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10.1111/nyas.14475 http://scihub22266oqcxt.onion/10.1111/nyas.14475 32885420!9109234!32885420     free     free     free Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Ann+N+Y+Acad+Sci 2020 ; 1480 (1): 155-169 Nephropedia Template TP {{tp|p=32885420|t=2020. Protective role of HO-1 against acute kidney injury caused by cutaneous exposure to arsenicals |pdf=|usr=}}{{32885420}} gab.com Text Protective role of HO-1 against acute kidney injury caused by cutaneous exposure to arsenicals JO: Ann N Y Acad Sci http://www.kidney.de/pget.php?&tw=1&pmid=32885420 #FOAvip Lewisite and many other similar arsenicals are warfare vesicants developed and weaponized for use in World Wars I and II. These chemicals, when exposed to the skin and other epithelial tissues, cause rapid severe inflammation and systemic damage. Here, we show that topically applied arsenicals in a murine model produce significant acute kidney injury (AKI), as determined by an increase in the AKI biomarkers NGAL and KIM-1. An increase in reactive oxygen species and ER stress proteins, such as ATF4 and CHOP, correlated with the induction of these AKI biomarkers. Also, TUNEL staining of CHOP-positive renal tubular cells suggests CHOP mediates apoptosis in these cells. A systemic inflammatory response characterized by a significant elevation in inflammatory mediators, such as IL-6, IFN-alpha, and COX-2, in the kidney could be the underlying cause of AKI. The mechanism of arsenical-mediated inflammation involves activation of AMPK/Nrf2 signaling pathways, which regulate heme oxygenase-1 (HO-1). Indeed, HO-1 induction with cobalt protoporphyrin (CoPP) treatment in arsenical-treated HEK293 cells afforded cytoprotection by attenuating CHOP-associated apoptosis and cytokine mRNA levels. These results demonstrate that topical exposure to arsenicals causes AKI and that HO-1 activation may serve a protective role in this setting. Twit Text FOAVip Protective role of HO-1 against acute kidney injury caused by cutaneous exposure to arsenicals ????Ann N Y Acad Sci http://www.kidney.de/pget.php?&tw=1&pmid=32885420 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32885420 #FOAvip English Wikipedia <ref>{{Cite pmid|32885420}}</ref> Protective role of HO-1 against acute kidney injury caused by cutaneous exposure to arsenicals #MMPMID32885420 Srivastava RK; Muzaffar S; Khan J; Traylor AM; Zmijewski JW; Curtis LM; George JF; Ahmad A; Antony VB; Agarwal A; Athar M Ann N Y Acad Sci 2020[Nov]; 1480 (1): 155-169 PMID32885420show ga Lewisite and many other similar arsenicals are warfare vesicants developed and weaponized for use in World Wars I and II. These chemicals, when exposed to the skin and other epithelial tissues, cause rapid severe inflammation and systemic damage. Here, we show that topically applied arsenicals in a murine model produce significant acute kidney injury (AKI), as determined by an increase in the AKI biomarkers NGAL and KIM-1. An increase in reactive oxygen species and ER stress proteins, such as ATF4 and CHOP, correlated with the induction of these AKI biomarkers. Also, TUNEL staining of CHOP-positive renal tubular cells suggests CHOP mediates apoptosis in these cells. A systemic inflammatory response characterized by a significant elevation in inflammatory mediators, such as IL-6, IFN-alpha, and COX-2, in the kidney could be the underlying cause of AKI. The mechanism of arsenical-mediated inflammation involves activation of AMPK/Nrf2 signaling pathways, which regulate heme oxygenase-1 (HO-1). Indeed, HO-1 induction with cobalt protoporphyrin (CoPP) treatment in arsenical-treated HEK293 cells afforded cytoprotection by attenuating CHOP-associated apoptosis and cytokine mRNA levels. These results demonstrate that topical exposure to arsenicals causes AKI and that HO-1 activation may serve a protective role in this setting. |*Acute Kidney Injury/chemically induced/metabolism/pathology/prevention & control[MESH] |*Arsenicals[MESH] |AMP-Activated Protein Kinases/metabolism[MESH] |Activating Transcription Factor 4/metabolism[MESH] |Animals[MESH] |Apoptosis/*drug effects[MESH] |Biomarkers/metabolism[MESH] |Chemical Warfare Agents/*poisoning[MESH] |Cyclooxygenase 2/metabolism[MESH] |Enzyme Activation/drug effects[MESH] |HEK293 Cells[MESH] |Heme Oxygenase-1/*metabolism[MESH] |Hepatitis A Virus Cellular Receptor 1/metabolism[MESH] |Humans[MESH] |Interleukin-6/metabolism[MESH] |Membrane Proteins/*metabolism[MESH] |Mice[MESH] |Mice, Hairless[MESH] |NF-E2-Related Factor 2/metabolism[MESH] |Signal Transduction/*drug effects[MESH]Protective role of HO-1 against acute kidney injury caused by cutaneou(epmc).pdf DeepDyve Pubget Overpricing