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Journal articles on the topic 'Protein fibrillation'

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Author: Grafiati

Published: 1 April 2023

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1

Gorensek-Benitez, Annelise H., Bryan Kirk, and Jeffrey K. Myers. "Protein Fibrillation under Crowded Conditions." Biomolecules 12, no. 7 (July 6, 2022): 950. http://dx.doi.org/10.3390/biom12070950.

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Protein amyloid fibrils have widespread implications for human health. Over the last twenty years, fibrillation has been studied using a variety of crowding agents to mimic the packed interior of cells or to probe the mechanisms and pathways of the process. We tabulate and review these results by considering three classes of crowding agent: synthetic polymers, osmolytes and other small molecules, and globular proteins. While some patterns are observable for certain crowding agents, the results are highly variable and often depend on the specific pairing of crowder and fibrillating protein.

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2

St. Rammos, Kyriakos, George J. Koullias, Moustafa O. Hassan, Nikolaos P. Argyrakis, Christos G. Voucharas, Steven J. Scarupa, and Tomas G. Cowte. "Low Preoperative HSP70 Atrial Myocardial Levels Correlate Significantly with High Incidence of Postoperative Atrial Fibrillation after Cardiac Surgery." Cardiovascular Surgery 10, no. 3 (June 2002): 228–32. http://dx.doi.org/10.1177/096721090201000309.

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Purpose of the study. Atrial fibrillation after cardiac surgery is still a frequent encountered complication and has been associated with increased hospital length of stay and numerous postoperative complications. The pathogenesis of atrial fibrillation involves an overall sequence of perioperative events, collectively termed as ischemia-reperfusion injury. Heat-shock proteins have been found to provide increased protection during ischemia-reperfusion as well as increased postischemic cardiac functional recovery. We sought to determine whether preoperative atrial heat shock levels were correlated with the appearance of postoperative atrial fibrillation Basic methods. Preoperative atrial myocardial samples obtained just before cannulation from 101 patients were used to detect immunohistochemically the expression of heat-shock proteins. The derived results were compared statistically with the incidence of postoperative atrial fibrillation, its time of appearance, duration and resistance to administered antiarrhythmics. Principal findings. The overall incidence of postoperative atrial fibrillation was 22.3%. Of these patients, 58.3% had no detectable heat shock proteins in their cytoplasm, in sharp contrast with 100% of the patients with no atrial fibrillation who were positive for heat shock proteins ( p<0.01). Four percent of our patient group had prolonged atrial fibrillation (defined as duration >48 h). These patients had significantly less ( p<0.01) nuclear heat shock protein expression compared with the non-atrial fibrillation group. However, the difference of the heat shock protein expression between the prolonged atrial fibrillation and the rest of the atrial fibrillation patients was not significant ( p = 0.891). Conclusions. Our results indicate that patients with low preoperative atrial heat shock protein expression have a significantly greater incidence of postoperative atrial fibrillation. Heat shock protein expression did not, however, correlate with the onset of atrial fibrillation and the resistance to administered medications. Heat shock protein preoperative induction as a measure of myocardial preconditioning may potentially decrease the incidence of postoperative atrial fibrillation.

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3

Ohkubo, Kimie, Ichiro Watanabe, Yasuo Okumura, Keiko Takahashi, Kazuki Iso, Rikitake Kogawa, Kazumasa Sonoda, et al. "High-Sensitivity C-Reactive Protein: A Novel Predictor of Recurrence of Atrial Fibrillation After Initial Catheter Ablation of Paroxysmal Atrial Fibrillation." Journal of Nihon University Medical Association 75, no. 3 (2016): 118–22. http://dx.doi.org/10.4264/numa.75.3_118.

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4

Tachibana, Hideki, Shunta Kubomura, Kaoru Shinohara, and Ryohei Kono. "3P081 Seeded-Fibrillation of Lysozyme Disulfide-Variant Proteins(Protein: Property,The 48th Annual Meeting of the Biophysical Society of Japan)." Seibutsu Butsuri 50, supplement2 (2010): S159. http://dx.doi.org/10.2142/biophys.50.s159_1.

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5

Dev, Shubhda. "MOLECULAR DOCKING ANALYSIS OF NATRIURETIC PEPTIDE RECEPTOR-C TOWARDS THE DESIGN OF POTENTIAL ATRIAL FIBRILLATION INHIBITORS." Journal of Medical Pharmaceutical And Allied Sciences 9, no. 5 (October 15, 2020): 2595–600. http://dx.doi.org/10.22270/jmpas.v9i5.974.

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Atrial fibrillation (AF) stands the most widely recognized kind of clinical arrhythmia. Right now accessible anti-Atrial Fibrillation drugs are restricted by just moderate adequacy and an unfavorable safety profile. There is a perceived requirement for enhanced antiarrhythmic agents including activities that are specific for the fibrillating atrium. Therefore, it is of interest to design an appropriate medication for the disease Atrial Fibrillation using Molecular Docking techniques through protein-ligand interaction analysis. Hence, we document the Molecular docking analysis of natriuretic peptide receptor-C towards the design of potential Atrial Fibrillation inhibitors (Aprindine, Inclacumab, and Budiodarone) with the most favorable binding features for further consideration. This study centers around the process for drug discovery finding appropriate medication for the disease Atrial Fibrillation by Molecular Docking technique through protein-ligand interaction. The examination uncovered that out of a couple of molecules that were chosen as target, three of them were seen as most reasonable having the least energies compared to the other molecules. Aprindine, which is utilized in arrhythmia patients as a cardiac depressant. Inclacumab, which is an investigational sedate utilized in trials to look at the treatment and evasion of Myocardial Infarction, Peripheral Arterial Disease (PAD), and Coronary Heart Disease. Budiodarone, which is an antiarrhythmic drug at present in clinical preliminaries identified with amiodarone.

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6

Sata, Naoyuki, Naokazu Hamada, Takashi Horinouchi, Shigeru Amitani, Takuya Yamashita, Yukinori Moriyama, and Kenkichi Miyahara. "C-reactive Protein and Atrial Fibrillation." Japanese Heart Journal 45, no. 3 (2004): 441–45. http://dx.doi.org/10.1536/jhj.45.441.

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7

Huang, Kun, Jian Dong, Nelson B. Phillips, Paul R. Carey, and Michael A. Weiss. "Proinsulin Is Refractory to Protein Fibrillation." Journal of Biological Chemistry 280, no. 51 (October 20, 2005): 42345–55. http://dx.doi.org/10.1074/jbc.m507110200.

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8

Linse, S., C. Cabaleiro-Lago, W. F. Xue, I. Lynch, S. Lindman, E. Thulin, S. E. Radford, and K. A. Dawson. "Nucleation of protein fibrillation by nanoparticles." Proceedings of the National Academy of Sciences 104, no. 21 (May 7, 2007): 8691–96. http://dx.doi.org/10.1073/pnas.0701250104.

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9

Hernández Madrid, Antonio, and Concepción Moro. "Atrial Fibrillation and C-Reactive Protein." Journal of the American College of Cardiology 49, no. 15 (April 2007): 1649–50. http://dx.doi.org/10.1016/j.jacc.2007.02.009.

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10

Wood, Mark A., Kenneth A. Ellenbogen, and Bruce S. Stambler. "Atrial fibrillation from liquid protein diet." American Heart Journal 127, no. 6 (June 1994): 1667–68. http://dx.doi.org/10.1016/0002-8703(94)90422-7.

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11

Colvin, V. L., and K. M. Kulinowski. "Nanoparticles as catalysts for protein fibrillation." Proceedings of the National Academy of Sciences 104, no. 21 (May 14, 2007): 8679–80. http://dx.doi.org/10.1073/pnas.0703194104.

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12

Galea, Roberto, Maria Teresa Cardillo, Annalisa Caroli, Maria Giulia Marini, Chiara Sonnino, Maria L. Narducci, and Luigi M. Biasucci. "Inflammation and C-Reactive Protein in Atrial Fibrillation: Cause or Effect?" Texas Heart Institute Journal 41, no. 5 (October 1, 2014): 461–68. http://dx.doi.org/10.14503/thij-13-3466.

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Atrial fibrillation is associated with substantial morbidity and mortality rates. The incompletely understood pathogenesis of this cardiac dysrhythmia makes it difficult to improve approaches to primary and secondary prevention. Evidence has accumulated in regard to a relationship between inflammation and atrial fibrillation. Investigators have correlated the dysrhythmia with myocarditis, pericardiotomy, and C-reactive protein levels, suggesting that inflammation causes atrial fibrillation or participates in its onset and continuation. Conversely, other investigators suggest that atrial fibrillation induces an inflammatory response. In this review, we summarize and critically discuss the nature and clinical role of inflammation and C-reactive protein in atrial fibrillation.

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13

Namsrai, Javkhlantugs, Ganchimeg Lkhamsuren, Kazuyoshi Ueda, and Akira Naito. "3P022 Structure and Interactions in Fibrillation of Human Calcitonin Hormone(01A. Protein: Structure,Poster)." Seibutsu Butsuri 53, supplement1-2 (2013): S215. http://dx.doi.org/10.2142/biophys.53.s215_4.

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14

Badran, Hala Mahfouz, and Magdi Elsayed Mahfouz. "Cytotoxin-associated gene-A bearing strains of Helicobacter pylori and atrial fibrillation due to ischemic origin: is there a link?" European Journal of Cardiovascular Prevention & Rehabilitation 14, no. 4 (August 2007): 518–20. http://dx.doi.org/10.1097/hjr.0b013e328011a2a0.

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Background Helicobacter pylori CagA strains could increase the risk for atrial fibrillation in patients with coronary artery disease Methods Serological status for H. pylori CagA using enzyme-linked immunosorbent assay, C-reactive protein, total leucocytic count and atrial size were determined in 185 coronary artery disease patients (with and without atrial fibrillation) and 80 healthy subjects (control). Results CagA strain showed a higher prevalence in the atrial fibrillation group. Atrial dimension and C-reactive protein (independent predictors of atrial fibrillation) were significantly increased in the CagA seropositive subgroup Conclus ons There is a strong liaison between H. pylori CagA infection and atrial fibrillation in coronary artery disease. Increased C reactive protein and atrial size in atrial fibrillation patients may reflect atrial inflammatory remodeling.

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15

Mari, Eleonora, Caterina Ricci, Silvia Pieraccini, Francesco Spinozzi, Paolo Mariani, and Maria Grazia Ortore. "Trehalose Effect on The Aggregation of Model Proteins into Amyloid Fibrils." Life 10, no. 5 (May 13, 2020): 60. http://dx.doi.org/10.3390/life10050060.

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Protein aggregation into amyloid fibrils is a phenomenon that attracts attention from a wide and composite part of the scientific community. Indeed, the presence of mature fibrils is associated with several neurodegenerative diseases, and in addition these supramolecular aggregates are considered promising self-assembling nanomaterials. In this framework, investigation on the effect of cosolutes on protein propensity to aggregate into fibrils is receiving growing interest, and new insights on this aspect might represent valuable steps towards comprehension of highly complex biological processes. In this work we studied the influence exerted by the osmolyte trehalose on fibrillation of two model proteins, that is, lysozyme and insulin, investigated during concomitant variation of the solution ionic strength due to NaCl. In order to monitor both secondary structures and the overall tridimensional conformations, we have performed UV spectroscopy measurements with Congo Red, Circular Dichroism, and synchrotron Small Angle X-ray Scattering. For both proteins we describe the effect of trehalose in changing the fibrillation pattern and, as main result, we observe that ionic strength in solution is a key factor in determining trehalose efficiency in slowing down or blocking protein fibrillation. Ionic strength reveals to be a competitive element with respect to trehalose, being able to counteract its inhibiting effects toward amyloidogenesis. Reported data highlight the importance of combining studies carried out on cosolutes with valuation of other physiological parameters that may affect the aggregation process. Also, the obtained experimental results allow to hypothesize a plausible mechanism adopted by the osmolyte to preserve protein surface and prevent protein fibrillation.

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16

Rho, Hoon Suk, Henk-Willem Veltkamp, Alexander Thomas Hanke, Marcel Ottens, Christian Breukers, Pamela Habibović, and Han Gardeniers. "Systematic Investigation of Insulin Fibrillation on a Chip." Molecules 25, no. 6 (March 18, 2020): 1380. http://dx.doi.org/10.3390/molecules25061380.

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A microfluidic protein aggregation device (microPAD) that allows the user to perform a series of protein incubations with various concentrations of two reagents is demonstrated. The microfluidic device consists of 64 incubation chambers to perform individual incubations of the protein at 64 specific conditions. Parallel processes of metering reagents, stepwise concentration gradient generation, and mixing are achieved simultaneously by pneumatic valves. Fibrillation of bovine insulin was selected to test the device. The effect of insulin and sodium chloride (NaCl) concentration on the formation of fibrillar structures was studied by observing the growth rate of partially folded protein, using the fluorescent marker Thioflavin-T. Moreover, dual gradients of different NaCl and hydrochloric acid (HCl) concentrations were formed, to investigate their interactive roles in the formation of insulin fibrils and spherulites. The chip-system provides a bird’s eye view on protein aggregation, including an overview of the factors that affect the process and their interactions. This microfluidic platform is potentially useful for rapid analysis of the fibrillation of proteins associated with many misfolding-based diseases, such as quantitative and qualitative studies on amyloid growth.

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17

Macchi, Francesca, Maike Eisenkolb, Hans Kiefer, and Daniel E. Otzen. "The Effect of Osmolytes on Protein Fibrillation." International Journal of Molecular Sciences 13, no. 3 (March 21, 2012): 3801–19. http://dx.doi.org/10.3390/ijms13033801.

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18

DERNELLIS, John, and Maria PANARETOU. "C-reactive protein and paroxysmal atrial fibrillation." Acta Cardiologica 56, no. 6 (December 1, 2001): 375–80. http://dx.doi.org/10.2143/ac.56.6.2005701.

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19

Jeppesen, Martin D., Peter Westh, and Daniel E. Otzen. "The role of protonation in protein fibrillation." FEBS Letters 584, no. 4 (January 11, 2010): 780–84. http://dx.doi.org/10.1016/j.febslet.2010.01.002.

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20

Ellinor, Patrick T., Adrian Low, Kristen K. Patton, Marisa A. Shea, and Calum A. MacRae. "C-Reactive Protein in Lone Atrial Fibrillation." American Journal of Cardiology 97, no. 9 (May 2006): 1346–50. http://dx.doi.org/10.1016/j.amjcard.2005.11.052.

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21

Pagano, Rodrigo S., Máximo López Medus, Gabriela E. Gómez, Paula M. Couto, María S. Labanda, Lucas Landolfo, Cecilia D’Alessio, and Julio J. Caramelo. "Protein Fibrillation Lag Times During Kinetic Inhibition." Biophysical Journal 107, no. 3 (August 2014): 711–20. http://dx.doi.org/10.1016/j.bpj.2014.06.029.

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22

Heegaard, Peter M. H., Ulrik Boas, and Daniel E. Otzen. "Dendrimer Effects on Peptide and Protein Fibrillation." Macromolecular Bioscience 7, no. 8 (August 7, 2007): 1047–59. http://dx.doi.org/10.1002/mabi.200700051.

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23

Landreh, Michael, Jan Johansson, Anna Rising, Jenny Presto, and Hans Jörnvall. "Control of amyloid assembly by autoregulation." Biochemical Journal 447, no. 2 (September 26, 2012): 185–92. http://dx.doi.org/10.1042/bj20120919.

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The assembly of proteins into amyloid fibrils can be an element of both protein aggregation diseases and a functional unit in healthy biological pathways. In both cases, it must be kept under tight control to prevent undesired aggregation. In normophysiology, proteins can self-chaperone amyloidogenic segments by restricting their conformational flexibility in an overall stabilizing protein fold. However, some aggregation-prone segments cannot be controlled in this manner and require additional regulatory elements to limit fibrillation. The present review summarizes different molecular mechanisms that proteins use to control their own assembly into fibrils, such as the inclusion of a chaperoning domain or a blocking segment in the proform, the controlled release of an amyloidogenic region from the folded protein, or the adjustment of fibrillation propensity according to pH. Autoregulatory elements can control disease-related as well as functional fibrillar protein assemblies and distinguish a group of self-regulating amyloids across a wide range of biological functions and organisms.

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24

Barros, Heloise R., Maria Kokkinopoulou, Izabel C. Riegel-Vidotti, Katharina Landfester, and Héloïse Thérien-Aubin. "Gold nanocolloid–protein interactions and their impact on β-sheet amyloid fibril formation." RSC Advances 8, no. 2 (2018): 980–86. http://dx.doi.org/10.1039/c7ra11219j.

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Formation of amyloid protein fibrils is associated with degenerative diseases. Here, the interaction mechanism between globular and fibrillar proteins with AuNPs were investigated in order to potentially control and reverse the fibrillation process.

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25

Li, Qiaoqiao, Yingyu Lai, Xiaoyan Gao, Xin Li, Chun-Yu Deng, Huiming Guo, Junfei Zhao, et al. "Involvement of plasminogen activator inhibitor-1 and its related molecules in atrial fibrosis in patients with atrial fibrillation." PeerJ 9 (June 2, 2021): e11488. http://dx.doi.org/10.7717/peerj.11488.

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Atrial fibrillation is the most common form of cardiac arrhythmia. Atrial fibrosis is a significant feature of atrial fibrillation though its mechanism is not well understood. We searched the Gene Expression Omnibus database to compare mRNA expression patterns between atrial fibrillation and sinus rhythm samples; one hundred and forty eight differentially expressed genes were identified. Most of these genes were significantly enriched in the extracellular matrix organization process and collagen-activated tyrosine kinase receptor signaling pathway. To screen hub genes involved in atrial fibrosis, we constructed a protein-protein interaction network and found that three hub genes (SERPINE1/plasminogen activator inhibitor-1/PAI-1, TIMP Metallopeptidase Inhibitor 3/TIMP3 and decorin/DCN) play vital roles in atrial fibrosis, especially plasminogen activator inhibitor-1. Elevated plasminogen activator inhibitor-1 expression was positively correlated with the p53 signaling pathway. Plasminogen activator inhibitor-1 and p53 protein expression levels were verified in patients with sinus rhythm and atrial fibrillation by Western blot analysis. Compared with the sinus rhythm controls, p53 and plasminogen activator inhibitor-1 protein expressions were upregulated in the atrial tissues of patients with atrial fibrillation. p53 was also found to regulate plasminogen activator inhibitor-1 based on the results of cellular and molecular experiments. Thus, the p53/plasminogen activator inhibitor-1 signaling axis may participate in the pathophysiological processes of atrial fibrillation, and plasminogen activator inhibitor-1 may serve as a new therapeutic biomarker in atrial fibrillation.

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26

Tykhomyrov, A. A., Yu S. Kushnir, V. S. Nedzvetsky, T. V. Grinenko, and O. V. Kuryata. "Citicoline affects serum angiostatin and neurospecific protein levels in patients with atrial fibrillation and ischemic stroke." Ukrainian Biochemical Journal 91, no. 5 (September 13, 2019): 34–45. http://dx.doi.org/10.15407/ubj91.05.034.

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27

Ohkubo, Kimie, Ichiro Watanabe, Yasuo Okumura, Keiko Takahashi, Kazuki Iso, Rikitake Kogawa, Kazumasa Sonoda, et al. "Usefulness of High Sensitivity C-Reactive Protein in Predicting Recurrence of Atrial Fibrillation after Electrical Cardioversion." Journal of Nihon University Medical Association 74, no. 5 (2015): 233–37. http://dx.doi.org/10.4264/numa.74.5_233.

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28

Borges, Jordana I., Malka S. Suster, and Anastasios Lymperopoulos. "Cardiac RGS Proteins in Human Heart Failure and Atrial Fibrillation: Focus on RGS4." International Journal of Molecular Sciences 24, no. 7 (March 24, 2023): 6136. http://dx.doi.org/10.3390/ijms24076136.

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The regulator of G protein signaling (RGS) proteins are crucial for the termination of G protein signals elicited by G protein-coupled receptors (GPCRs). This superfamily of cell membrane receptors, by far the largest and most versatile in mammals, including humans, play pivotal roles in the regulation of cardiac function and homeostasis. Perturbations in both the activation and termination of their G protein-mediated signaling underlie numerous heart pathologies, including heart failure (HF) and atrial fibrillation (AFib). Therefore, RGS proteins play important roles in the pathophysiology of these two devasting cardiac diseases, and several of them could be targeted therapeutically. Although close to 40 human RGS proteins have been identified, each RGS protein seems to interact only with a specific set of G protein subunits and GPCR types/subtypes in any given tissue or cell type. Numerous in vitro and in vivo studies in animal models, and also in diseased human heart tissue obtained from transplantations or tissue banks, have provided substantial evidence of the roles various cardiomyocyte RGS proteins play in cardiac normal homeostasis as well as pathophysiology. One RGS protein in particular, RGS4, has been reported in what are now decades-old studies to be selectively upregulated in human HF. It has also been implicated in protection against AFib via knockout mice studies. This review summarizes the current understanding of the functional roles of cardiac RGS proteins and their implications for the treatment of HF and AFib, with a specific focus on RGS4 for the aforementioned reasons but also because it can be targeted successfully with small organic molecule inhibitors.

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Mahmoudi, Morteza, Hamid R. Kalhor, Sophie Laurent, and Iseult Lynch. "Protein fibrillation and nanoparticle interactions: opportunities and challenges." Nanoscale 5, no. 7 (2013): 2570. http://dx.doi.org/10.1039/c3nr33193h.

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30

Kashchiev, Dimo. "Kinetics of protein fibrillation controlled by fibril elongation." Proteins: Structure, Function, and Bioinformatics 82, no. 9 (May 2, 2014): 2229–39. http://dx.doi.org/10.1002/prot.24586.

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31

Li, Jun, Junjie Xiao, Dandan Liang, Hong Zhang, Gaofeng Zhang, Yi Liu, Yangyang Zhang, et al. "Inhibition of mitochondrial translocator protein prevents atrial fibrillation." European Journal of Pharmacology 632, no. 1-3 (April 2010): 60–64. http://dx.doi.org/10.1016/j.ejphar.2010.01.014.

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32

Vasilets, L. M., A. V. Agafonov, O. V. Khlynova, E. A. Ratanova, N. E. Grigoriadi, A. A. Krivaya, and K. V. Trenogina. "Prediction of atrial fibrillation according to levels of serum markers of inflammation during arterial hypertension." Kazan medical journal 93, no. 4 (August 15, 2012): 642–46. http://dx.doi.org/10.17816/kmj1561.

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Aim. To study the parameters of inflammation during atrial fibrillation in patients with arterial hypertension and to determine the possibility of their predictive significance in relation to development of the arrhythmia. Methods. Examined were 97 individuals with arterial hypertension, mean age 50.53±8.10 years. Formed were two groups: patients with arterial hypertension without the arrhythmia and patients with atrial fibrillation on the background of arterial hypertension. Among the examined patients with atrial fibrillation revealed were patients with persistent or recurrent persistent forms of atrial fibrillation, the latter were examined both without and during the paroxysm of arrhythmia. The comparison group was comprised of 21 practically healthy individuals. In all patients determined was the content of C-reactive protein, tumor necrosis factor-alpha, and fibrinogen. Results. Paroxysms of atrial fibrillation were accompanied by a significant increase in the concentration of the tumor necrosis factor-alpha. The level of C-reactive protein had an inverse correlation with the severity of atrial fibrillation, that is, in cases of persistent atrial fibrillation it was lower than in cases of paroxysmal forms of atrial fibrillation, as well as in patients with arterial hypertension without the arrhythmia. Conclusion. Variation in the levels of inflammation markers is an independent predictor of atrial fibrillation in patients with arterial hypertension.

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33

van Wijk, Stan W., Wei Su, Leonoor F. J. M. Wijdeveld, Kennedy S. Ramos, and Bianca J. J. M. Brundel. "Cytoskeletal Protein Variants Driving Atrial Fibrillation: Potential Mechanisms of Action." Cells 11, no. 3 (January 25, 2022): 416. http://dx.doi.org/10.3390/cells11030416.

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The most common clinical tachyarrhythmia, atrial fibrillation (AF), is present in 1–2% of the population. Although common risk factors, including hypertension, diabetes, and obesity, frequently underlie AF onset, it has been recognized that in 15% of the AF population, AF is familial. In these families, genome and exome sequencing techniques identified variants in the non-coding genome (i.e., variant regulatory elements), genes encoding ion channels, as well as genes encoding cytoskeletal (-associated) proteins. Cytoskeletal protein variants include variants in desmin, lamin A/C, titin, myosin heavy and light chain, junctophilin, nucleoporin, nesprin, and filamin C. These cytoskeletal protein variants have a strong association with the development of cardiomyopathy. Interestingly, AF onset is often represented as the initial manifestation of cardiac disease, sometimes even preceding cardiomyopathy by several years. Although emerging research findings reveal cytoskeletal protein variants to disrupt the cardiomyocyte structure and trigger DNA damage, exploration of the pathophysiological mechanisms of genetic AF is still in its infancy. In this review, we provide an overview of cytoskeletal (-associated) gene variants that relate to genetic AF and highlight potential pathophysiological pathways that drive this arrhythmia.

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34

Savelieva, Irina, and A. John Camm. "A New Biomarker in Atrial Fibrillation: Monocyte Chemoattractant Protein-1-Induced Protein." Cardiology 144, no. 3-4 (2019): 122–24. http://dx.doi.org/10.1159/000502253.

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35

Psychari, Stavroula N., Dionysios Tsoukalas, Dimitrios Varvarousis, Anastasios Papaspyropoulos, Eleni Gkika, Athanasios Kotsakis, Ioannis A. Paraskevaidis, and Efstathios K. Iliodromitis. "Opposite relations of epicardial adipose tissue to left atrial size in paroxysmal and permanent atrial fibrillation." SAGE Open Medicine 6 (January 2018): 205031211879990. http://dx.doi.org/10.1177/2050312118799908.

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Objectives: Atrial fibrillation has been associated with obesity in epidemiological studies. Epicardial adipose tissue is an ectopic fat depot in the proximity of atria, with endocrine and inflammatory properties that is implicated in the pathophysiology of atrial fibrillation. Inflammation also has a role in atrial arrhythmogenesis. The aim of this study was to investigate the potential relations of epicardial adipose tissue to left atrial size and to adiponectin and the pro-inflammatory mediators, high-sensitivity C-reactive protein, and interleukin-6 in paroxysmal and permanent atrial fibrillation. Methods: This was a cross-sectional study of 103 atrial fibrillation patients, divided into two subgroups of paroxysmal and permanent atrial fibrillation, and 81 controls, in sinus rhythm. Echocardiography was used for estimation of epicardial adipose tissue and left atrial size and high-sensitivity C-reactive protein, interleukin-6 and adiponectin were measured in all subjects. Results: Atrial fibrillation patients had significantly larger epicardial adipose tissue compared with controls (0.43 ± 0.17 vs 0.34 ± 0.17 cm, p = 0.002). Atrial fibrillation presence was independently related to epicardial adipose tissue thickness ( b = 0.09, p = 0.002). Opposite associations of epicardial adipose tissue with left atrial volume existed in atrial fibrillation subgroups; in the paroxysmal subgroup, epicardial adipose tissue was directly related to left atrial volume ( R = 0.3, p = 0.03), but in the permanent one the relation was inverse ( R = −0.7, p < 0.0001). Adiponectin, high-sensitivity C-reactive protein and interleukin-6 were elevated in both atrial fibrillation groups. Only interleukin-6 was related to epicardial adipose tissue size. Conclusion: Opposite associations of epicardial adipose tissue with left atrial size in paroxysmal and permanent Atrial fibrillation and elevated inflammatory markers, suggest a role of epicardial adipose tissue and inflammation in the fibrotic and remodeling process.

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Chen, Yongqing, Fangju Su, Juanping Han, Piqi Jiao, and Wenyun Guo. "Expression of Rho Kinase and Its Mechanism in the Left Atrial Appendage in Patients with Atrial Fibrillation." Heart Surgery Forum 21, no. 1 (February 19, 2018): 044. http://dx.doi.org/10.1532/hsf.1851.

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Aim: To study the expression of Rho kinase (Rho associated coil forming protein kinase-1, ROCK-1) and its substrate myosin phosphatase target subunit 1 (myosin phosphatase target subunit-1, MYPT-1), connexin 40 (Cx40) and connexin 43 (Cx43) in the left atrial appendage of patients with atrial fibrillation, and explore the role of ROCK signaling pathway in patients with atrial fibrillation and its underlying mechanism. Methods: 40 patients undergoing open heart surgery were divided into two groups; atrial fibrillation group (AF group) and sinus rhythm group (SR group). About 100 mg of left atrial appendage tissue was taken during surgery and quickly frozen in liquid nitrogen. Immunohistochemistry and western blot were performed to evaluate the expression and location of ROCK-1, MYPT-1, Cx40 and Cx43 in the left atrial appendage tissue. Results: The results indicated that the expression of ROCK-1, MYPT-1, and Cx40 in the left atrial appendage in patients with atrial fibrillation was significantly upregulated (P < .01), the difference in the two groups was statistically significant, and ROCK-1, Cx40, and MYPT-1 expression in the AF group were higher than those in sinus rhythm group; there was a weakly positive expression of Cx43 protein in the AF group and sinus rhythm group, the difference was not statistically significant, and ROCK-1 and MYPT-1 expression showed a significant positive correlation (r = 0.968, P < .05), MYPT 1 and Cx40 protein expression was also positively correlated (r = 0.983, P < .05). Evidence in the left atrial appendage tissue of patients with atrial fibrillation showed that some proteins in Rho/ROCK pathway were upregulated, and MYPT-1 and Cx40 protein expression in AF group were significantly higher than that of SR group, which was also positively correlated; Cx43 showed a weak positive expression in both the SR group and AF group, which indicates that Rho kinase may induce expression of Cx40 by phosphorylation of MYPT-1; Cx43 may not be involved, suggesting that Rho kinase signaling pathway may activate and play an important role in the pathogenesis of atrial fibrillation lesions.

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Panigrahi, Gitanjali P., Ankita R. Rane, Sirisha L. Vavilala, and Sinjan Choudhary. "Deciphering the anti-Parkinson’s activity of sulphated polysaccharides from Chlamydomonas reinhardtii on the α-Synuclein mutants A30P, A53T, E46K, E57K and E35K." Journal of Biochemistry 166, no. 6 (August 6, 2019): 463–74. http://dx.doi.org/10.1093/jb/mvz064.

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Abstract Parkinsonism-linked mutations in alanine and glutamic acid residues of the pre-synaptic protein α-Synuclein (α-Syn) affect specific tertiary interactions essential for stability of the native state and make it prone to more aggregation. Many of the currently available drugs used for the treatment of Parkinson’s disease (PD) are not very effective and are associated with multiple side effects. Recently, marine algae have been reported to have sulphated polysaccharides which offers multiple pharmaceutical properties. With this background, we have isolated sulphated polysaccharides from Chlamydomonas reinhardtii (Cr-SPs) and investigated their effects on inhibition of fibrillation/aggregation of α-Syn mutants through a combination of spectroscopic and microscopic techniques. The kinetics of α-Syn fibrillation establishes that Cr-SPs are very effective in inhibiting fibrillation of α-Syn mutants. The morphological changes associated with the fibrillation/aggregation process have been monitored by transmission electron microscopy. Sodium dodecyl sulphate-polyacrylamide gel electrophoresis gel image suggests that Cr-SPs increase the amount of soluble protein after completion of the fibrillation/aggregation process. The circular dichroism results showed that Cr-SPs efficiently delay the conversion of native protein into β-sheet-rich structures. Thus, the current work has considerable therapeutic implications towards deciphering the potential of Cr-SPs to act against PD and other protein aggregation-related disorders.

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Pala, Arda Aybars. "C-reactive protein/albumin ratio in predicting atrial fibrillation after coronary artery bypass grafting." Cardiovascular Surgery and Interventions 9, no. 2 (July 7, 2022): 66–72. http://dx.doi.org/10.5606/e-cvsi.2022.1233.

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Objectives: In the present study, the purpose was to investigate the usability of the preoperative C-reactive protein/albumin ratio as a predictor of the development of postoperative atrial fibrillation in patients who undergo coronary artery bypass grafting. Patients and methods: A total of 336 patients (228 males, 108 females; mean age: 58.1±8.5 years; range 35 to 88 years) who underwent isolated coronary artery bypass grafting with cardiopulmonary bypass between January 2019 and January 2021 were reviewed in the single-center, retrospective study. Those with postoperative sinus rhythm were considered Group 1 (n=258), and patients with postoperative atrial fibrillation were defined as Group 2 (n=78). Preoperative routine biochemical tests of the patient groups were evaluated. Results: The incidence of postoperative atrial fibrillation was 23.2%. Statistically significant differences were detected between the two groups in terms of age (p<0.001) and previous percutaneous coronary intervention (p=0.028). In multivariate analysis, age, hemoglobin, mean platelet volume, neutrophil/lymphocyte ratio, and C-reactive protein/albumin ratio variables were found to be independent predictive factors of postoperative atrial fibrillation development (p<0.001, p=0.005, p=0.002, p<0.001, and p<0.001, respectively). Conclusion: Preoperative hemoglobin, mean platelet volume, calculated neutrophil/lymphocyte ratio, and C-reactive protein/albumin ratio values can be used as predictors of postoperative atrial fibrillation development in patients who will undergo coronary artery bypass grafting.

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Milošević, Jelica, Radivoje Prodanović, and Natalija Polović. "On the Protein Fibrillation Pathway: Oligomer Intermediates Detection Using ATR-FTIR Spectroscopy." Molecules 26, no. 4 (February 12, 2021): 970. http://dx.doi.org/10.3390/molecules26040970.

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Oligomeric intermediates on the pathway of amyloid fibrillation are suspected as the main cytotoxins responsible for amyloid-related pathogenicity. As they appear to be a part of the lag phase of amyloid fibrillation when analyzed using standard methods such as Thioflavin T (ThT) fluorescence, a more sensitive method is needed for their detection. Here we apply Fourier transform infrared spectroscopy (FTIR) in attenuated total reflectance (ATR) mode for fast and cheap analysis of destabilized hen-egg-white lysozyme solution and detection of oligomer intermediates of amyloid fibrillation. Standard methods of protein aggregation analysis— Thioflavin T (ThT) fluorescence, atomic force microscopy (AFM), and 8-anilinonaphthalene-1-sulphonic acid (ANS) fluorescence were applied and compared to FTIR spectroscopy data. Results show the great potential of FTIR for both, qualitative and quantitative monitoring of oligomer formation based on the secondary structure changes. While oligomer intermediates do not induce significant changes in ThT fluorescence, their secondary structure changes were very prominent. Normalization of specific Amide I region peak intensities by using Amide II peak intensity as an internal standard provides an opportunity to use FTIR spectroscopy for both qualitative and quantitative analysis of biological samples and detection of potentially toxic oligomers, as well as for screening of efficiency of fibrillation procedures.

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Bai, Juan, Chongyu Ren, Wei Hao, Rui Wang, and Ji-Min Cao. "Chemical sympathetic denervation, suppression of myocardial transient outward potassium current, and ventricular fibrillation in the rat." Canadian Journal of Physiology and Pharmacology 86, no. 10 (October 2008): 700–709. http://dx.doi.org/10.1139/y08-075.

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Sympathetic denervation is frequently observed in heart disease. To investigate the linkage of sympathetic denervation and cardiac arrhythmia, we developed a rat model of chemical sympathectomy by subcutaneous injections of 6-hydroxydopamine (6-OHDA). Cardiac sympathetic innervation was visualized by means of a glyoxylic catecholaminergic histofluorescence method. Transient outward current (Ito) of ventricular myocytes was recorded with the whole-cell configuration of the patch clamp technique. We observed that sympathectomy (i) decreased cardiac sympathetic nerve density and norepinephrine level, (ii) reduced the protein expression of Kv4.2, Kv1.4, and Kv channel-interacting protein 2 (KChIP2), (iii) decreased current densities and delayed activation of Ito channels, (iv) reduced the phosphorylation of extracellular signal-regulated kinase 1 and 2 (ERK1/2) and cAMP response element-binding protein (CREB), and (v) increased the severity of ventricular fibrillation induced by rapid pacing. Three weeks after 6-OHDA injections, which allowed time for sympathetic regeneration, we found cardiac sympathetic nerve density, norepinephrine levels, expression levels of Kv4.2 and KChIP2 proteins, and Ito densities were partially normalized and ventricular fibrillation severity was decreased. We conclude that chemical sympathectomy downregulates the expression of selective Kv channel subunits and decreases myocardial Ito channel activities, contributing to the elevated susceptibility to ventricular fibrillation.

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SO, Masatomo, Hisashi YAGI, and Yuji GOTO. "Ultrasonication-Induced Acceleration of Amyloid Fibrillation and Protein Crystallization." Seibutsu Butsuri 54, no. 6 (2014): 297–302. http://dx.doi.org/10.2142/biophys.54.297.

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Fändrich, M., and C. M. Dobson. "Amyloid-type fibrillation of the all alpha protein myoglobin." Biochemical Society Transactions 28, no. 5 (October 1, 2000): A408. http://dx.doi.org/10.1042/bst028a408c.

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Cabaleiro-Lago, Celia, Fiona Quinlan-Pluck, Iseult Lynch, Stina Lindman, Aedin M. Minogue, Eva Thulin, Dominic M. Walsh, Kenneth A. Dawson, and Sara Linse. "Inhibition of Amyloid β Protein Fibrillation by Polymeric Nanoparticles." Journal of the American Chemical Society 130, no. 46 (November 19, 2008): 15437–43. http://dx.doi.org/10.1021/ja8041806.

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Korantzopoulos, Panagiotis, Dimitrios Galaris, Dimitrios Papaioannides, and Stelianos Kokkoris. "C-reactive protein and oxidative stress in atrial fibrillation." International Journal of Cardiology 88, no. 1 (March 2003): 103–4. http://dx.doi.org/10.1016/s0167-5273(02)00386-8.

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Boos, Christopher J., and Gregory Y. H. Lip. "C-Reactive Protein and Lone Atrial Fibrillation: Potential Confounders." American Journal of Cardiology 98, no. 7 (October 2006): 991–92. http://dx.doi.org/10.1016/j.amjcard.2006.05.005.

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Marott, Sarah C. W., Børge G. Nordestgaard, Jeppe Zacho, Jens Friberg, Gorm B. Jensen, Anne Tybjærg-Hansen, and Marianne Benn. "Does Elevated C-Reactive Protein Increase Atrial Fibrillation Risk?" Journal of the American College of Cardiology 56, no. 10 (August 2010): 789–95. http://dx.doi.org/10.1016/j.jacc.2010.02.066.

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Volpatti, Lisa R., Ulyana Shimanovich, Francesco Simone Ruggeri, Sreenath Bolisetty, Thomas Müller, Thomas O. Mason, Thomas C. T. Michaels, Raffaele Mezzenga, Giovanni Dietler, and Tuomas P. J. Knowles. "Micro- and nanoscale hierarchical structure of core–shell protein microgels." Journal of Materials Chemistry B 4, no. 48 (2016): 7989–99. http://dx.doi.org/10.1039/c6tb02683d.

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Akbarian, Mohsen, Ehsan Rezaie, Fatemeh Farjadian, Zahra Bazyar, Mona Hosseini-Sarvari, Ehsan Malek Ara, Seyed Ali Mirhosseini, and Jafar Amani. "Inhibitory effect of coumarin and its analogs on insulin fibrillation /cytotoxicity is depend on oligomerization states of the protein." RSC Advances 10, no. 63 (2020): 38260–74. http://dx.doi.org/10.1039/d0ra07710k.

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The effect of the applied compounds on insulin fibrillation at two pHs. By and large, the compounds through changing the oligomerization states and altering structure integrity of insulin can govern the fibrillation process.

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Meng, Xiaoyun, Larissa A. Munishkina, Anthony L. Fink, and Vladimir N. Uversky. "Effects of Various Flavonoids on theα-Synuclein Fibrillation Process." Parkinson's Disease 2010 (2010): 1–16. http://dx.doi.org/10.4061/2010/650794.

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α-Synuclein aggregation and fibrillation are closely associated with the formation of Lewy bodies in neurons and are implicated in the causative pathogenesis of Parkinson's disease and other synucleinopathies. Currently, there is no approved therapeutic agent directed toward preventing the protein aggregation, which has been recently shown to have a key role in the cytotoxic nature of amyloidogenic proteins. Flavonoids, known as plant pigments, belong to a broad family of polyphenolic compounds. Over 4,000 flavonoids have been identified from various plants and foodstuffs derived from plants and have been demonstrated as potential neuroprotective agents. In this study 48 flavonoids belonging to several classes with structures differing in the position of double bonds and ring substituents were tested for their ability to inhibit the fibrillation ofα-synuclein in vitro. A variety of flavonoids inhibitedα-synuclein fibrillation, and most of the strong inhibitory flavonoids were also found to disaggregate preformed fibrils.

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Basu, Aalok, Sagar Bhayye, Sonia Kundu, Aatryee Das, and Arup Mukherjee. "Andrographolide inhibits human serum albumin fibril formations through site-specific molecular interactions." RSC Advances 8, no. 54 (2018): 30717–24. http://dx.doi.org/10.1039/c8ra04637a.

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