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10.1038/s41598-017-15424-3 http://scihub22266oqcxt.onion/10.1038/s41598-017-15424-3 C5688098!5688098 !29142197     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29142197 &cmd=llinks): Failed to open stream: HTTP request failed! 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Proteotoxicity in cardiac amyloidosis: amyloidogenic light chains affect the levels of intracellular proteins in human heart cells |pdf=|usr=}}{{29142197 }} gab.com Text Proteotoxicity in cardiac amyloidosis: amyloidogenic light chains affect the levels of intracellular proteins in human heart cells JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=29142197 #FOAvip AL amyloidosis is characterized by widespread deposition of immunoglobulin light chains (LCs) as amyloid fibrils. Cardiac involvement is frequent and leads to life-threatening cardiomyopathy. Besides the tissue alteration caused by fibrils, clinical and experimental evidence indicates that cardiac damage is also caused by proteotoxicity of prefibrillar amyloidogenic species. As in other amyloidoses, the damage mechanisms at cellular level are complex and largely undefined. We have characterized the molecular changes in primary human cardiac fibroblasts (hCFs) exposed in vitro to soluble amyloidogenic cardiotoxic LCs from AL cardiomyopathy patients. To evaluate proteome alterations caused by a representative cardiotropic LC, we combined gel-based with label-free shotgun analysis and performed bioinformatics and data validation studies. To assess the generalizability of our results we explored the effects of multiple LCs on hCF viability and on levels of a subset of cellular proteins. Our results indicate that exposure of hCFs to cardiotropic LCs translates into proteome remodeling, associated with apoptosis activation and oxidative stress. The proteome alterations affect proteins involved in cytoskeletal organization, protein synthesis and quality control, mitochondrial activity and metabolism, signal transduction and molecular trafficking. These results support and expand the concept that soluble amyloidogenic cardiotropic LCs exert toxic effects on cardiac cells. Twit Text FOAVip Proteotoxicity in cardiac amyloidosis: amyloidogenic light chains affect the levels of intracellular proteins in human heart cells ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=29142197 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29142197 #FOAvip English Wikipedia <ref>{{Cite pmid|29142197 }}</ref> Proteotoxicity in cardiac amyloidosis: amyloidogenic light chains affect the levels of intracellular proteins in human heart cells #MMPMID29142197 Imperlini E ; Gnecchi M ; Rognoni P ; Sabidò E ; Ciuffreda MC ; Palladini G ; Espadas G ; Mancuso FM ; Bozzola M ; Malpasso G ; Valentini V ; Palladini G ; Orrù S ; Ferraro G ; Milani P ; Perlini S ; Salvatore F ; Merlini G ; Lavatelli F Sci Rep 2017[Nov]; 7 (1 ): 15661 PMID29142197 show ga AL amyloidosis is characterized by widespread deposition of immunoglobulin light chains (LCs) as amyloid fibrils. Cardiac involvement is frequent and leads to life-threatening cardiomyopathy. Besides the tissue alteration caused by fibrils, clinical and experimental evidence indicates that cardiac damage is also caused by proteotoxicity of prefibrillar amyloidogenic species. As in other amyloidoses, the damage mechanisms at cellular level are complex and largely undefined. We have characterized the molecular changes in primary human cardiac fibroblasts (hCFs) exposed in vitro to soluble amyloidogenic cardiotoxic LCs from AL cardiomyopathy patients. To evaluate proteome alterations caused by a representative cardiotropic LC, we combined gel-based with label-free shotgun analysis and performed bioinformatics and data validation studies. To assess the generalizability of our results we explored the effects of multiple LCs on hCF viability and on levels of a subset of cellular proteins. Our results indicate that exposure of hCFs to cardiotropic LCs translates into proteome remodeling, associated with apoptosis activation and oxidative stress. The proteome alterations affect proteins involved in cytoskeletal organization, protein synthesis and quality control, mitochondrial activity and metabolism, signal transduction and molecular trafficking. These results support and expand the concept that soluble amyloidogenic cardiotropic LCs exert toxic effects on cardiac cells. |Amyloid/metabolism [MESH] |Amyloidogenic Proteins/*metabolism [MESH] |Cardiomyopathies/genetics/metabolism/pathology [MESH] |Cardiotoxicity [MESH] |Cytoplasm/metabolism [MESH] |Fibroblasts/metabolism/pathology [MESH] |Heart/physiopathology [MESH] |Humans [MESH] |Immunoglobulin Light Chains/*metabolism [MESH] |Immunoglobulin Light-chain Amyloidosis/genetics/*metabolism/pathology [MESH] |Mitochondria/metabolism/pathology [MESH] |Myocardium/metabolism/pathology [MESH] |Myocytes, Cardiac/*metabolism/pathology [MESH] |Oxidative Stress/genetics [MESH]Proteotoxicity in cardiac amyloidosis: amyloidogenic light chains affe(epmc).pdf DeepDyve Pubget Overpricing