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https://www.readbyqxmd.com/read/29768048/hypoxic-stress-up-regulates-kir2-1-expression-by-a-pathway-including-hypoxic-inducible-factor-1-and-dynamin2-in-brain-capillary-endothelial-cells
#1
Hideto Yamamura, Yoshiaki Suzuki, Hisao Yamamura, Kiyofumi Asai, Wayne Giles, Yuji Imaizumi
Brain capillary endothelial cells (BCECs) play a central role in maintenance of blood-brain barrier (BBB) function and therefore are essential for central nervous system homeostasis and integrity. Although brain ischemia damages BCECs and causes disruption of BBB, the related influence of hypoxia on BCECs is not well understood. Hypoxic stress can up-regulate functional expression of specific K+ currents in endothelial cells, e.g., Kir2.1 channels without any alterations in the mRNA level, in t-BBEC117, a cell line derived from bovine BCECs...
May 16, 2018: American Journal of Physiology. Cell Physiology
https://www.readbyqxmd.com/read/29719087/regulation-of-inward-rectifier-potassium-current-ionic-channel-remodeling-by-at-1-calcineurin-nfat-signaling-pathway-in-stretch-induced-hypertrophic-atrial-myocytes
#2
Jionghong He, Yanan Xu, Long Yang, Guiling Xia, Na Deng, Yongyao Yang, Ye Tian, Zenan Fu, Yongqi Huang
Previous studies have shown that the activation of angiotensin II receptor type I (AT1 ) is attributed to cardiac remodeling stimulated by increased heart load, and that it is followed by the activation of the calcineurin-nuclear factor of activated T-cells (NFAT) signaling pathway. Additionally, AT1 has been found to be a regulator of cardiocyte ionic channel remodeling, and calcineurin-NFAT signals participate in the regulation of cardiocyte ionic channel expression. A hypothesis therefore follows that stretch stimulation may regulate cardiocyte ionic channel remodeling by activating the AT1 -calcineurin-NFAT pathway...
May 2, 2018: Cell Biology International
https://www.readbyqxmd.com/read/29650538/kir-channel-blockages-by-proflavine-derivatives-via-multiple-modes-of-interaction
#3
Atsushi Inanobe, Hideaki Itamochi, Yoshihisa Kurachi
Many compounds inhibit tetrameric and pseudo-tetrameric cation channels by associating with the central cavity located in the middle of the membrane plane. They traverse the ion conduction pathway from intracellular side and access to the cavity. Previously we reported that the bacteriostatic agent, proflavine, preferentially blocked a subset of Kir channels. However, the development of the inhibition of Kir1.1 by the compound was obviously different from that operating in Kir3.2 as a pore blocker. To gain mechanistic insights into the compound-channel interaction, we analyzed its chemical specificity, subunit selectivity, and voltage dependency using 13 different combinations of Kir-channel family members and 11 proflavine derivatives...
April 12, 2018: Molecular Pharmacology
https://www.readbyqxmd.com/read/29615871/a-novel-kcnj2-mutation-identified-in-an-autistic-proband-affects-the-single-channel-properties-of-kir2-1
#4
Anna Binda, Ilaria Rivolta, Chiara Villa, Elisa Chisci, Massimiliano Beghi, Cesare M Cornaggia, Roberto Giovannoni, Romina Combi
Inwardly rectifying potassium channels (Kir) have been historically associated to several cardiovascular disorders. In particular, loss-of-function mutations in the Kir2.1 channel have been reported in cases affected by Andersen-Tawil syndrome while gain-of-function mutations in the same channel cause the short QT3 syndrome. Recently, a missense mutation in Kir2.1, as well as mutations in the Kir4.1, were reported to be involved in autism spectrum disorders (ASDs) suggesting a role of potassium channels in these diseases and introducing the idea of the existence of K+ channel ASDs...
2018: Frontiers in Cellular Neuroscience
https://www.readbyqxmd.com/read/29581290/osr1-regulates-a-subset-of-inward-rectifier-potassium-channels-via-a-binding-motif-variant
#5
Clinton A Taylor, Sung-Wan An, Sachith Gallolu Kankanamalage, Steve Stippec, Svetlana Earnest, Ashesh T Trivedi, Jonathan Zijiang Yang, Hamid Mirzaei, Chou-Long Huang, Melanie H Cobb
The with-no-lysine (K) (WNK) signaling pathway to STE20/SPS1-related proline- and alanine-rich kinase (SPAK) and oxidative stress-responsive 1 (OSR1) kinase is an important mediator of cell volume and ion transport. SPAK and OSR1 associate with upstream kinases WNK 1-4, substrates, and other proteins through their C-terminal domains which interact with linear R-F-x-V/I sequence motifs. In this study we find that SPAK and OSR1 also interact with similar affinity with a motif variant, R-x-F-x-V/I. Eight of 16 human inward rectifier K+ channels have an R-x-F-x-V motif...
April 10, 2018: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/29581272/endothelial-gqpcr-activity-controls-capillary-electrical-signaling-and-brain-blood-flow-through-pip-2-depletion
#6
Osama F Harraz, Thomas A Longden, Fabrice Dabertrand, David Hill-Eubanks, Mark T Nelson
Brain capillaries play a critical role in sensing neural activity and translating it into dynamic changes in cerebral blood flow to serve the metabolic needs of the brain. The molecular cornerstone of this mechanism is the capillary endothelial cell inward rectifier K+ (Kir2.1) channel, which is activated by neuronal activity-dependent increases in external K+ concentration, producing a propagating hyperpolarizing electrical signal that dilates upstream arterioles. Here, we identify a key regulator of this process, demonstrating that phosphatidylinositol 4,5-bisphosphate (PIP2 ) is an intrinsic modulator of capillary Kir2...
March 26, 2018: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/29571612/kir2-1-is-important-for-efficient-bmp-signaling-in-mammalian-face-development
#7
Matthew T Belus, Madison A Rogers, Alaaeddin Elzubeir, Megan Josey, Steven Rose, Viktoria Andreeva, Pamela C Yelick, Emily A Bates
Mutations that disrupt the inwardly rectifying potassium channel Kir2.1 lead to Andersen-Tawil syndrome that includes periodic paralysis, cardiac arrhythmia, cognitive deficits, craniofacial dysmorphologies and limb defects. The molecular mechanism that underlies the developmental consequences of inhibition of these channels has remained a mystery. We show that while loss of Kir2.1 function does not affect expression of several early facial patterning genes, the domain in which Pou3f3 is expressed in the maxillary arch is reduced...
March 20, 2018: Developmental Biology
https://www.readbyqxmd.com/read/29549164/kir2-1-interaction-with-stk38-promotes-invasion-and-metastasis-of-human-gastric-cancer-by-enhancing-mekk2-mek1-2-erk1-2-signaling
#8
Cheng-Dong Ji, Yan-Xia Wang, Dong-Fang Xiang, Qiang Liu, Zhi-Hua Zhou, Feng Qian, Lang Yang, Yong Ren, Wei Cui, Sen-Lin Xu, Xi-Long Zhao, Xia Zhang, Yan Wang, Peng Zhang, Ji-Ming Wang, You-Hong Cui, Xiu-Wu Bian
Potassium ion channels are emerging as pro-malignant factors involved in cancer progression. In this study, we found that invading human gastric cancer (GC) cells express high level of inwardly rectifying potassium channel 2.1 (Kir2.1). Silencing Kir2.1 markedly reduced the invasive and metastatic capabilities as well as the epithelial-mesenchymal transition (EMT) of GC cells. The pro-malignant nature of Kir2.1 in GC cells was independent of potassium permeation but relied on its interaction with serine/threonine-protein kinase 38 (Stk38) to inhibit ubiquitination and degradation of mitogen-activated protein kinase kinase kinase 2 (MEKK2)...
March 16, 2018: Cancer Research
https://www.readbyqxmd.com/read/29514831/cardiac-kir2-1-and-na-v-1-5-channels-traffic-together-to-the-sarcolemma-to-control-excitability
#9
Daniela Ponce-Balbuena, Guadalupe Guerrero-Serna, Carmen R Valdivia, Ricardo Caballero, F J Díez-Guerra, Eric N Jiménez-Vázquez, Rafael J Ramirez, Andre Monteiro da Rocha, Todd J Herron, Katherine F Campbell, B C Willis, Francisco J Alvarado, Manuel Zarzoso, Kuljeet Kaur, Marta Pérez-Hernández, Marcos Matamoros, Héctor H Valdivia, Eva Delpón, José Jalife
<u>Rationale:</u> In cardiomyocytes, NaV 1.5 and Kir2.1 channels interact dynamically as part of membrane bound macromolecular complexes. <u>Objective:</u> To test whether NaV 1.5 and Kir2.1 preassemble during early forward trafficking and travel together to common membrane microdomains. <u>Methods and Results:</u> In patch-clamp experiments, co-expression of trafficking deficient mutants Kir2.1Δ314-315 or Kir2.1R44A/R46A with wildtype (WT) NaV 1.5WT in heterologous cells reduced INa , compared to NaV 1...
March 7, 2018: Circulation Research
https://www.readbyqxmd.com/read/29502108/regulation-of-kir2-1-function-under-shear-stress-and-cholesterol-loading
#10
EDITORIAL
Nhat-Tu Le, Jun-Ichi Abe
No abstract text is available yet for this article.
March 3, 2018: Journal of the American Heart Association
https://www.readbyqxmd.com/read/29502106/hypercholesterolemia-induced-loss-of-flow-induced-vasodilation-and-lesion-formation-in-apolipoprotein-e-deficient-mice-critically-depend-on-inwardly-rectifying-k-channels
#11
Ibra S Fancher, Sang Joon Ahn, Crystal Adamos, Catherine Osborn, Myung-Jin Oh, Yun Fang, Catherine A Reardon, Godfrey S Getz, Shane A Phillips, Irena Levitan
BACKGROUND: Hypercholesterolemia-induced decreased availability of nitric oxide (NO) is a major factor in cardiovascular disease. We previously established that cholesterol suppresses endothelial inwardly rectifying K+ (Kir) channels and that Kir2.1 is an upstream mediator of flow-induced NO production. Therefore, we tested the hypothesis that suppression of Kir2.1 is responsible for hypercholesterolemia-induced inhibition of flow-induced NO production and flow-induced vasodilation (FIV)...
March 3, 2018: Journal of the American Heart Association
https://www.readbyqxmd.com/read/29405004/genetically-encoding-unnatural-amino-acids-in-neurons-in-vitro-and-in-the-embryonic-mouse-brain-for-optical-control-of-neuronal-proteins
#12
Ji-Yong Kang, Daichi Kawaguchi, Lei Wang
Deciphering neuronal networks governing specific brain functions is a longstanding mission in neuroscience, yet global manipulation of protein functions pharmacologically or genetically lacks sufficient specificity to reveal a neuronal protein's function in a particular neuron or a circuitry. Photostimulation presents a great venue for researchers to control neuronal proteins with high temporal and spatial resolution. Recently, an approach to optically control the function of a neuronal protein directly in neurons has been demonstrated using genetically encoded light-sensitive Unnatural amino acids (Uaas)...
2018: Methods in Molecular Biology
https://www.readbyqxmd.com/read/29401592/kir2-inward-rectification-controlled-precise-and-dynamic-balances-between-kir2-and-hcn-currents-initiate-pacemaking-activity
#13
Kuihao Chen, Dongchuan Zuo, Sho-Ya Wang, Haijun Chen
Spontaneous rhythmic action potential or pacemaking activity of pacemaker cells controls rhythmic signaling such as heartbeat. The mechanism underlying the origin of pacemaking activity is not well understood. In this study, we created human embryonic kidney (HEK) 293 cells that show pacemaking activity through heterologous expression of strong inward rectifier K+ channels (Kir2.1), hyperpolarization-activated cyclic nucleotide-gated nonselective cation channels (HCN2), and voltage-gated Na+ or Ca2+ channels (Nav 1...
January 12, 2018: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/29358197/impact-of-renal-denervation-on-atrial-arrhythmogenic-substrate-in-ischemic-model-of-heart-failure
#14
Shinya Yamada, Man-Cai Fong, Ya-Wen Hsiao, Shih-Lin Chang, Yung-Nan Tsai, Li-Wei Lo, Tze-Fan Chao, Yenn-Jiang Lin, Yu-Feng Hu, Fa-Po Chung, Jo-Nan Liao, Yao-Ting Chang, Hsing-Yuan Li, Satoshi Higa, Shih-Ann Chen
BACKGROUND: Myocardial infarction increases the risk of heart failure (HF) and atrial fibrillation. Renal denervation (RDN) might suppress the development of atrial remodeling. This study aimed to elucidate the molecular mechanism of RDN in the suppression of atrial fibrillation in a HF model after myocardial infarction. METHODS AND RESULTS: HF rabbits were created 4 weeks after coronary ligation. Rabbits were classified into 3 groups: normal control (n=10), HF (n=10), and HF-RDN (n=6)...
January 22, 2018: Journal of the American Heart Association
https://www.readbyqxmd.com/read/29355592/down-regulation-of-inwardly-rectifying-k-currents-in-astrocytes-derived-from-patients-with-monge-s-disease
#15
Wei Wu, Hang Yao, Helen W Zhao, Juan Wang, Gabriel G Haddad
Chronic mountain sickness (CMS) or Monge's disease is a disease in highlanders. These patients have a variety of neurologic symptoms such as migraine, mental fatigue, confusion, dizziness, loss of appetite, memory loss and neuronal degeneration. The cellular and molecular mechanisms underlying CMS neuropathology is not understood. In the previous study, we demonstrated that neurons derived from CMS patients' fibroblasts have a decreased expression and altered gating properties of voltage-gated sodium channel...
March 15, 2018: Neuroscience
https://www.readbyqxmd.com/read/29339676/electrical-and-histological-remodeling-of-the-pulmonary-vein-in-2k1c-hypertensive-rats-indication-of-initiation-and-maintenance-of-atrial-fibrillation
#16
Pan Pan Xia, Lian Jing Li, Run Di Qi, Jiao Jiao Shi, Wei Zhu Ju, Ming Long Chen
OBJECTIVE: Hypertension is a significant risk factor for atrial fibrillation (AF). The role of pulmonary vein (PV) remodeling in the mechanistic association between hypertension and AF is not definitive. In this study, we aimed to identify changes in the electrophysiology and histology in PVs in two-kidney, one-clip (2K1C) hypertensive rats. METHODS: Fifty male Sprague-Dawley rats were classified into the 2K1C and sham-operated groups. The systolic blood pressure was measured every 2 weeks...
January 17, 2018: Anatolian Journal of Cardiology
https://www.readbyqxmd.com/read/29326130/inward-rectifier-potassium-channels-kir2-x-and-caveolin-3-domain-specific-interaction-implications-for-purkinje-cell-dependent-ventricular-arrhythmias
#17
Ravi Vaidyanathan, Hanora Van Ert, Kazi T Haq, Stefano Morotti, Samuel Esch, Elise C McCune, Eleonora Grandi, Lee L Eckhardt
BACKGROUND: In human cardiac ventricle, I K1 is mainly comprised Kir2.1, but Kir2.2 and Kir2.3 heterotetramers occur and modulate I K1 . Long-QT syndrome-9-associated CAV3 mutations cause decreased Kir2.1 current density, but Kir2.x heterotetramers have not been studied. Here, we determine the effect of long-QT syndrome-9- CAV3 mutation F97C on Kir2.x homo- and heterotetramers and model-associated arrhythmia mechanisms. METHODS AND RESULTS: Super-resolution microscopy, co-immunoprecipitation, cellular electrophysiology, on-cell Western blotting, and simulation of Purkinje and ventricular myocyte mathematical models were used...
January 2018: Circulation. Arrhythmia and Electrophysiology
https://www.readbyqxmd.com/read/29317494/hydrogen-sulfide-inhibits-kir2-and-kir3-channels-by-decreasing-sensitivity-to-the-phospholipid-phosphatidylinositol-4-5-bisphosphate-pip-2
#18
Junghoon Ha, Yu Xu, Takeharu Kawano, Tyler Hendon, Lia Baki, Sumanta Garai, Andreas Papapetropoulos, Ganesh A Thakur, Leigh D Plant, Diomedes E Logothetis
Inwardly rectifying potassium (Kir) channels establish and regulate the resting membrane potential of excitable cells in the heart, brain, and other peripheral tissues. Phosphatidylinositol 4,5-bisphosphate (PIP2 ) is a key direct activator of ion channels, including Kir channels. The gasotransmitter carbon monoxide has been shown to regulate Kir channel activity by altering channel-PIP2 interactions. Here, we tested in two cellular models the effects and mechanism of action of another gasotransmitter, hydrogen sulfide (H2 S), thought to play a key role in cellular responses under ischemic conditions...
March 9, 2018: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/29290967/modelling-the-effects-of-chloroquine-on-kcnj2-linked-short-qt-syndrome
#19
Cunjin Luo, Kuanquan Wang, Henggui Zhang
A gain-of-function KCNJ2 D172N mutation in KCNJ2-encoded Kir2.1 channels underlies one form of short QT syndrome (SQT3), which is associated with increased susceptibility to arrhythmias and sudden death. Anti-malarial drug chloroquine was reported as an effective inhibitor of Kir2.1 channels. Using biophysically-detailed human ventricle computer models, this study assessed the effects of chloroquine on SQT3. The ten Tusscher et al. model of human ventricular cell action potential was modified to recapitulate functional changes in the inward rectifier K+ current ( I K1 ) due to heterozygous and homozygous forms of the D172N mutation...
December 5, 2017: Oncotarget
https://www.readbyqxmd.com/read/29282531/kir2-1-channels-set-two-levels-of-resting-membrane-potential-with-inward-rectification
#20
Kuihao Chen, Dongchuan Zuo, Zheng Liu, Haijun Chen
Strong inward rectifier K+ channels (Kir2.1) mediate background K+ currents primarily responsible for maintenance of resting membrane potential. Multiple types of cells exhibit two levels of resting membrane potential. Kir2.1 and K2P1 currents counterbalance, partially accounting for the phenomenon of human cardiomyocytes in subphysiological extracellular K+ concentrations or pathological hypokalemic conditions. The mechanism of how Kir2.1 channels contribute to the two levels of resting membrane potential in different types of cells is not well understood...
April 2018: Pflügers Archiv: European Journal of Physiology
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