Only in Titles

Search results for: CX40 (1 236aa)

paperclip

#32923963   2019/11/07 To Up

Endothelial connexins in vascular function.

Gap junctions are essential for intercellular crosstalk in blood and lymphatic vasculature. These clusters of intercellular channels ensure direct communication among endothelial cells and between endothelial and smooth muscle cells, and the synchronization of their behavior along the vascular tree. Gap junction channels are formed by connexins; six connexins form a connexon or hemichannel and the docking of two connexons result in a full gap junction channel allowing for the exchange of ions and small metabolites between neighboring cells. Recent evidence indicates that the intracellular domains of connexins may also function as an interaction platform (interactome) for other proteins, thereby regulating their function. Interestingly, fragments of Cx proteins generated by alternative internal translation were recently described, although their functions in the vascular wall remain to be uncovered. Variations in connexin expression are observed along different types of blood and lymphatic vessels; the most commonly found endothelial connexins are Cx37, Cx40, Cx43 and Cx47. Physiological studies on connexin-knockout mice demonstrated the essential roles of these channel-forming proteins in the coordination of vasomotor activity, endothelial permeability and inflammation, angiogenesis and in the maintenance of fluid balance in the body.
Aurélie Hautefort, Anna Pfenniger, Brenda R Kwak

1572 related Products with: Endothelial connexins in vascular function.

1.00 flask2ug1.00 flask100 μg96 tests1.00 flask96T2ug2ug1.00 flask2ug2ug x 20

Related Pathways

paperclip

#32710379   2020/07/24 To Up

3D Bioprinting the Cardiac Purkinje System Using Human Adipogenic Mesenchymal Stem Cell Derived Purkinje Cells.

The objective of this study was to reprogram human adipogenic mesenchymal stem cells (hADMSCs) to form Purkinje cells and to use the reprogrammed Purkinje cells to bioprint Purkinje networks.
Evan P Tracy, Brian C Gettler, Joseph S Zakhari, Robert J Schwartz, Stuart K Williams, Ravi K Birla

1955 related Products with: 3D Bioprinting the Cardiac Purkinje System Using Human Adipogenic Mesenchymal Stem Cell Derived Purkinje Cells.

1.00 flask5 x 10A5 cells/vial4 x 96-well plate1.00 flask1 mg10 ug124 wells0.1ml (1mg/ml)25 TESTS1.00 flask100 ug

Related Pathways

paperclip

#32687896   2020/07/18 To Up

Conjugated activation of myocardial-specific transcription of Gja5 by a pair of Nkx2-5-Shox2 co-responsive elements.

The sinoatrial node (SAN) is the primary pacemaker in the heart. During cardiogenesis, Shox2 and Nkx2-5 are co-expressed in the junction domain of the SAN and regulate pacemaker cell fate through a Shox2-Nkx2-5 antagonism. Cx40 is a marker of working myocardium and an Nkx2-5 transcriptional output antagonized by Shox2, but the underlying regulatory mechanisms remain elusive. Here we characterized a bona fide myocardial-specific Gja5 (coding gene of Cx40) distal enhancer consisting of a pair of Nkx2-5 and Shox2 co-bound elements in the regulatory region of Gja5. Transgenic reporter assays revealed that neither element alone, but the conjugation of both elements together, drives myocardial-specific transcription. Genetic analyses confirmed that the activation of this enhancer depends on Nkx2-5 but is inhibited by Shox2 in vivo, and its presence is essential for Gja5 expression in the myocardium but not the endothelial cells of the heart. Furthermore, chromatin conformation analysis showed an Nkx2-5-dependent loop formation between these two elements and the Gja5 promoter in vivo, indicating that Nkx2-5 bridges the conjugated activation of this enhancer by pairing the two elements to the Gja5 promoter.
Tianfang Yang, Zhen Huang, Hua Li, Linyan Wang, YiPing Chen

1240 related Products with: Conjugated activation of myocardial-specific transcription of Gja5 by a pair of Nkx2-5-Shox2 co-responsive elements.

100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized

Related Pathways

paperclip

#32650696   2020/07/10 To Up

Prolonged duration of repolarization and decreased conduction velocity in the atrial myocardium after hypothermic ischemia-reperfusion may be related to expressions of inward rectifier potassium channel 2.1 protein and connexin 40.

The study aimed to determine the role of inward rectifier potassium channel 2.1 protein and connexin 40 expressions in regulating the duration of repolarization and conduction velocity of right atrial myocardium in rats following hypothermic ischemia-reperfusion.
Youqin He, Guilong Wang, Hong Gao, Yanqiu Liu, Huayu Li, Yurong Feng, Jian Tang

1829 related Products with: Prolonged duration of repolarization and decreased conduction velocity in the atrial myocardium after hypothermic ischemia-reperfusion may be related to expressions of inward rectifier potassium channel 2.1 protein and connexin 40.

100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized

Related Pathways

paperclip

#32471989   2020/05/29 To Up

Spatio-temporal patterning of different connexins in developing and postnatal human kidneys and in nephrotic syndrome of the Finnish type (CNF).

Connexins (Cxs) are membrane-spanning proteins which enable flow of information important for kidney homeostasis. Changes in their spatiotemporal patterning characterize blood vessel abnormalities and chronic kidney diseases (CKD). We analysed spatiotemporal expression of Cx37, Cx40, Cx43 and Cx45 in nephron and glomerular cells of developing, postnatal kidneys, and nephrotic syndrome of the Finnish type (CNF) by using immunohistochemistry, statistical methods and electron microscopy. During kidney development, strong Cx45 expression in proximal tubules and decreasing expression in glomeruli was observed. In developing distal nephron, Cx37 and Cx40 showed moderate-to-strong expression, while weak Cx43 expression gradually increased. Cx45/Cx40 co-localized in mesangial and granular cells. Cx43 /Cx45 co-localized in podocytes, mesangial and parietal epithelial cells, and with podocyte markers (synaptopodin, nephrin). Different Cxs co-expressed with endothelial (CD31) and VSMC (α -SMA) markers in vascular walls. Peak signalling of Cx37, Cx43 and Cx40 accompanied kidney nephrogenesis, while strongest Cx45 signalling paralleled nephron maturation. Spatiotemporal Cxs patterning indicate participation of Cx45 in differentiation of proximal tubules, and Cx43, Cx37 and Cx40 in distal tubules differentiation. CNF characterized disorganized Cx45 expression in proximal tubules, increased Cx43 expression in distal tubules and overall elevation of Cx40 and Cx37, while Cx40 co-localized with increased number of interstitial myofibroblasts.
Ivona Kosovic, Natalija Filipovic, Benjamin Benzon, Katarina Vukojevic, Marijan Saraga, Merica Glavina Durdov, Ivana Bocina, Mirna Saraga-Babic

2601 related Products with: Spatio-temporal patterning of different connexins in developing and postnatal human kidneys and in nephrotic syndrome of the Finnish type (CNF).

100 μg96T1 mg10 ug50ul100 μg100 μg100 μg100 1 kit(96 Wells)1 mg

Related Pathways

paperclip

#32347164   2020/04/29 To Up

ZO-1 Regulates Intercalated Disc Composition and Atrioventricular Node Conduction.

ZO-1 (Zona occludens 1), encoded by the tight junction protein 1 () gene, is a regulator of paracellular permeability in epithelia and endothelia. ZO-1 interacts with the actin cytoskeleton, gap, and adherens junction proteins and localizes to intercalated discs in cardiomyocytes. However, the contribution of ZO-1 to cardiac physiology remains poorly defined.
Wenli Dai, Rangarajan D Nadadur, Jaclyn A Brennan, Heather L Smith, Kaitlyn M Shen, Margaret Gadek, Brigitte Laforest, Mingyi Wang, Joanna Gemel, Ye Li, Jing Zhang, Bruce D Ziman, Jiajie Yan, Xun Ai, Eric C Beyer, Edward G Lakata, Narayanan Kasthuri, Igor R Efimov, Michael T Broman, Ivan P Moskowitz, Le Shen, Christopher R Weber

2930 related Products with: ZO-1 Regulates Intercalated Disc Composition and Atrioventricular Node Conduction.

25 mg10 mg100ul100 mg100μg1 mg50 mg100ug10 mg100ug100 mg1000 tests

Related Pathways

paperclip

#32270355   2020/04/08 To Up

Vascular smooth muscle cell phenotypic transition regulates gap junctions of cardiomyocyte.

Atrial fibrillation (AF) is one of the most prevalent arrhythmias. Myocardial sleeves of the pulmonary vein are critical in the occurrence of AF. Our study aims to investigate the effect of synthetic vascular smooth muscle cells (SMCs) on gap junction proteins in cardiomyocytes. (1) Extraction of vascular SMCs from the pulmonary veins of Norway rats. TGF-β was used to induce the vascular SMCs switching to the synthetic phenotype and 18-α-GA was used to inhibit gap junctions of SMCs. The contractile and synthetic phenotype vascular SMCs were cocultured with HL-1 cells; (2) Western blotting was used to detect the expression of Cx43, Cx40 and Cx45 in HL-1 cells, and RT-PCR to test microRNA 27b in vascular SMCs or in HL-1 cells; (3) Lucifer yellow dye transfer experiment was used to detect the function of gap junctions. (1) TGF- β induced the vascular SMCs switching to synthetic phenotype; (2) Cx43 was significantly increased, and Cx40 and Cx45 were decreased in HL-1 cocultured with synthetic SMCs; (3) The fluorescence intensity of Lucifer yellow was higher in HL-1 cocultured with synthetic SMCs than that in the cells cocultured with contractile SMCs, which was inhibited by18-α-GA; (4) the expression of microRNA 27b was increased in HL-1 cocultured with synthetic SMCs, which was attenuated markedly by 18-α-GA. (5) the expression of ZFHX3 was decreased in HL-1 cocultured with synthetic SMCs, which was reversed by 18-α-GA. The gap junction proteins of HL-1 were regulated by pulmonary venous SMCs undergoing phenotypic transition in this study, accompanied with the up-regulation of microRNA 27b and the down-regulation of ZFHX3 in HL-1 cells, which was associated with heterocellular gap junctions between HL-1 and pulmonary venous SMCs.
En Zhou, Tiantian Zhang, Changlong Bi, Changqian Wang, Zongqi Zhang

1927 related Products with: Vascular smooth muscle cell phenotypic transition regulates gap junctions of cardiomyocyte.

100ul200ul100ul96tests 6 ml Ready-to-use 100ul100ul1 ml100ul100ul100 μg

Related Pathways

paperclip

#31936157   2020/01/07 To Up

Rho Kinase Activity, Connexin 40, and Atrial Fibrillation: Mechanistic Insights from End-Stage Renal Disease on Dialysis Patients.

Evidence on cellular/molecular mechanisms leading to atrial fibrillation (AF) are scanty. Increased expression of Rho kinase (ROCK) and myosin-phosphatase-target subunit-1 (MYPT-1), ROCK activity's marker, were shown in AF patients, which correlated with connexin 40 (Cx40) expression, membrane protein of heart gap junctions, key for rapid action potential's cell-cell transfer. AF is the most frequent arrhythmia in dialysis patients who present increased MYPT-1 phosphorylation, which correlates with left ventricular (LV) mass. Given ROCK's established role in cardiovascular-renal remodeling, induction of impaired cell-to-cell coupling/potential conduction promoting AF initiation/perpetuation, we evaluated in dialysis patients with AF, MYPT-1 phosphorylation, Cx40 expression, and their relationships to support their involvement in AF. Mononuclear cells' MYPT-1 phosphorylation, Cx40 expression, and the ROCK inhibitor fasudil's effect were assessed in dialysis patients with AF (DPAFs), dialysis patients with sinus rhythm (DPs), and healthy subjects (C) (western blot). M-mode echocardiography assessed LV mass and left atrial systolic volume. DPAF's phospho-MYPT-1 was increased vs. that of DPs and C (1.57 ± 0.17 d.u. vs. 0.69 ± 0.04 vs. 0.51 ± 0.05 respectively, < 0.0001). DP's phospho-MYPT-1 was higher vs. that of C, = 0.009. DPAF's Cx40 was higher vs. that of DPs and C (1.23 ± 0.12 vs. 0.74 ± 0.03 vs. 0.69 ± 0.03, < 0.0001). DPAF's phospho-MYPT-1 correlated with Cx40 ( < 0.001), left atrial systolic volume ( = 0.013), and LV mass ( = 0.014). In DPAFs, fasudil reduced MYPT-1 phosphorylation ( < 0.01) and Cx40 expression ( = 0.03). These data point toward ROCK and Cx40's role in the mechanism(s) leading to AF in dialysis patients. Exploration of the ROCK pathway in AF could contribute to AF generation's mechanistic explanations and likely identify potential pharmacologic targets for translation into treatment.
Lorenzo A Calò, Verdiana Ravarotto, Giovanni Bertoldi, Elisa Pagnin, Barbara Rossi, Matteo Rigato, Paul A Davis, Riccardo Proietti

2743 related Products with: Rho Kinase Activity, Connexin 40, and Atrial Fibrillation: Mechanistic Insights from End-Stage Renal Disease on Dialysis Patients.

400Tests40 assays100 assays

Related Pathways

paperclip

#31916853   2020/01/09 To Up

and Reprogram Human-Induced Pluripotent Stem Cells-Derived Cardiomyocytes into Pacemaker-Like Cells.

reprograms cardiac myocytes into cells that possess sinoatrial node phenotype, but no specific funny current (If) was detected. We explore whether overexpression of alone or combined with can reprogram human-induced pluripotent stem cells-derived cardiomyocytes (hiPSC-CMs) into pacemaker-like cells. HiPSC-CMs were transfected with and/or in this study. Expression analysis showed that overexpression of induces a reduced reduction expression profile of working cardiomyocytes into that of pacemaker cells. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and electrophysiological analyses showed a reduced expression of connexins subunits (CX40, CX43), the sodium current (, INa), the inward rectified potassium channels (, IK1), and an increased expression of connexins subunits (CX30.2, CX45). No If was detected. The reduction of IK1 resulted in a more depolarized maximum diastolic potential together with an expression of If (generated by ), which they work in synergy to generate spontaneous diastolic depolarization that was the most typical characteristic of pacemaker cells. In conclusion, overexpression of and could reprogram hiPSC-CMs into pacemaker-like cells. The ability to enable diastolic depolarization formation provides a new strategy for the construction of a biological pacemaker.
Hongyi Zhao, Fengyuan Wang, Yanhong Tang, Xi Wang, Teng Wang, Qingyan Zhao, Congxin Huang

1654 related Products with: and Reprogram Human-Induced Pluripotent Stem Cells-Derived Cardiomyocytes into Pacemaker-Like Cells.

4 x 96-well plate1.00 flask1 mg10 ug11.00 flask25 1.00 flask1mg1.00 flask1.00 flask200

Related Pathways

paperclip

#31862763   2020/03/12 To Up

Connexin-43 is a promising target for pulmonary hypertension due to hypoxaemic lung disease.

The mechanisms underlying pulmonary hypertension (PH) are complex and multifactorial, and involve different cell types that are interconnected through gap junctional channels. Although connexin (Cx)-43 is the most abundant gap junction protein in the heart and lungs, and critically governs intercellular signalling communication, its contribution to PH remains unknown. The focus of the present study is thus to evaluate Cx43 as a potential new target in PH.Expressions of Cx37, Cx40 and Cx43 were studied in lung specimens from patients with idiopathic pulmonary arterial hypertension (IPAH) or PH associated with chronic hypoxaemic lung diseases (chronic hypoxia-induced pulmonary hypertension (CH-PH)). Heterozygous Cx43 knockdown CD1 (Cx43) and wild-type littermate (Cx43) mice at 12 weeks of age were randomly divided into two groups, one of which was maintained in room air and the other exposed to hypoxia (10% oxygen) for 3 weeks. We evaluated pulmonary haemodynamics, remodelling processes in cardiac tissues and pulmonary arteries (PAs), lung inflammation and PA vasoreactivity.Cx43 levels were increased in PAs from CH-PH patients and decreased in PAs from IPAH patients; however, no difference in Cx37 or Cx40 levels was noted. Upon hypoxia treatment, the Cx43 mice were partially protected against CH-PH when compared to Cx43 mice, with reduced pulmonary arterial muscularisation and inflammatory infiltration. Interestingly, the adaptive changes in cardiac remodelling in Cx43 mice were not affected. PA contraction due to endothelin-1 (ET-1) was increased in Cx43 mice under normoxic and hypoxic conditions.Taken together, these results indicate that targeting Cx43 may have beneficial therapeutic effects in PH without affecting compensatory cardiac hypertrophy.
Claire Bouvard, Nafiisha Genet, Carole Phan, Baptiste Rode, Raphaël Thuillet, Ly Tu, Paul Robillard, Marilyne Campagnac, Raffaella Soleti, Eric Dumas De La Roque, Frédéric Delcambre, Laurent Cronier, Thibaud Parpaite, Elise Maurat, Patrick Berger, Jean-Pierre Savineau, Roger Marthan, Christophe Guignabert, Véronique Freund-Michel, Christelle Guibert

1649 related Products with: Connexin-43 is a promising target for pulmonary hypertension due to hypoxaemic lung disease.

100 ml100 TESTS0.1 mg0.2 mg25 µg250 ml0.1ml (1.3mg/ml)1 ml0.1 mg0.25 mg

Related Pathways