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10.1681/ASN.2015040397 http://scihub22266oqcxt.onion/10.1681/ASN.2015040397 C4926972!4926972 !26574047     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26574047 &cmd=llinks): Failed to open stream: HTTP request failed! 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Renal 2 ,3 -Cyclic Nucleotide 3 -Phosphodiesterase Is an Important Determinant of AKI Severity after Ischemia-Reperfusion |pdf=|usr=}}{{26574047 }} gab.com Text Renal 2 ,3 -Cyclic Nucleotide 3 -Phosphodiesterase Is an Important Determinant of AKI Severity after Ischemia-Reperfusion JO: J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=26574047 #FOAvip A positional isomer of 3',5'-cAMP, 2',3'-cAMP, is produced by kidneys in response to energy depletion, and renal 2',3'-cyclic nucleotide 3'-phosphodiesterase (CNPase) metabolizes 2',3'-cAMP to 2'-AMP; 2',3'-cAMP is a potent opener of mitochondrial permeability transition pores (mPTPs), which can stimulate autophagy. Because autophagy protects against AKI, it is conceivable that inhibition of CNPase protects against ischemia-reperfusion (IR) -induced AKI. Therefore, we investigated renal outcomes, mitochondrial function, number, area, and autophagy in CNPase-knockout (CNPase(-/-)) versus wild-type (WT) mice using a unique two-kidney, hanging-weight model of renal bilateral IR (20 minutes of ischemia followed by 48 hours of reperfusion). Analysis of urinary purines showed attenuated metabolism of 2',3'-cAMP to 2'-AMP in CNPase(-/-) mice. Neither genotype nor IR affected BP, heart rate, urine volume, or albumin excretion. In WT mice, renal IR reduced (14)C-inulin clearance (index of GFR) and increased renal vascular resistance (measured by transit time nanoprobes) and urinary excretion of kidney injury molecule-1 and neutrophil gelatinase-associated lipocalin. IR did not affect these parameters in CNPase(-/-) mice. Histologic analysis revealed that IR induced severe damage in kidneys from WT mice, whereas histologic changes were minimal after IR in CNPase(-/-) mice. Measurements of renal cardiolipin levels, citrate synthase activity, rotenone-sensitive NADH oxidase activity, and proximal tubular mitochondrial and autophagosome area and number (by transmission electron microscopy) indicted accelerated autophagy/mitophagy in injured CNPase(-/-) mice. We conclude that CNPase deletion attenuates IR-induced AKI, in part by accelerating autophagy with targeted removal of damaged mitochondria. Twit Text FOAVip Renal 2 ,3 -Cyclic Nucleotide 3 -Phosphodiesterase Is an Important Determinant of AKI Severity after Ischemia-Reperfusion ????J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=26574047 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26574047 #FOAvip English Wikipedia <ref>{{Cite pmid|26574047 }}</ref> Renal 2 ,3 -Cyclic Nucleotide 3 -Phosphodiesterase Is an Important Determinant of AKI Severity after Ischemia-Reperfusion #MMPMID26574047 Jackson EK ; Menshikova EV ; Mi Z ; Verrier JD ; Bansal R ; Janesko-Feldman K ; Jackson TC ; Kochanek PM J Am Soc Nephrol 2016[Jul]; 27 (7 ): 2069-81 PMID26574047 show ga A positional isomer of 3',5'-cAMP, 2',3'-cAMP, is produced by kidneys in response to energy depletion, and renal 2',3'-cyclic nucleotide 3'-phosphodiesterase (CNPase) metabolizes 2',3'-cAMP to 2'-AMP; 2',3'-cAMP is a potent opener of mitochondrial permeability transition pores (mPTPs), which can stimulate autophagy. Because autophagy protects against AKI, it is conceivable that inhibition of CNPase protects against ischemia-reperfusion (IR) -induced AKI. Therefore, we investigated renal outcomes, mitochondrial function, number, area, and autophagy in CNPase-knockout (CNPase(-/-)) versus wild-type (WT) mice using a unique two-kidney, hanging-weight model of renal bilateral IR (20 minutes of ischemia followed by 48 hours of reperfusion). Analysis of urinary purines showed attenuated metabolism of 2',3'-cAMP to 2'-AMP in CNPase(-/-) mice. Neither genotype nor IR affected BP, heart rate, urine volume, or albumin excretion. In WT mice, renal IR reduced (14)C-inulin clearance (index of GFR) and increased renal vascular resistance (measured by transit time nanoprobes) and urinary excretion of kidney injury molecule-1 and neutrophil gelatinase-associated lipocalin. IR did not affect these parameters in CNPase(-/-) mice. Histologic analysis revealed that IR induced severe damage in kidneys from WT mice, whereas histologic changes were minimal after IR in CNPase(-/-) mice. Measurements of renal cardiolipin levels, citrate synthase activity, rotenone-sensitive NADH oxidase activity, and proximal tubular mitochondrial and autophagosome area and number (by transmission electron microscopy) indicted accelerated autophagy/mitophagy in injured CNPase(-/-) mice. We conclude that CNPase deletion attenuates IR-induced AKI, in part by accelerating autophagy with targeted removal of damaged mitochondria. |2',3'-Cyclic Nucleotide 3'-Phosphodiesterase/*physiology [MESH] |Acute Kidney Injury/*enzymology/etiology [MESH] |Animals [MESH] |Female [MESH] |Kidney/blood supply [MESH] |Male [MESH] |Mice [MESH] |Mice, Knockout [MESH] |Reperfusion Injury/complications [MESH]Renal 2 ,3 -Cyclic Nucleotide 3 -Phosphodiesterase Is an Important Det(epmc).pdf DeepDyve Pubget Overpricing