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10.1152/ajpendo.00604.2012 http://scihub22266oqcxt.onion/10.1152/ajpendo.00604.2012 C3680700!3680700!23632630     free     free     free 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 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 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Am+J+Physiol+Endocrinol+Metab 2013 ; 304 (12): E1365-78 Nephropedia Template TP {{tp|p=23632630|t=2013. Hydrogen sulfide deficiency and diabetic renal remodeling: role of matrix metalloproteinase-9 |pdf=|usr=}}{{23632630}} gab.com Text Hydrogen sulfide deficiency and diabetic renal remodeling: role of matrix metalloproteinase-9 JO: Am J Physiol Endocrinol Metab http://www.kidney.de/pget.php?&tw=1&pmid=23632630 #FOAvip Matrix metalloproteinase-9 (MMP-9) causes adverse remodeling, whereas hydrogen sulfide (H2S) rescues organs in vascular diseases. The involvement of MMP-9 and H2S in diabetic renovascular remodeling is, however, not well characterized. We determined whether MMP-9 regulates H2S generation and whether H2S modulates connexin through N-methyl-d-aspartate receptor (NMDA-R)-mediated pathway in the diabetic kidney. Wild-type (WT, C57BL/6J), diabetic (Akita, C57BL/6J-Ins2Akita), MMP-9?/? (M9KO), double knockout (DKO) of Akita/MMP-9?/? mice and in vitro cell culture were used in our study. Hyperglycemic Akita mice exhibited increased level of MMP-9 and decreased production of H2S. H2S-synthesizing enzymes cystathionine-?-synthase and cystathionine-?-lyase were also diminished. In addition, increased expressions of NMDA-R1 and connexin-40 and -43 were observed in diabetic kidney. As expected, MMP-9 mRNA was not detected in M9KO kidneys. However, very thin protein expression and activity were detected. No other changes were noticed in M9KO kidney. In DKO mice, all the above molecules showed a trend toward baseline despite hyperglycemia. In vitro, glomerular endothelial cells treated with high glucose showed induction of MMP-9, attenuated H2S production, NMDA-R1 induction, and dysregulated conexin-40 and -43 expressions. Silencing MMP-9 by siRNA or inhibition of NMDA-R1 by MK801 or H2S treatment preserved connexin-40 and -43. We conclude that in diabetic renovascular remodeling MMP-9 plays a major role and that H2S has therapeutic potential to prevent adverse diabetic renal remodeling. Twit Text FOAVip Hydrogen sulfide deficiency and diabetic renal remodeling: role of matrix metalloproteinase-9 ????Am J Physiol Endocrinol Metab http://www.kidney.de/pget.php?&tw=1&pmid=23632630 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=23632630 #FOAvip English Wikipedia <ref>{{Cite pmid|23632630}}</ref> Hydrogen sulfide deficiency and diabetic renal remodeling: role of matrix metalloproteinase-9 #MMPMID23632630 Kundu S; Pushpakumar SB; Tyagi A; Coley D; Sen U Am J Physiol Endocrinol Metab 2013[Jun]; 304 (12): E1365-78 PMID23632630show ga Matrix metalloproteinase-9 (MMP-9) causes adverse remodeling, whereas hydrogen sulfide (H2S) rescues organs in vascular diseases. The involvement of MMP-9 and H2S in diabetic renovascular remodeling is, however, not well characterized. We determined whether MMP-9 regulates H2S generation and whether H2S modulates connexin through N-methyl-d-aspartate receptor (NMDA-R)-mediated pathway in the diabetic kidney. Wild-type (WT, C57BL/6J), diabetic (Akita, C57BL/6J-Ins2Akita), MMP-9?/? (M9KO), double knockout (DKO) of Akita/MMP-9?/? mice and in vitro cell culture were used in our study. Hyperglycemic Akita mice exhibited increased level of MMP-9 and decreased production of H2S. H2S-synthesizing enzymes cystathionine-?-synthase and cystathionine-?-lyase were also diminished. In addition, increased expressions of NMDA-R1 and connexin-40 and -43 were observed in diabetic kidney. As expected, MMP-9 mRNA was not detected in M9KO kidneys. However, very thin protein expression and activity were detected. No other changes were noticed in M9KO kidney. In DKO mice, all the above molecules showed a trend toward baseline despite hyperglycemia. In vitro, glomerular endothelial cells treated with high glucose showed induction of MMP-9, attenuated H2S production, NMDA-R1 induction, and dysregulated conexin-40 and -43 expressions. Silencing MMP-9 by siRNA or inhibition of NMDA-R1 by MK801 or H2S treatment preserved connexin-40 and -43. We conclude that in diabetic renovascular remodeling MMP-9 plays a major role and that H2S has therapeutic potential to prevent adverse diabetic renal remodeling. äHydrogen sulfide deficiency and diabetic renal remodeling: role of mat(epmc).pdf DeepDyve Pubget Overpricing