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10.1152/ajpheart.00339.2015 http://scihub22266oqcxt.onion/10.1152/ajpheart.00339.2015 C4666985!4666985 !26432840     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26432840 &cmd=llinks): Failed to open stream: HTTP request failed! 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N-acetylcysteine reverses diastolic dysfunction and hypertrophy in familial hypertrophic cardiomyopathy |pdf=|usr=}}{{26432840 }} gab.com Text N-acetylcysteine reverses diastolic dysfunction and hypertrophy in familial hypertrophic cardiomyopathy JO: Am J Physiol Heart Circ Physiol http://www.kidney.de/pget.php?&tw=1&pmid=26432840 #FOAvip S-glutathionylation of cardiac myosin-binding protein C (cMyBP-C) induces Ca(2+) sensitization and a slowing of cross-bridge kinetics as a result of increased oxidative signaling. Although there is evidence for a role of oxidative stress in disorders associated with hypertrophic cardiomyopathy (HCM), this mechanism is not well understood. We investigated whether oxidative myofilament modifications may be in part responsible for diastolic dysfunction in HCM. We administered N-acetylcysteine (NAC) for 30 days to 1-mo-old wild-type mice and to transgenic mice expressing a mutant tropomyosin (Tm-E180G) and nontransgenic littermates. Tm-E180G hearts demonstrate a phenotype similar to human HCM. After NAC administration, the morphology and diastolic function of Tm-E180G mice was not significantly different from controls, indicating that NAC had reversed baseline diastolic dysfunction and hypertrophy in our model. NAC administration also increased sarco(endo)plasmic reticulum Ca(2+) ATPase protein expression, reduced extracellular signal-related kinase 1/2 phosphorylation, and normalized phosphorylation of phospholamban, as assessed by Western blot. Detergent-extracted fiber bundles from NAC-administered Tm-E180G mice showed nearly nontransgenic (NTG) myofilament Ca(2+) sensitivity. Additionally, we found that NAC increased tension cost and rate of cross-bridge reattachment. Tm-E180G myofilaments were found to have a significant increase in S-glutathionylation of cMyBP-C, which was returned to NTG levels upon NAC administration. Taken together, our results indicate that oxidative myofilament modifications are an important mediator in diastolic function, and by relieving this modification we were able to reverse established diastolic dysfunction and hypertrophy in HCM. Twit Text FOAVip N-acetylcysteine reverses diastolic dysfunction and hypertrophy in familial hypertrophic cardiomyopathy ????Am J Physiol Heart Circ Physiol http://www.kidney.de/pget.php?&tw=1&pmid=26432840 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26432840 #FOAvip English Wikipedia <ref>{{Cite pmid|26432840 }}</ref> N-acetylcysteine reverses diastolic dysfunction and hypertrophy in familial hypertrophic cardiomyopathy #MMPMID26432840 Wilder T ; Ryba DM ; Wieczorek DF ; Wolska BM ; Solaro RJ Am J Physiol Heart Circ Physiol 2015[Nov]; 309 (10 ): H1720-30 PMID26432840 show ga S-glutathionylation of cardiac myosin-binding protein C (cMyBP-C) induces Ca(2+) sensitization and a slowing of cross-bridge kinetics as a result of increased oxidative signaling. Although there is evidence for a role of oxidative stress in disorders associated with hypertrophic cardiomyopathy (HCM), this mechanism is not well understood. We investigated whether oxidative myofilament modifications may be in part responsible for diastolic dysfunction in HCM. We administered N-acetylcysteine (NAC) for 30 days to 1-mo-old wild-type mice and to transgenic mice expressing a mutant tropomyosin (Tm-E180G) and nontransgenic littermates. Tm-E180G hearts demonstrate a phenotype similar to human HCM. After NAC administration, the morphology and diastolic function of Tm-E180G mice was not significantly different from controls, indicating that NAC had reversed baseline diastolic dysfunction and hypertrophy in our model. NAC administration also increased sarco(endo)plasmic reticulum Ca(2+) ATPase protein expression, reduced extracellular signal-related kinase 1/2 phosphorylation, and normalized phosphorylation of phospholamban, as assessed by Western blot. Detergent-extracted fiber bundles from NAC-administered Tm-E180G mice showed nearly nontransgenic (NTG) myofilament Ca(2+) sensitivity. Additionally, we found that NAC increased tension cost and rate of cross-bridge reattachment. Tm-E180G myofilaments were found to have a significant increase in S-glutathionylation of cMyBP-C, which was returned to NTG levels upon NAC administration. Taken together, our results indicate that oxidative myofilament modifications are an important mediator in diastolic function, and by relieving this modification we were able to reverse established diastolic dysfunction and hypertrophy in HCM. |Acetylcysteine/*pharmacology [MESH] |Animals [MESH] |Calcium-Binding Proteins/drug effects/metabolism [MESH] |Calcium/metabolism [MESH] |Cardiomyopathy, Hypertrophic, Familial/genetics/*metabolism/physiopathology [MESH] |Carrier Proteins/drug effects/metabolism [MESH] |Diastole/*drug effects [MESH] |Disease Models, Animal [MESH] |Female [MESH] |Free Radical Scavengers/*pharmacology [MESH] |Heart Ventricles/*drug effects/metabolism/physiopathology [MESH] |Male [MESH] |Mice [MESH] |Mice, Transgenic [MESH] |Mitogen-Activated Protein Kinase 1/drug effects/metabolism [MESH] |Mitogen-Activated Protein Kinase 3/drug effects/metabolism [MESH] |Myofibrils/*drug effects/metabolism [MESH] |Oxidative Stress/drug effects [MESH] |Phosphorylation/drug effects [MESH] |Sarcoplasmic Reticulum Calcium-Transporting ATPases/drug effects/metabolism [MESH]N-acetylcysteine reverses diastolic dysfunction and hypertrophy in fam(epmc).pdf DeepDyve Pubget Overpricing