ArticleThe journal of histochemistry and cytochemistry : official journal of the Histochemistry Society2014
Quantitative Imaging of Preamyloid Oligomers, a Novel Structural Abnormality, in Human Atrial Samples.
Article in The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Highly Reactive Isolevuglandins Promote Atrial Fibrillation Caused by Hypertension.JACC. Basic to translational science · 2020Article
- Desmin Phosphorylation Triggers Preamyloid Oligomers Formation and Myocyte Dysfunction in Acquired Heart Failure.Circulation research · 2018Article
- Cardiomyocyte-Specific Human Bcl2-Associated Anthanogene 3 P209L Expression Induces Mitochondrial Fragmentation, Bcl2-Associated Anthanogene 3 Haploinsufficiency, and Activates p38 Signaling.The American journal of pathology · 2016Article
- A new mechanism links preamyloid oligomer formation in the myocyte stress response associated with atrial fibrillation.Journal of molecular and cellular cardiology · 2015Article
- Reactive γ-ketoaldehydes promote protein misfolding and preamyloid oligomer formation in rapidly-activated atrial cells.Journal of molecular and cellular cardiology · 2015Article
- Hypertension is associated with preamyloid oligomers in human atrium: a missing link in atrial pathophysiology?Journal of the American Heart Association · 2014Article
- BRG1 and BRM SWI/SNF ATPases redundantly maintain cardiomyocyte homeostasis by regulating cardiomyocyte mitophagy and mitochondrial dynamics in vivo.Cardiovascular pathology : the official journal of the Society for Cardiovascular PathologyArticle
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
Abstract
Abnormalities in atrial myocardium increase the likelihood of arrhythmias, including atrial fibrillation (AF). The deposition of misfolded protein, or amyloidosis, plays an important role in the pathophysiology of many diseases, including human cardiomyopathies. We have shown that genes implicated in amyloidosis are activated in a cellular model of AF, with the development of preamyloid oligomers (PAOs). PAOs are intermediates in the formation of amyloid fibrils, and they are now recognized to be the cytotoxic species during amyloidosis. To investigate the presence of PAOs in human atrium, we developed a microscopic imaging-based protocol to enable robust and reproducible quantitative analysis of PAO burden in atrial samples harvested at the time of elective cardiac surgery. Using PAO- and myocardial-specific antibodies, we found that PAO distribution was typically heterogeneous within a myocardial sample. Rigorous imaging and analysis protocols were developed to quantify the relative area of myocardium containing PAOs, termed the Green/Red ratio (G/R), for a given sample. Using these methods, reproducible G/R values were obtained when different sections of a sample were independently processed, imaged, and analyzed by different investigators. This robust technique will enable studies to investigate the role of this novel structural abnormality in the pathophysiology of and arrhythmia generation in human atrial tissue.
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Registered trials
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