Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1165/rcmb.2021-0219OC http://scihub22266oqcxt.onion/10.1165/rcmb.2021-0219OC 34890296!8937245!34890296     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Am+J+Respir+Cell+Mol+Biol 2022 ; 66 (3): 323-336 Nephropedia Template TP {{tp|p=34890296|t=2022. Thioredoxin Prevents Loss of UCP2 in Hyperoxia via MKK4-p38 MAPK-PGC1alpha Signaling and Limits Oxygen Toxicity |pdf=|usr=}}{{34890296}} gab.com Text Thioredoxin Prevents Loss of UCP2 in Hyperoxia via MKK4-p38 MAPK-PGC1alpha Signaling and Limits Oxygen Toxicity JO: Am J Respir Cell Mol Biol http://www.kidney.de/pget.php?&tw=1&pmid=34890296 #FOAvip Administration of high concentrations of oxygen (hyperoxia) is one of few available options to treat acute hypoxemia-related respiratory failure, as seen in the current coronavirus disease (COVID-19) pandemic. Although hyperoxia can cause acute lung injury through increased production of superoxide anion (O(2)(*-)), the choice of high-concentration oxygen administration has become a necessity in critical care. The objective of this study was to test the hypothesis that UCP2 (uncoupling protein 2) has a major function of reducing O(2)(*-) generation in the lung in ambient air or in hyperoxia. Lung epithelial cells and wild-type; UCP2(-/-); or transgenic, hTrx overexpression-bearing mice (Trx-Tg) were exposed to hyperoxia and O(2)(*-) generation was measured by using electron paramagnetic resonance, and lung injury was measured by using histopathologic analysis. UCP2 expression was analyzed by using RT-PCR analysis, Western blotting analysis, and RNA interference. The signal transduction pathways leading to loss of UCP2 expression were analyzed by using IP, phosphoprotein analysis, and specific inhibitors. UCP2 mRNA and protein expression were acutely decreased in hyperoxia, and these decreases were associated with a significant increase in O(2)(*-) production in the lung. Treatment of cells with rhTrx (recombinant human thioredoxin) or exposure of Trx-Tg mice prevented the loss of UCP2 protein and decreased O(2)(*-) generation in the lung. Trx is also required to maintain UCP2 expression in normoxia. Loss of UCP2 in UCP2(-/-) mice accentuated lung injury in hyperoxia. Trx activates the MKK4-p38MAPK (p38 mitogen-activated protein kinase)-PGC1alpha (PPARgamma [peroxisome proliferator-activated receptor gamma] coactivator 1alpha) pathway, leading to rescue of UCP2 and decreased O(2)(*-) generation in hyperoxia. Loss of UCP2 in hyperoxia is a major mechanism of O(2)(*-) production in the lung in hyperoxia. rhTrx can protect against lung injury in hyperoxia due to rescue of the loss of UCP2. Twit Text FOAVip Thioredoxin Prevents Loss of UCP2 in Hyperoxia via MKK4-p38 MAPK-PGC1alpha Signaling and Limits Oxygen Toxicity ????Am J Respir Cell Mol Biol http://www.kidney.de/pget.php?&tw=1&pmid=34890296 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34890296 #FOAvip English Wikipedia <ref>{{Cite pmid|34890296}}</ref> Thioredoxin Prevents Loss of UCP2 in Hyperoxia via MKK4-p38 MAPK-PGC1alpha Signaling and Limits Oxygen Toxicity #MMPMID34890296 Raghavan S; Kundumani-Sridharan V; Kumar S; White CW; Das KC Am J Respir Cell Mol Biol 2022[Mar]; 66 (3): 323-336 PMID34890296show ga Administration of high concentrations of oxygen (hyperoxia) is one of few available options to treat acute hypoxemia-related respiratory failure, as seen in the current coronavirus disease (COVID-19) pandemic. Although hyperoxia can cause acute lung injury through increased production of superoxide anion (O(2)(*-)), the choice of high-concentration oxygen administration has become a necessity in critical care. The objective of this study was to test the hypothesis that UCP2 (uncoupling protein 2) has a major function of reducing O(2)(*-) generation in the lung in ambient air or in hyperoxia. Lung epithelial cells and wild-type; UCP2(-/-); or transgenic, hTrx overexpression-bearing mice (Trx-Tg) were exposed to hyperoxia and O(2)(*-) generation was measured by using electron paramagnetic resonance, and lung injury was measured by using histopathologic analysis. UCP2 expression was analyzed by using RT-PCR analysis, Western blotting analysis, and RNA interference. The signal transduction pathways leading to loss of UCP2 expression were analyzed by using IP, phosphoprotein analysis, and specific inhibitors. UCP2 mRNA and protein expression were acutely decreased in hyperoxia, and these decreases were associated with a significant increase in O(2)(*-) production in the lung. Treatment of cells with rhTrx (recombinant human thioredoxin) or exposure of Trx-Tg mice prevented the loss of UCP2 protein and decreased O(2)(*-) generation in the lung. Trx is also required to maintain UCP2 expression in normoxia. Loss of UCP2 in UCP2(-/-) mice accentuated lung injury in hyperoxia. Trx activates the MKK4-p38MAPK (p38 mitogen-activated protein kinase)-PGC1alpha (PPARgamma [peroxisome proliferator-activated receptor gamma] coactivator 1alpha) pathway, leading to rescue of UCP2 and decreased O(2)(*-) generation in hyperoxia. Loss of UCP2 in hyperoxia is a major mechanism of O(2)(*-) production in the lung in hyperoxia. rhTrx can protect against lung injury in hyperoxia due to rescue of the loss of UCP2. |Animals[MESH] |COVID-19/metabolism/therapy[MESH] |Cell Line[MESH] |Humans[MESH] |Hyperoxia/metabolism[MESH] |Lung/cytology/*metabolism[MESH] |MAP Kinase Kinase 4/genetics/metabolism[MESH] |Mice[MESH] |Mice, Inbred C57BL[MESH] |Mice, Knockout[MESH] |Mice, Transgenic[MESH] |Oxygen/*metabolism/toxicity[MESH] |Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha/genetics/metabolism[MESH] |Phosphorylation[MESH] |Signal Transduction[MESH] |Superoxides/metabolism[MESH] |Thioredoxins/genetics/*metabolism/pharmacology[MESH] |Uncoupling Protein 2/genetics/*metabolism[MESH]Thioredoxin Prevents Loss of UCP2 in Hyperoxia via MKK4-p38 MAPK-PGC1a(epmc).pdf DeepDyve Pubget Overpricing