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https://www.readbyqxmd.com/read/27806967/neuronal-nav1-8-channels-as-a-novel-therapeutic-target-of-acute-atrial-fibrillation-prevention
#1
XiaoMeng Chen, LiLei Yu, ShaoBo Shi, Hong Jiang, CongXin Huang, Mayurika Desai, YiGang Li, Hector Barajas-Martinez, Dan Hu
BACKGROUND: Ganglionated plexus have been developed as additional ablation targets to improve the outcome of atrial fibrillation (AF) besides pulmonary vein isolation. Recent studies implicated an intimate relationship between neuronal sodium channel Nav1.8 (encoded by SCN10A) and AF. The underlying mechanism between Nav1.8 and AF remains unclear. This study aimed to determine the role of Nav1.8 in cardiac electrophysiology in an acute AF model and explore possible therapeutic targets...
November 2, 2016: Journal of the American Heart Association
https://www.readbyqxmd.com/read/27806966/contrasting-nav1-8-activity-in-scn10a-ventricular-myocytes-and-the-intact-heart
#2
Dina Myers Stroud, Tao Yang, Kevin Bersell, Dymtro O Kryshtal, Satomi Nagao, Christian Shaffer, Laura Short, Lynn Hall, Thomas C Atack, Wei Zhang, Bjorn C Knollmann, Franz Baudenbacher, Dan M Roden
BACKGROUND: Genome-wide association studies have implicated variants in SCN10A, which encodes Nav1.8, as modulators of cardiac conduction. Follow-up work has indicated the SCN10A sequence includes an intronic enhancer for SCN5A. Yet the role of the Nav1.8 protein in the myocardium itself is still unclear. To investigate this, we use homozygous knockout mice (Scn10a(-/-)) generated by disruption of exons 4 and 5, leaving the Scn5a enhancer intact. METHODS AND RESULTS: We previously reported that pharmacologic blockade of Nav1...
November 2, 2016: Journal of the American Heart Association
https://www.readbyqxmd.com/read/27729462/association-and-interaction-analysis-of-diabetes-mellitus-and-scn10a-for-cardiovascular-autonomic-neuropathy-in-a-chinese-population
#3
Yubao Lv, Linuo Zhou, Zihui Tang, Jingcheng Dong
BACKGROUND: This study assessed the extent to which diabetes mellitus (DM) and SCN10A (rs7375036) and their interaction impact on cardiovascular autonomic neuropathy (CAN) susceptibility in a Chinese Han sample. METHOD: We performed a study in a cross-sectional dataset that included 419 patients with DM and 1557 controls who were genotyped for the presence of the SCN10A rs7375036 polymorphisms. Genotyping was performed by iPLEX technology. The associations of rs7375036 and DM with CAN was assessed by using univariate and multivariate logistic regression controlling for confounders...
October 11, 2016: Postgraduate Medical Journal
https://www.readbyqxmd.com/read/27725708/the-rs6771157-c-g-polymorphism-in-scn10a-is-associated-with-the-risk-of-atrial-fibrillation-in-a-chinese-han-population
#4
Zhen Fang, Yue Jiang, Yifeng Wang, Yuan Lin, Yaowu Liu, Liyan Zhao, Yan Xu, Mohammad Bilaal Toorabally, Shenghu He, Fengxiang Zhang
A recent genome wide associated study in European descent population identified the association of Atrial fibrillation (AF) risk with a single nucleotide polymorphism (SNP) in SCN10A. The aim of this study was to evaluate whether SCN10A polymorphisms are associated with AF risk in the Chinese Han population. A total of 2,300 individuals of Chinese Han origin were recruited and three potentially functional SNPs were genotyped. Logistic regression models were utilized to calculate odds ratios (ORs) at a 95% confidence intervals (CIs)...
October 11, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27667030/enhanced-cardiac-tbc1d10c-expression-lowers-heart-rate-and-enhances-exercise-capacity-and-survival
#5
Cornelia Volland, Sebastian Bremer, Kristian Hellenkamp, Nico Hartmann, Nataliya Dybkova, Sara Khadjeh, Anna Kutschenko, David Liebetanz, Stefan Wagner, Bernhard Unsöld, Michael Didié, Karl Toischer, Samuel Sossalla, Gerd Hasenfuß, Tim Seidler
TBC1D10C is a protein previously demonstrated to bind and inhibit Ras and Calcineurin. In cardiomyocytes, also CaMKII is inhibited and all three targeted enzymes are known to promote maladaptive cardiomyocyte hypertrophy. Here, in accordance with lack of Calcineurin inhibition in vivo, we did not observe a relevant anti-hypertrophic effect despite inhibition of Ras and CaMKII. However, cardiomyocyte-specific TBC1D10C overexpressing transgenic mice exhibited enhanced longevity. Ejection fraction and exercise capacity were enhanced in transgenic mice, but shortening of isolated cardiomyocytes was not increased...
September 26, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27659466/52-genetic-loci-influencing-myocardial%C3%A2-mass
#6
Pim van der Harst, Jessica van Setten, Niek Verweij, Georg Vogler, Lude Franke, Matthew T Maurano, Xinchen Wang, Irene Mateo Leach, Mark Eijgelsheim, Nona Sotoodehnia, Caroline Hayward, Rossella Sorice, Osorio Meirelles, Leo-Pekka Lyytikäinen, Ozren Polašek, Toshiko Tanaka, Dan E Arking, Sheila Ulivi, Stella Trompet, Martina Müller-Nurasyid, Albert V Smith, Marcus Dörr, Kathleen F Kerr, Jared W Magnani, Fabiola Del Greco M, Weihua Zhang, Ilja M Nolte, Claudia T Silva, Sandosh Padmanabhan, Vinicius Tragante, Tõnu Esko, Gonçalo R Abecasis, Michiel E Adriaens, Karl Andersen, Phil Barnett, Joshua C Bis, Rolf Bodmer, Brendan M Buckley, Harry Campbell, Megan V Cannon, Aravinda Chakravarti, Lin Y Chen, Alessandro Delitala, Richard B Devereux, Pieter A Doevendans, Anna F Dominiczak, Luigi Ferrucci, Ian Ford, Christian Gieger, Tamara B Harris, Eric Haugen, Matthias Heinig, Dena G Hernandez, Hans L Hillege, Joel N Hirschhorn, Albert Hofman, Norbert Hubner, Shih-Jen Hwang, Annamaria Iorio, Mika Kähönen, Manolis Kellis, Ivana Kolcic, Ishminder K Kooner, Jaspal S Kooner, Jan A Kors, Edward G Lakatta, Kasper Lage, Lenore J Launer, Daniel Levy, Alicia Lundby, Peter W Macfarlane, Dalit May, Thomas Meitinger, Andres Metspalu, Stefania Nappo, Silvia Naitza, Shane Neph, Alex S Nord, Teresa Nutile, Peter M Okin, Jesper V Olsen, Ben A Oostra, Josef M Penninger, Len A Pennacchio, Tune H Pers, Siegfried Perz, Annette Peters, Yigal M Pinto, Arne Pfeufer, Maria Grazia Pilia, Peter P Pramstaller, Bram P Prins, Olli T Raitakari, Soumya Raychaudhuri, Ken M Rice, Elizabeth J Rossin, Jerome I Rotter, Sebastian Schafer, David Schlessinger, Carsten O Schmidt, Jobanpreet Sehmi, Herman H W Silljé, Gianfranco Sinagra, Moritz F Sinner, Kamil Slowikowski, Elsayed Z Soliman, Timothy D Spector, Wilko Spiering, John A Stamatoyannopoulos, Ronald P Stolk, Konstantin Strauch, Sian-Tsung Tan, Kirill V Tarasov, Bosco Trinh, Andre G Uitterlinden, Malou van den Boogaard, Cornelia M van Duijn, Wiek H van Gilst, Jorma S Viikari, Peter M Visscher, Veronique Vitart, Uwe Völker, Melanie Waldenberger, Christian X Weichenberger, Harm-Jan Westra, Cisca Wijmenga, Bruce H Wolffenbuttel, Jian Yang, Connie R Bezzina, Patricia B Munroe, Harold Snieder, Alan F Wright, Igor Rudan, Laurie A Boyer, Folkert W Asselbergs, Dirk J van Veldhuisen, Bruno H Stricker, Bruce M Psaty, Marina Ciullo, Serena Sanna, Terho Lehtimäki, James F Wilson, Stefania Bandinelli, Alvaro Alonso, Paolo Gasparini, J Wouter Jukema, Stefan Kääb, Vilmundur Gudnason, Stephan B Felix, Susan R Heckbert, Rudolf A de Boer, Christopher Newton-Cheh, Andrew A Hicks, John C Chambers, Yalda Jamshidi, Axel Visel, Vincent M Christoffels, Aaron Isaacs, Nilesh J Samani, Paul I W de Bakker
BACKGROUND: Myocardial mass is a key determinant of cardiac muscle function and hypertrophy. Myocardial depolarization leading to cardiac muscle contraction is reflected by the amplitude and duration of the QRS complex on the electrocardiogram (ECG). Abnormal QRS amplitude or duration reflect changes in myocardial mass and conduction, and are associated with increased risk of heart failure and death. OBJECTIVES: This meta-analysis sought to gain insights into the genetic determinants of myocardial mass...
September 27, 2016: Journal of the American College of Cardiology
https://www.readbyqxmd.com/read/27598514/scn10a-mutation-in-a-patient-with-erythromelalgia-enhances-c-fiber-activity-dependent-slowing
#7
Andreas M Kist, Dagrun Sagafos, Anthony M Rush, Cristian Neacsu, Esther Eberhardt, Roland Schmidt, Lars Kristian Lunden, Kristin Ørstavik, Luisa Kaluza, Jannis Meents, Zhiping Zhang, Thomas Hedley Carr, Hugh Salter, David Malinowsky, Patrik Wollberg, Johannes Krupp, Inge Petter Kleggetveit, Martin Schmelz, Ellen Jørum, Angelika Lampert, Barbara Namer
Gain-of-function mutations in the tetrodotoxin (TTX) sensitive voltage-gated sodium channel (Nav) Nav1.7 have been identified as a key mechanism underlying chronic pain in inherited erythromelalgia. Mutations in TTX resistant channels, such as Nav1.8 or Nav1.9, were recently connected with inherited chronic pain syndromes. Here, we investigated the effects of the p.M650K mutation in Nav1.8 in a 53 year old patient with erythromelalgia by microneurography and patch-clamp techniques. Recordings of the patient's peripheral nerve fibers showed increased activity dependent slowing (ADS) in CMi and less spontaneous firing compared to a control group of erythromelalgia patients without Nav mutations...
2016: PloS One
https://www.readbyqxmd.com/read/27590072/a-scn10a-snp-biases-human-pain-sensitivity
#8
Guangyou Duan, Chongyang Han, Qingli Wang, Shanna Guo, Yuhao Zhang, Ying Ying, Penghao Huang, Li Zhang, Lawrence Macala, Palak Shah, Mi Zhang, Ningbo Li, Sulayman D Dib-Hajj, Stephen G Waxman, Xianwei Zhang
BACKGROUND: Nav1.8 sodium channels, encoded by SCN10A, are preferentially expressed in nociceptive neurons and play an important role in human pain. Although rare gain-of-function variants in SCN10A have been identified in individuals with painful peripheral neuropathies, whether more common variants in SCN10A can have an effect at the channel level and at the dorsal root ganglion, neuronal level leading to a pain disorder or an altered normal pain threshold has not been determined. RESULTS: Candidate single nucleotide polymorphism association approach together with experimental pain testing in human subjects was used to explore possible common SCN10A missense variants that might affect human pain sensitivity...
2016: Molecular Pain
https://www.readbyqxmd.com/read/27577874/fine-mapping-novel-loci-identification-and-snp-association-transferability-in-a-genome-wide-association-study-of-qrs-duration-in-african-americans
#9
Daniel S Evans, Christy L Avery, Mike A Nalls, Guo Li, John Barnard, Erin N Smith, Toshiko Tanaka, Anne M Butler, Sarah G Buxbaum, Alvaro Alonso, Dan E Arking, Gerald S Berenson, Joshua C Bis, Steven Buyske, Cara L Carty, Wei Chen, Mina K Chung, Steven R Cummings, Rajat Deo, Charles B Eaton, Ervin R Fox, Susan R Heckbert, Gerardo Heiss, Lucia A Hindorff, Wen-Chi Hsueh, Aaron Isaacs, Yalda Jamshidi, Kathleen F Kerr, Felix Liu, Yongmei Liu, Kurt K Lohman, Jared W Magnani, Joseph F Maher, Reena Mehra, Yan A Meng, Solomon K Musani, Christopher Newton-Cheh, Kari E North, Bruce M Psaty, Susan Redline, Jerome I Rotter, Renate B Schnabel, Nicholas J Schork, Ralph V Shohet, Andrew B Singleton, Jonathan D Smith, Elsayed Z Soliman, Sathanur R Srinivasan, Herman A Taylor, David R Van Wagoner, James G Wilson, Taylor Young, Zhu-Ming Zhang, Alan B Zonderman, Michele K Evans, Luigi Ferrucci, Sarah S Murray, Gregory J Tranah, Eric A Whitsel, Alex P Reiner, Nona Sotoodehnia
The electrocardiographic QRS duration, a measure of ventricular depolarization and conduction, is associated with cardiovascular mortality. While genome-wide association studies (GWAS) have identified single nucleotide polymorphisms (SNPs) associated with QRS duration at 22 loci among those of European descent, the genetic architecture of QRS duration in non-European populations is largely unknown. We therefore performed a GWAS meta-analysis of QRS duration in 13,031 African Americans from ten cohorts and a transethnic GWAS meta-analysis with additional results from populations of European descent...
August 29, 2016: Human Molecular Genetics
https://www.readbyqxmd.com/read/27272739/association-of-common-and-rare-variants-of-scn10a-gene-with-sudden-unexplained-nocturnal-death-syndrome-in-chinese-han-population
#10
Liyong Zhang, Feng Zhou, Lei Huang, Qiuping Wu, Jinxiang Zheng, Yeda Wu, Kun Yin, Jianding Cheng
Sudden unexplained nocturnal death syndrome (SUNDS) remains an autopsy negative entity with unknown etiology to both forensic pathologists and physicians. The electrocardiogram (ECG) characteristics and clinical phenotype of SUNDS survivors strongly suggest that SUNDS shares some similarities with Brugada syndrome (BrS). Recently, the variants of sodium channel Nav 1.8 coding gene SCN10A were identified to be associated with BrS. Here, we investigated the association of SCN10A gene variants with 105 sporadic SUNDS victims and 22 BrS cases in the Chinese Han population...
June 7, 2016: International Journal of Legal Medicine
https://www.readbyqxmd.com/read/26971948/psychiatric-risk-gene-transcription-factor-4-regulates-intrinsic-excitability-of-prefrontal-neurons-via-repression-of-scn10a-and-kcnq1
#11
Matthew D Rannals, Gregory R Hamersky, Stephanie Cerceo Page, Morganne N Campbell, Aaron Briley, Ryan A Gallo, BaDoi N Phan, Thomas M Hyde, Joel E Kleinman, Joo Heon Shin, Andrew E Jaffe, Daniel R Weinberger, Brady J Maher
Transcription Factor 4 (TCF4) is a clinically pleiotropic gene associated with schizophrenia and Pitt-Hopkins syndrome (PTHS). To gain insight about the neurobiology of TCF4, we created an in vivo model of PTHS by suppressing Tcf4 expression in rat prefrontal neurons immediately prior to neurogenesis. This cell-autonomous genetic insult attenuated neuronal spiking by increasing the afterhyperpolarization. At the molecular level, using a novel technique called iTRAP that combined in utero electroporation and translating ribosome affinity purification, we identified increased translation of two ion channel genes, Kcnq1 and Scn10a...
April 6, 2016: Neuron
https://www.readbyqxmd.com/read/26962151/twenty-eight-genetic-loci-associated-with-st-t-wave-amplitudes-of-the-electrocardiogram
#12
Niek Verweij, Irene Mateo Leach, Aaron Isaacs, Dan E Arking, Joshua C Bis, Tune H Pers, Marten E van den Berg, Leo-Pekka Lyytikäinen, Phil Barnett, Xinchen Wang, Elsayed Z Soliman, Cornelia M van Duijn, Mika Kähönen, Dirk J van Veldhuisen, Jan A Kors, Olli T Raitakari, Claudia T Silva, Terho Lehtimäki, Hans L Hillege, Joel N Hirschhorn, Laurie A Boyer, Wiek H van Gilst, Alvaro Alonso, Nona Sotoodehnia, Mark Eijgelsheim, Rudolf A de Boer, Paul I W de Bakker, Lude Franke, Pim van der Harst
The ST segment and adjacent T wave amplitudes (ST-T wave) of the electrocardiogram are quantitative characteristics of cardiac repolarization. Repolarization abnormalities have been linked to ventricular arrhythmias and sudden cardiac death. We performed the first GWA meta-analysis of ST-T wave amplitudes in up to 37,977 individuals identifying 71 robust genotype-phenotype associations clustered within 28 independent loci. Fifty-four genes were prioritized as candidates underlying the phenotypes, including genes with established roles in the cardiac repolarization phase (SCN5A/SCN10A, KCND3, KCNB1, NOS1AP and HEY2) and others with as yet undefined cardiac function...
March 8, 2016: Human Molecular Genetics
https://www.readbyqxmd.com/read/26917719/corrigendum-to-role-of-common-and-rare-variants-in-scn10a-results-from-the-brugada-syndrome-qrs-locus-gene-discovery-collaborative-study
#13
(no author information available yet)
No abstract text is available yet for this article.
May 1, 2016: Cardiovascular Research
https://www.readbyqxmd.com/read/26747884/sodium-channel-nav1-8-emerging-links-to-human-disease
#14
REVIEW
Chongyang Han, Jianying Huang, Stephen G Waxman
The NaV1.8 sodium channel, encoded by gene SCN10A, was initially termed sensory neuron-specific (SNS) due to prominent expression in primary sensory neurons including dorsal root ganglion (DRG) neurons. Early studies on rodent NaV1.8 demonstrated depolarized voltage dependence of channel inactivation, a slow rate of inactivation, and rapid recovery from inactivation. As a result of these biophysical properties, NaV1.8 supports repetitive firing in response to sustained depolarization. This article reviews recent studies that reveal multiple links of NaV1...
February 2, 2016: Neurology
https://www.readbyqxmd.com/read/26740675/channelopathy-related-scn10a-gene-variants-predict-cerebellar-dysfunction-in-multiple-sclerosis
#15
Tina Roostaei, Shokufeh Sadaghiani, Min Tae M Park, Rahil Mashhadi, Aria Nazeri, Sina Noshad, Mohammad Javad Salehi, Maryam Naghibzadeh, Abdorreza Naser Moghadasi, Mahsa Owji, Rozita Doosti, Amir Pejman Hashemi Taheri, Ali Shakouri Rad, Amirreza Azimi, M Mallar Chakravarty, Aristotle N Voineskos, Arash Nazeri, Mohammad Ali Sahraian
OBJECTIVE: To determine the motor-behavioral and neural correlates of putative functional common variants in the sodium-channel NaV1.8 encoding gene (SCN10A) in vivo in patients with multiple sclerosis (MS). METHODS: We recruited 161 patients with relapsing-onset MS and 94 demographically comparable healthy participants. All patients with MS underwent structural MRI and clinical examinations (Expanded Disability Status Scale [EDSS] and Multiple Sclerosis Functional Composite [MSFC])...
February 2, 2016: Neurology
https://www.readbyqxmd.com/read/26733327/absence-of-a-primary-role-for-scn10a-mutations-in-arrhythmogenic-right-ventricular-dysplasia-cardiomyopathy
#16
LETTER
Anneline S J M Te Riele, Cynthia A James, Brittney Murray, Crystal Tichnell, Nuria Amat-Alarcon, Kathleen Burks, Harikrishna Tandri, Hugh Calkins, Michael Polydefkis, Daniel P Judge
Prior reports have identified associations between SCN10A and cardiac disorders, such as atrial fibrillation and Brugada syndrome. We evaluated SCN10A in 151 probands with ARVD/C. In this cohort, 10 putatively pathogenic SCN10A variants were identified, including a novel frameshift insertion. Despite a known role for the encoded protein in peripheral nerve function, the proband with the frameshift variant had no discernible neurological abnormalities. Arrhythmic phenotypes were not different between those with a rare variant in SCN10A and those without...
February 2016: Journal of Cardiovascular Translational Research
https://www.readbyqxmd.com/read/26711856/painful-small-fiber-neuropathy-with-gastroparesis-a-new-phenotype-with-a-novel-mutation-in-the-scn10a-gene
#17
Ron Dabby, Menachem Sadeh, Yelena Broitman, Keren Yosovich, Ram Dickman, Esther Leshinsky-Silver
Gain-of-function mutations in the SCN10A gene (encoding the Nav1.8 voltage gated sodium channel) have been reported in a small number of patients. All presented with predominantly painful sensory neuropathy, congruent with the expression of Nav1.8 in nociceptive sensory neurons of the dorsal root ganglion. Only a few had mild autonomic symptoms, including dry eyes and mouth, orthostatic dizziness, palpitations, diarrhea and constipation. The underlying mechanism of the autonomic symptoms in these patients is unclear...
April 2016: Journal of Clinical Neuroscience: Official Journal of the Neurosurgical Society of Australasia
https://www.readbyqxmd.com/read/26423924/genetic-investigation-of-sudden-unexpected-death-in-epilepsy-cohort-by-panel-target-resequencing
#18
Monica Coll, Catarina Allegue, Sara Partemi, Jesus Mates, Bernat Del Olmo, Oscar Campuzano, Vincenzo Pascali, Anna Iglesias, Pasquale Striano, Antonio Oliva, Ramon Brugada
Sudden unexpected death in epilepsy (SUDEP) is defined as the abrupt, no traumatic, witnessed or unwitnessed death, occurring in benign circumstances, in an individual with epilepsy, with or without evidence for a seizure and excluding documented status epilepticus (seizure duration ≥ 30 min or seizures without recovery), and in which postmortem examination does not reveal a cause of death. Although the physiopathological mechanisms that underlie SUDEP remain to be clarified, the genetic background has been described to play a role in this disorder...
March 2016: International Journal of Legal Medicine
https://www.readbyqxmd.com/read/26194361/carboplatin-taxane-induced-gastrointestinal-toxicity-a-pharmacogenomics-study-on-the-scotroc1-trial
#19
Y J He, S J Winham, J M Hoskins, S Glass, J Paul, R Brown, A Motsinger-Reif, H L McLeod
Carboplatin/taxane combination is first-line therapy for ovarian cancer. However, patients can encounter treatment delays, impaired quality of life, even death because of chemotherapy-induced gastrointestinal (GI) toxicity. A candidate gene study was conducted to assess potential association of genetic variants with GI toxicity in 808 patients who received carboplatin/taxane in the Scottish Randomized Trial in Ovarian Cancer 1 (SCOTROC1). Patients were randomized into discovery and validation cohorts consisting of 404 patients each...
June 2016: Pharmacogenomics Journal
https://www.readbyqxmd.com/read/26167069/gene-polymorphisms-associated-with-functional-dyspepsia
#20
REVIEW
Anastasia Kourikou, George P Karamanolis, George D Dimitriadis, Konstantinos Triantafyllou
Functional dyspepsia (FD) is a constellation of functional upper abdominal complaints with poorly elucidated pathophysiology. However, there is increasing evidence that susceptibility to FD is influenced by hereditary factors. Genetic association studies in FD have examined genotypes related to gastrointestinal motility or sensation, as well as those related to inflammation or immune response. G-protein b3 subunit gene polymorphisms were first reported as being associated with FD. Thereafter, several gene polymorphisms including serotonin transporter promoter, interlukin-17F, migration inhibitory factor, cholecystocynine-1 intron 1, cyclooxygenase-1, catechol-o-methyltransferase, transient receptor potential vanilloid 1 receptor, regulated upon activation normal T cell expressed and secreted, p22PHOX, Toll like receptor 2, SCN10A, CD14 and adrenoreceptors have been investigated in relation to FD; however, the results are contradictory...
July 7, 2015: World Journal of Gastroenterology: WJG
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