 cells. Expression of ?- and ?-ENaC was measured at protein and mRNA levels by western blot and real-time PCR, respectively. Intracellular ROS levels were detected by the dichlorofluorescein assay. Heterologous ???-ENaC activity was observed in an oocyte model. RESULTS: Our results showed that crotonaldehyde reduced transalveolar fluid clearance in mice. Furthermore, ENaC activity in H441 cells was inhibited by crotonaldehyde dose-dependently. Expression of ?- and ?-subunits of ENaC was decreased at the protein and mRNA level in H441 cells exposed to crotonaldehyde, which was probably mediated by the increase in phosphorylated extracellular signal-regulated protein kinases 1 and 2. ROS levels increased time-dependently in cells exposed to crotonaldehyde. Heterologous ???-ENaC activity was rapidly eliminated by crotonaldehyde. CONCLUSION: Our findings suggest that crotonaldehyde causes edematous acute lung injury by eliminating ENaC activity at least partly via facilitating the phosphorylation of extracellular signal-regulated protein kinases 1 and 2 signal molecules. Long-term exposure may decrease the expression of ENaC subunits and damage the cell membrane integrity, as well as increase the levels of cellular ROS products. äNovel mechanisms for crotonaldehyde-induced lung edema (epmc).pdf DeepDyve Pubget Overpricing