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10.1089/ars.2012.4598 http://scihub22266oqcxt.onion/10.1089/ars.2012.4598 C3638512!3638512 !22657153     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 278.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 278.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 278.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 278.79999999999995 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\22657153 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Antioxid+Redox+Signal 2013 ; 18 (17 ): 2241-50 Nephropedia Template TP {{tp|p=22657153 |t=2013. Protective role of methionine sulfoxide reductase A against ischemia/reperfusion injury in mouse kidney and its involvement in the regulation of trans-sulfuration pathway |pdf=|usr=}}{{22657153 }} gab.com Text Protective role of methionine sulfoxide reductase A against ischemia/reperfusion injury in mouse kidney and its involvement in the regulation of trans-sulfuration pathway JO: Antioxid Redox Signal http://www.kidney.de/pget.php?&tw=1&pmid=22657153 #FOAvip AIMS: Methionine sulfoxide reductase A (MsrA) and methionine metabolism are associated with oxidative stress, a principal cause of ischemia/reperfusion (I/R) injury. Herein, we investigated the protective role of MsrA against kidney I/R injury and the involvement of MsrA in methionine metabolism and the trans-sulfuration pathway during I/R. RESULTS: We found that MsrA gene-deleted mice (MsrA(-/-)) were more susceptible to kidney I/R injury than wild-type mice (MsrA(+/+)). Deletion of MsrA enhanced renal functional and morphological impairments, congestion, inflammatory responses, and oxidative stress under I/R conditions. Concentrations of homocysteine and H(2)S in the plasma of control MsrA(-/-) mice were significantly lower than those in control MsrA(+/+) mice. I/R reduced the levels of homocysteine and H(2)S in both MsrA(+/+) and MsrA(-/-) mice, and these reductions were significantly more profound in MsrA(-/-) than in MsrA(+/+) mice. I/R reduced the expression and activities of cystathionine-?-synthase (CBS) and cystathionine-?-lyase (CSE), both of which are H(2)S-producing enzymes, in the kidneys. These reductions were more profound in the MsrA(-/-) mice than in the MsrA(+/+)mice. INNOVATION: The data provided herein constitute the first in vivo evidence for the involvement of MsrA in regulating methionine metabolism and the trans-sulfuration pathway under normal and I/R conditions. CONCLUSION: Our data demonstrate that MsrA protects the kidney against I/R injury, and that this protection is associated with reduced oxidative stress and inflammatory responses. The data indicate that MsrA regulates H(2)S production during I/R by modulating the expression and activity of the CBS and CSE enzymes. Twit Text FOAVip Protective role of methionine sulfoxide reductase A against ischemia/reperfusion injury in mouse kidney and its involvement in the regulation of trans-sulfuration pathway ????Antioxid Redox Signal http://www.kidney.de/pget.php?&tw=1&pmid=22657153 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=22657153 #FOAvip English Wikipedia <ref>{{Cite pmid|22657153 }}</ref> Protective role of methionine sulfoxide reductase A against ischemia/reperfusion injury in mouse kidney and its involvement in the regulation of trans-sulfuration pathway #MMPMID22657153 Kim JI ; Choi SH ; Jung KJ ; Lee E ; Kim HY ; Park KM Antioxid Redox Signal 2013[Jun]; 18 (17 ): 2241-50 PMID22657153 show ga AIMS: Methionine sulfoxide reductase A (MsrA) and methionine metabolism are associated with oxidative stress, a principal cause of ischemia/reperfusion (I/R) injury. Herein, we investigated the protective role of MsrA against kidney I/R injury and the involvement of MsrA in methionine metabolism and the trans-sulfuration pathway during I/R. RESULTS: We found that MsrA gene-deleted mice (MsrA(-/-)) were more susceptible to kidney I/R injury than wild-type mice (MsrA(+/+)). Deletion of MsrA enhanced renal functional and morphological impairments, congestion, inflammatory responses, and oxidative stress under I/R conditions. Concentrations of homocysteine and H(2)S in the plasma of control MsrA(-/-) mice were significantly lower than those in control MsrA(+/+) mice. I/R reduced the levels of homocysteine and H(2)S in both MsrA(+/+) and MsrA(-/-) mice, and these reductions were significantly more profound in MsrA(-/-) than in MsrA(+/+) mice. I/R reduced the expression and activities of cystathionine-?-synthase (CBS) and cystathionine-?-lyase (CSE), both of which are H(2)S-producing enzymes, in the kidneys. These reductions were more profound in the MsrA(-/-) mice than in the MsrA(+/+)mice. INNOVATION: The data provided herein constitute the first in vivo evidence for the involvement of MsrA in regulating methionine metabolism and the trans-sulfuration pathway under normal and I/R conditions. CONCLUSION: Our data demonstrate that MsrA protects the kidney against I/R injury, and that this protection is associated with reduced oxidative stress and inflammatory responses. The data indicate that MsrA regulates H(2)S production during I/R by modulating the expression and activity of the CBS and CSE enzymes. |Animals [MESH] |Antigens, Ly/metabolism [MESH] |Disease Models, Animal [MESH] |Enzyme Activation [MESH] |Gene Deletion [MESH] |Gene Expression Regulation [MESH] |Homocysteine/blood/metabolism [MESH] |Hydrogen Sulfide/blood/metabolism [MESH] |Inflammation/genetics/metabolism/pathology [MESH] |Kidney/blood supply/*metabolism/pathology [MESH] |Male [MESH] |Methionine Sulfoxide Reductases/genetics/*metabolism [MESH] |Mice [MESH] |Mice, Knockout [MESH] |Oxidative Stress/genetics [MESH]Protective role of methionine sulfoxide reductase A against ischemia/r(epmc).pdf DeepDyve Pubget Overpricing