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https://www.readbyqxmd.com/read/28107665/a-%C3%AF-%C3%AF-conjugation-containing-soft-and-conductive-injectable-polymer-hydrogel-highly-efficiently-rebuilds-cardiac-function-after-myocardial-infarction
#1
Rui Bao, Baoyu Tan, Shuang Liang, Ning Zhang, Wei Wang, Wenguang Liu
Previous studies suggested that a stiffer hydrogel system exhibited a better performance to promote heart function after myocardial infarction (MI). However, the nature of myocardium, a tissue that alternately contracts and relaxes with electrical impulses, leads us to hypothesize that a soft and conductive hydrogel may be in favor of mechanical and electrical signals transmission to enhance heart function after MI. In this work, π-π conjugation interaction was first employed to produce a soft injectable hydrogel with conductive property...
January 12, 2017: Biomaterials
https://www.readbyqxmd.com/read/28100454/gene-therapy-targeting-oligodendrocytes-provides-therapeutic-benefit-in-a-leukodystrophy-model
#2
Elena Georgiou, Kyriaki Sidiropoulou, Jan Richter, Christos Papaneophytou, Irene Sargiannidou, Alexia Kagiava, Georg von Jonquieres, Christina Christodoulou, Matthias Klugmann, Kleopas A Kleopa
Pelizaeus-Merzbacher-like disease or hypomyelinating leukodystrophy-2 is an autosomal recessively inherited leukodystrophy with childhood onset resulting from mutations in the gene encoding the gap junction protein connexin 47 (Cx47, encoded by GJC2). Cx47 is expressed specifically in oligodendrocytes and is crucial for gap junctional communication throughout the central nervous system. Previous studies confirmed that a cell autonomous loss-of-function mechanism underlies hypomyelinating leukodystrophy-2 and that transgenic oligodendrocyte-specific expression of another connexin, Cx32 (GJB1), can restore gap junctions in oligodendrocytes to achieve correction of the pathology in a disease model...
January 18, 2017: Brain: a Journal of Neurology
https://www.readbyqxmd.com/read/28098880/the-role-of-gap-junctions-in-inflammatory-and-neoplastic-disorders-review
#3
Pui Wong, Victoria Laxton, Saurabh Srivastava, Yin Wah Fiona Chan, Gary Tse
Gap junctions are intercellular channels made of connexin proteins, mediating both electrical and biochemical signals between cells. The ability of gap junction proteins to regulate immune responses, cell proliferation, migration, apoptosis and carcinogenesis makes them attractive therapeutic targets for treating inflammatory and neoplastic disorders in different organ systems. Alterations in gap junction profile and expression levels are observed in hyperproliferative skin disorders, lymphatic vessel diseases, inflammatory lung diseases, liver injury and neoplastic disorders...
January 17, 2017: International Journal of Molecular Medicine
https://www.readbyqxmd.com/read/28096472/myosin-vi-facilitates-connexin-43-gap-junction-accretion
#4
Bennett Waxse, Prabuddha Sengupta, Geoffrey G Hesketh, Jennifer Lippincott-Schwartz, Folma Buss
In this study, we demonstrate myosin VI enrichment at Cx43 gap junctions in heart tissue, primary cardiomyocytes and cell culture models. The loss of myosin VI via siRNA-mediated knock down or isolation of primary cardiac tissue and fibroblasts from the myosin VI-null mouse results in reduced GJ plaque size with a concomitant reduction in intercellular communication as shown by FRAP and a new method of selective calcein administration. Analysis of the molecular role of myosin VI in Cx43 trafficking indicates that myosin VI is dispensable in the delivery of Cx43 to the cell surface and connexon movement in the plasma membrane...
January 17, 2017: Journal of Cell Science
https://www.readbyqxmd.com/read/28096261/tuning-collective-cell-migration-by-cell-cell-junction-regulation
#5
Peter Friedl, Roberto Mayor
Collective cell migration critically depends on cell-cell interactions coupled to a dynamic actin cytoskeleton. Important cell-cell adhesion receptor systems implicated in controlling collective movements include cadherins, immunoglobulin superfamily members (L1CAM, NCAM, ALCAM), Ephrin/Eph receptors, Slit/Robo, connexins and integrins, and an adaptive array of intracellular adapter and signaling proteins. Depending on molecular composition and signaling context, cell-cell junctions adapt their shape and stability, and this gradual junction plasticity enables different types of collective cell movements such as epithelial sheet and cluster migration, branching morphogenesis and sprouting, collective network migration, as well as coordinated individual-cell migration and streaming...
January 17, 2017: Cold Spring Harbor Perspectives in Biology
https://www.readbyqxmd.com/read/28096061/connexin37-deficiency-alters-organic-bone-matrix-cortical-bone-geometry-and-increases-wnt-%C3%AE-catenin-signaling
#6
Rafael Pacheco-Costa, Jay R Kadakia, Emily G Atkinson, Joseph M Wallace, Lilian I Plotkin, Rejane D Reginato
Deletion of connexin (Cx) 37 in mice leads to increased cancellous bone mass due to defective osteoclast differentiation. Paradoxically; however, Cx37-deficient mice exhibit reduced cortical thickness accompanied by higher bone strength, suggesting a contribution of Cx37 to bone matrix composition. Thus, we investigated whether global deletion of Cx37 alters the composition of organic bone extracellular matrix. Five-month-old Cx37(-/-) mice exhibited increased marrow cavity area, and periosteal and endocortical bone surface resulting in higher total area in tibia compared to Cx37(+/+) control mice...
January 13, 2017: Bone
https://www.readbyqxmd.com/read/28089824/mitochondrial-uncoupling-protein-2-in-human-cumulus-cells-is-associated-with-regulating-autophagy-and-apoptosis-maintaining-gap-junction-integrity-and-progesterone-synthesis
#7
Hongshan Ge, Fan Zhang, Duan Ping, Nan Zhu, Jiayan Zhang, Feijun Ye, Dan Shan, Hua Chen, XiaoSheng Lu, ChunFang Zhu, Renshan Ge, Zhenkun Lin
To explore the roles of mitochondrial Uncoupling Protein 2 (UCP2) in cumulus cells (CCs), human CCs were cultured in vitro, and the UCP2 was inhibited by treatment with Genipin, a special UCP inhibitor, or by RNA interference targeting UCP2. No significant differences in adenosine triphosphate levels and the ratio of ADP/ATP were observed after UCP2 inhibition. UCP2 inhibition caused a significant increase in cellular oxidative damage, which was reflected in alterations to several key parameters, including reactive oxygen species (ROS) and lipid peroxidation levels and the ratio of reduced GSH to GSSG...
January 12, 2017: Molecular and Cellular Endocrinology
https://www.readbyqxmd.com/read/28086997/enamel-renal-syndrome-in-2-patients-with-a-mutation-in-fam20-a-and-atypical-hypertrichosis-and-hearing-loss-phenotypes
#8
Sabina Pena B Pêgo, Ricardo D Coletta, Simona Dumitriu, Daniela Iancu, Saleh Albanyan, Robert Kleta, Maria Teresa Auricchio, Luis Antônio Santos, Breno Rocha, Hercílio Martelli-Júnior
Enamel-renal syndrome (OMIM #204690) is an uncommon disorder characterized by amelogenesis imperfecta and nephrocalcinosis and is caused by mutations in FAM20 A. We report 2 patients with enamel-renal syndrome who exhibited the typical features of this syndrome and a homozygous nonsense mutation in the FAM20 A gene (c.406 C>T), genetically confirming the diagnosis. They also exhibited 2 undescribed clinical features, hypertrichosis and hearing loss. Alterations in genes frequently associated with nonsyndromic hearing loss in the Brazilian population, including connexin 26 (GJB2), connexin 30 (GJB6) and mitochondrial 12 S rRNA (m...
February 2017: Oral Surgery, Oral Medicine, Oral Pathology and Oral Radiology
https://www.readbyqxmd.com/read/28081514/role-of-mirna-1-in-regulating-connexin-43-in-ischemia-reperfusion-heart-injury-a-rat-model
#9
Bo Bian, Xue-Fang Yu, Guo-Qin Wang, Tian-Ming Teng
MiRNA-1 may participate in regulating ischemia-reperfusion injury (IRI) by affecting the expression and distribution of connexin 43 (Cx43). The aim of this study is to investigate miR-1 expression and its potential role in regulating Cx43 during ischemic postconditioning (IPOST) in a rat model. Fifty-five Wistar male rats were randomly divided into five groups: N, IR, IPOST, agomir-1, and antagomir-1 group. The hearts were perfused with the Langendorff system. The reperfusion arrhythmia (RA) and myocardial infarct size were observed and recorded...
January 3, 2017: Cardiovascular Pathology: the Official Journal of the Society for Cardiovascular Pathology
https://www.readbyqxmd.com/read/28077706/connexin-mediated-signaling-in-nonsensory-cells-is-crucial-for-the-development-of-sensory-inner-hair-cells-in-the-mouse-cochlea
#10
Stuart L Johnson, Federico Ceriani, Oliver Houston, Roman Polishchuk, Elena Polishchuk, Giulia Crispino, Veronica Zorzi, Fabio Mammano, Walter Marcotti
: Mutations in the genes encoding for gap junction proteins connexin 26 (Cx26) and connexin 30 (Cx30) have been linked to syndromic and nonsyndromic hearing loss in mice and humans. The release of ATP from connexin hemichannels in cochlear nonsensory cells has been proposed to be the main trigger for action potential activity in immature sensory inner hair cells (IHCs), which is crucial for the refinement of the developing auditory circuitry. Using connexin knock-out mice, we show that IHCs fire spontaneous action potentials even in the absence of ATP-dependent intercellular Ca(2+) signaling in the nonsensory cells...
January 11, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/28077322/a-protein-kinase-a-ezrin-complex-regulates-connexin-43-gap-junction-communication-in-liver-epithelial-cells
#11
Aleksandra R Dukic, Linda Hofstad Haugen, Guillaume Pidoux, Edward Leithe, Oddmund Bakke, Kjetil Taskén
Communication between adjacent cells can occur via gap junctions (GJ) composed of connexin (Cx) hexamers that allow passage of small molecules. One of the most widely and highly expressed Cxs in human tissues is Cx43, shown to be regulated through phosphorylation by several kinases including PKA. Ezrin is a membrane associated protein that can serve as an A-kinase anchoring protein (AKAP) and hold an anchored pool of PKA. Here, we used the liver epithelial cell line IAR20, which expresses Cx43 as the predominant GJ protein, to test the hypothesis that Ezrin may associate with Cx43 in cell types that form stable GJs and serve as an AKAP...
January 8, 2017: Cellular Signalling
https://www.readbyqxmd.com/read/28076398/identification-of-a-novel-mutation-in-brd4-that-causes-autosomal-dominant-syndromic-congenital-cataracts-associated-with-other-neuro-skeletal-anomalies
#12
Hyun-Seok Jin, Jeonhyun Kim, Woori Kwak, Hyeonsoo Jeong, Gyu-Bin Lim, Cha Gon Lee
Congenital cataracts can occur as a non-syndromic isolated ocular disease or as a part of genetic syndromes accompanied by a multi-systemic disease. Approximately 50% of all congenital cataract cases have a heterogeneous genetic basis. Here, we describe three generations of a family with an autosomal dominant inheritance pattern and common complex phenotypes, including bilateral congenital cataracts, short stature, macrocephaly, and minor skeletal anomalies. We did not find any chromosomal aberrations or gene copy number abnormalities using conventional genetic tests; accordingly, we conducted whole-exome sequencing (WES) to identify disease-causing genetic alterations in this family...
2017: PloS One
https://www.readbyqxmd.com/read/28075455/tnf%C3%A2-%C3%AE-regulates-apoptosis-of-human-vascular-smooth-muscle-cells-through-gap-junctions
#13
Mei Tang, Jun Fang
Inflammatory cytokines are released by immune cells and are able to induce vascular smooth muscle cells (VSMCs) to undergo apoptosis, causing atherosclerotic plaque rupture. Changes in the expression levels of connexins (Cxs) have been demonstrated in VSMCs to be involved in the pathogenesis of atherosclerotic progression. The present study examined the effect of tumor necrosis factor‑α (TNF‑α) on Cx43 expression levels and apoptosis in human VSMCs. Overexpression of Cx43 plasmids notably stimulated VSMC proliferation...
January 5, 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/28075020/adenosine-receptors-regulate-gap-junction-coupling-of-the-human-cerebral-microvascular-endothelial-cells-hcmec-d3-by-ca-2-influx-through-cng-channels
#14
Almke Bader, Willem Bintig, Daniela Begandt, Anne Klett, Ina G Siller, Carola Gregor, Frank Schaarschmidt, Babette Weksler, Ignacio Romero, Pierre-Olivier Couraud, Stefan W Hell, Anaclet Ngezahayo
The human cerebral microvascular endothelial cell line hCMEC/D3 was used to characterize the physiological link between adenosine receptors and the gap junction coupling in endothelial cells of the blood-brain barrier. Expressed adenosine receptor subtypes and connexin (Cx) isoforms were identified by RT-PCR. Scrape loading/dye transfer was used to evaluate the impact of the A2A and A2B adenosine receptor subtype agonist 2-phenylaminoadenosine (2-PAA) on the gap junction coupling. We found that 2-PAA stimulated cAMP synthesis and enhanced gap junction coupling in a concentration-dependent manner...
January 11, 2017: Journal of Physiology
https://www.readbyqxmd.com/read/28074341/gap-junction-protein-connexin43-deregulation-contributes-to-bladder-carcinogenesis-via-targeting-mapk-pathway
#15
Xiao-Lin Ai, Qiang Chi, Yu Qiu, Hong-Yang Li, Dong-Jie Li, Jia-Xu Wang, Zhi-Yong Wang
High expression of connexins was found in a variety of cancers, but their role is still controversial. We investigated whether connexin43 (Cx43) contributed to bladder carcinogenesis through MAPK activation. In this study, we found that Cx43 expression was significantly increased in bladder cancer tissues and cell line. Overexpression of Cx43 in bladder cancer 5637 cells increased cell proliferation, promoted cell cycle progression, and inhibited apoptosis. Western blot showed that JNK and ERK pathways were dramatically activated in Cx43-overexpressed cells...
January 10, 2017: Molecular and Cellular Biochemistry
https://www.readbyqxmd.com/read/28071741/loss-of-coupling-distinguishes-gjb1-mutations-associated-with-cns-manifestations-of-cmt1x-from-those-without-cns-manifestations
#16
Charles K Abrams, Mikhail Goman, Sarah Wong, Steven S Scherer, Kleopas A Kleopa, Alejandro Peinado, Mona M Freidin
CMT1X, an X-linked inherited neuropathy, is caused by mutations in GJB1, which codes for Cx32, a gap junction protein expressed by Schwann cells and oligodendrocytes. Many GJB1 mutations cause central nervous system (CNS) abnormality in males, including stable subclinical signs and, less often, short-duration episodes characterized by motor difficulties and altered consciousness. However, some mutations have no apparent CNS effects. What distinguishes mutations with and without CNS manifestations has been unclear...
January 10, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28069793/decreased-wnt-%C3%AE-catenin-signalling-contributes-to-the-pathogenesis-of-dilated-cardiomyopathy-caused-by-mutations-in-the-lamin-a-c-gene
#17
Caroline Le Dour, Coline Macquart, Fusako Sera, Shunichi Homma, Gisele Bonne, John P Morrow, Howard J Worman, Antoine Muchir
Cardiomyopathy caused by lamin A/C gene (LMNA) mutations (hereafter referred as LMNA cardiomyopathy) is characterized by cardiac conduction abnormalities and left ventricular systolic dysfunction predisposing to heart failure. Previous cardiac transcriptional profiling of Lmna(H222P/H222P) mouse, a small animal model of LMNA cardiomyopathy, suggested decreased WNT/β-catenin signalling. We confirmed decreased WNT/β-catenin signalling in the hearts of these mice by demonstrating decreased β-catenin and WNT proteins...
January 9, 2017: Human Molecular Genetics
https://www.readbyqxmd.com/read/28068381/impairment-of-excitation-contraction-coupling-in-right-ventricular-hypertrophied-muscle-with-fibrosis-induced-by-pulmonary-artery-banding
#18
Yoichiro Kusakari, Takashi Urashima, Daisuke Shimura, Erika Amemiya, Genki Miyasaka, Shunsuke Yokota, Yoshitaka Fujimoto, Toru Akaike, Takahiro Inoue, Susumu Minamisawa
Interstitial myocardial fibrosis is one of the factors responsible for dysfunction of the heart. However, how interstitial fibrosis affects cardiac function and excitation-contraction coupling (E-C coupling) has not yet been clarified. We developed an animal model of right ventricular (RV) hypertrophy with fibrosis by pulmonary artery (PA) banding in rats. Two, four, and six weeks after the PA-banding operation, the tension and intracellular Ca2+ concentration of RV papillary muscles were simultaneously measured (n = 33)...
2017: PloS One
https://www.readbyqxmd.com/read/28066916/ammonia-mediates-cortical-hemichannel-dysfunction-in-rodent-models-of-chronic-liver-disease
#19
Anna Hadjihambi, Francesco De Chiara, Patrick S Hosford, Abeba Habtetion, Anastassios Karagiannis, Nathan Davies, Alexander V Gourine, Rajiv Jalan
: The pathogenesis of hepatic encephalopathy (HE) in cirrhosis is multifactorial and ammonia is thought to play a key role. Astroglial dysfunction is known to be present in HE. Astrocytes are extensively connected by gap junctions formed of connexins, which also exist as functional hemichannels allowing exchange of molecules between the cytoplasm and the extracellular milieu. The astrocyte-neuron lactate shuttle hypothesis suggests that neuronal activity is fuelled (at least in part) by lactate provided by neighbouring astrocytes...
January 9, 2017: Hepatology: Official Journal of the American Association for the Study of Liver Diseases
https://www.readbyqxmd.com/read/28066889/enteric-glial-activity-regulates-secretomotor-function-in-the-mouse-colon-but-does-not-acutely-affect-gut-permeability
#20
Vladimir Grubišić, Brian D Gulbransen
Enteric glial cells are often implicated in the regulation of epithelial barrier and secretomotor functions of the intestines. But whether glial cell activity regulates these functions acutely under physiological conditions is not clear. We addressed this issue by using transgenic animal models to modify the activity of enteric glia, either reducing glial expression of connexin 43 in Sox10::CreER(T2+/-) /Cx43(f/f) mice or activating glial calcium responses in GFAP::hM3Dq mice, and tested the effects on colonic barrier function and electrogenic ion transport in Ussing chambers...
January 8, 2017: Journal of Physiology
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