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mitochondrial connexin 43

Kerstin Boengler, Marko Bulic, Rolf Schreckenberg, Klaus-Dieter Schlüter, Rainer Schulz
BACKGROUND AND PURPOSE: Dysregulation of gap junction-mediated cell coupling contributes to development of arrhythmias and myocardial damage after ischaemia/reperfusion (I/R). Connexin 43 (Cx43) is present at ventricular gap junctions and also in the mitochondria of cardiomyocytes. The dipeptide (2S, 4R)-1-(2-aminoacetyl)-4-benzamidopyrrolidine-2-carboxylic acid (ZP1609) has antiarrhythmic properties and reduces infarct size when given at reperfusion. However, it is unclear, whether ZP1609 targets Cx43-containing mitochondria and affects cardiomyocyte hypercontracture following I/R...
March 30, 2017: British Journal of Pharmacology
Ashish Kumar Gadicherla, Nan Wang, Marco Bulic, Esperanza Agullo-Pascual, Alessio Lissoni, Maarten De Smet, Mario Delmar, Geert Bultynck, Dmitri V Krysko, Amadou Camara, Klaus-Dieter Schlüter, Rainer Schulz, Wai-Meng Kwok, Luc Leybaert
Mitochondrial connexin 43 (Cx43) plays a key role in cardiac cytoprotection caused by repeated exposure to short periods of non-lethal ischemia/reperfusion, a condition known as ischemic preconditioning. Cx43 also forms calcium (Ca(2+))-permeable hemichannels that may potentially lead to mitochondrial Ca(2+) overload and cell death. Here, we studied the role of Cx43 in facilitating mitochondrial Ca(2+) entry and investigated its downstream consequences. To that purpose, we used various connexin-targeting peptides interacting with extracellular (Gap26) and intracellular (Gap19, RRNYRRNY) Cx43 domains, and tested their effect on mitochondrial dye- and Ca(2+)-uptake, electrophysiological properties of plasmalemmal and mitochondrial Cx43 channels, and cell injury/cell death...
May 2017: Basic Research in Cardiology
Zhong-Jun Du, Guan-Qun Cui, Juan Zhang, Xiao-Mei Liu, Zhi-Hu Zhang, Qiang Jia, Jack C Ng, Cheng Peng, Cun-Xiang Bo, Hua Shao
Gap junction intercellular communication (GJIC) between cardiomyocytes is essential for synchronous heart contraction and relies on connexin-containing channels. Connexin 43 (Cx43) is a major component involved in GJIC in heart tissue, and its abnormal expression is closely associated with various cardiac diseases. Silica nanoparticles (SNPs) are known to induce cardiovascular toxicity. However, the mechanisms through which GJIC plays a role in cardiomyocytes apoptosis induced by SNPs remain unknown. The aim of the present study is to determine whether SNPs-decreased GJIC promotes apoptosis in rat cardiomyocytes cell line (H9c2 cells) via the mitochondrial pathway using CCK-8 Kit, scrape-loading dye transfer technique, Annexin V/PI double-staining assays, and Western blot analysis...
2017: International Journal of Nanomedicine
Camila de Moraes, Camila Andrea de Oliveira, Maria Esméria Corezola do Amaral, Gabriela Arcurio Landini, Rosana Catisti
Objective: Complexes like conjugated linoleic acid (CLA) reduce the percentage of body fat by increasing energy expenditure, fat oxidation, or both. The aim of this study was to verify if CLA is able to mimic caloric restriction (CR), and determine the effects of CLA on liver metabolic profile of young adult male Wistar rats. Materials and methods: We divided 36 animals into the following groups: 1) Control; 2) CLA (1% of daily food intake, 21 days, orogastric intubation); 3) Restr (fed 60% of the diet offered to controls); and 4) CLA Restr...
January 2017: Archives of Endocrinology and Metabolism
Hongshan Ge, Fan Zhang, Ping Duan, 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
Kenneth Andrew Sinclair, Stephanie Terase Yerkovich, Peter Mark-Anthony Hopkins, Daniel Charles Chambers
BACKGROUND: Bone marrow-derived mesenchymal stromal cells (BM-MSCs) are capable of repairing wounded lung epithelial cells by donating cytoplasmic material and mitochondria. Recently, we characterized two populations of human lung-derived mesenchymal stromal cells isolated from digested parenchymal lung tissue (LT-MSCs) from healthy individuals or from lung transplant recipients' bronchoalveolar lavage fluid (BAL-MSCs). The aim of this study was to determine whether LT-MSCs and BAL-MSCs are also capable of donating cytoplasmic content and mitochondria to lung epithelial cells...
July 12, 2016: Stem Cell Research & Therapy
Di Hu, Hui Zou, Tao Han, Junze Xie, Nannan Dai, Liling Zhuo, Jianhong Gu, Jianchun Bian, Yan Yuan, Xuezhong Liu, Zongping Liu
Gap junctions mediate direct communication between cells; however, toxicological cascade triggered by nonessential metals can abrogate cellular signaling mediated by gap junctions. Although cadmium (Cd) is known to induce apoptosis in organs and tissues, the mechanisms that underlie gap junction activity in Cd-induced apoptosis in BRL 3A rat liver cells has yet to be established. In this study, we showed that Cd treatment decreased the cell index (a measure of cellular electrical impedance) in BRL 3A cells...
March 2016: Journal of Veterinary Science
Amanda Denuc, Estefanía Núñez, Enrique Calvo, Marta Loureiro, Elisabet Miro-Casas, Adela Guarás, Jesús Vázquez, David Garcia-Dorado
Connexin 43 (Cx43), the gap junction protein involved in cell-to-cell coupling in the heart, is also present in the subsarcolemmal fraction of cardiomyocyte mitochondria. It has been described to regulate mitochondrial potassium influx and respiration and to be important for ischaemic preconditioning protection, although the molecular effectors involved are not fully characterized. In this study, we looked for potential partners of mitochondrial Cx43 in an attempt to identify new molecular pathways for cardioprotection...
May 2016: Journal of Cellular and Molecular Medicine
Sudhakar Veeranki, Srikanth Givvimani, Sourav Kundu, Naira Metreveli, Sathnur Pushpakumar, Suresh C Tyagi
AIMS: Although the cardiovascular benefits of exercise are well known, exercise induced effects and mechanisms in prevention of cardiomyopathy are less clear during obesity associated type-2 diabetes. The current study assessed the impact of moderate intensity exercise on diabetic cardiomyopathy by examining cardiac function and structure and mitochondrial function. METHODS: Obese-diabetic (db/db), and lean control (db/+) mice, were subjected to a 5 week, 300 m run on a tread-mill for 5 days/week at the speeds of 10-11 m/min...
March 2016: Journal of Molecular and Cellular Cardiology
Hua He, Nan Li, Zhihong Zhao, Fusheng Han, Xifu Wang, Yujie Zeng
To investigate the effects of cellular membrane connexin 43 (Cx43) and the potential details in ischemic postconditioning (IPOC)-induced cardioprotection, ischemia/reperfusion (IR) models were generated in 8-week-old male Sprague-Dawley rats by ligating the left coronary artery anterior descending branch. The serum levels of myocardial creatases, nitric oxide (NO) and malondialdehyde (MDA) levels, infarct size, arrhythmia events, expression and distribution of Cx43, ultrastructure and apoptosis in the myocardium in different treatments with IR, IR + IPOC, IR + diazoxide or IR + IPOC + 5-hydroxydecanoate acid (5-HD) were investigated...
September 2015: Biomedical Reports
Bo Bian, Xuefang Yu, Qing Wang, Tianming Teng, Jing Nie
Atorvastatin has protective effects against myocardial ischemia-reperfusion injuries and ischemia-reperfusion arrhythmia. This study was designed to investigate whether atorvastatin is able to protect against myocardial ischemia-reperfusion injury by enhancing the expression of Connexin 43 (Cx43) via the activation of the phosphatidylinositol-3-kinase (PI3K)/Akt pathway and mitochondrial ATP-sensitive potassium (K(ATP)) channels. Isolated perfused rat hearts were treated with classic ischemia postconditioning (IPOST), atorvastatin, and atorvastatin combined with inhibitor of PI3K and K(ATP) channels, respectively, after 30min of LAD ischemia and then subjected to reperfusion for 120min...
December 5, 2015: European Journal of Pharmacology
Hu Di, Zou Hui, Han Tao, Xie Junze, Dai Nannan, Zhuo Liling, Gu Jianhong, Bian Jianchun, Yuan Yan, Liu Xuezhong, Liu Zongping
Gap junctions mediate direct communication between cells. Toxicological cascade triggered by nonessential metals can abrogate cellular signaling mediated by gap junctions. Cadmium (Cd) is a cytotoxic industrial and environmental pollutant. Although Cd is known to induce apoptosis in organs and tissues, the mechanisms that underlie gap junction activity in Cd-induced apoptosis in BRL 3A cells is not established. In this study, we showed that Cd treatment decreased cell index (a measure of cellular electrical impedance) in BRL 3A cells...
August 4, 2015: Journal of Veterinary Science
Rainer Schulz, Philipp Maximilian Görge, Anikó Görbe, Péter Ferdinandy, Paul D Lampe, Luc Leybaert
Connexins are widely distributed proteins in the body that are crucially important for heart and brain functions. Six connexin subunits form a connexon or hemichannel in the plasma membrane. Interactions between two hemichannels in a head-to-head arrangement result in the formation of a gap junction channel. Gap junctions are necessary to coordinate cell function by passing electrical current flow between heart and nerve cells or by allowing exchange of chemical signals and energy substrates. Apart from its localization at the sarcolemma of cardiomyocytes and brain cells, connexins are also found in the mitochondria where they are involved in the regulation of mitochondrial matrix ion fluxes and respiration...
September 2015: Pharmacology & Therapeutics
Raquel Gago-Fuentes, Patricia Fernández-Puente, Diego Megias, Paula Carpintero-Fernández, Jesus Mateos, Benigno Acea, Eduardo Fonseca, Francisco Javier Blanco, Maria Dolores Mayan
We have previously reported that articular chondrocytes in tissue contain long cytoplasmic arms that physically connect two distant cells. Cell-to-cell communication occurs through connexin channels termed Gap Junction (GJ) channels, which achieve direct cellular communication by allowing the intercellular exchange of ions, small RNAs, nutrients, and second messengers. The Cx43 protein is overexpressed in several human diseases and inflammation processes and in articular cartilage from patients with osteoarthritis (OA)...
July 2015: Molecular & Cellular Proteomics: MCP
Youn Wook Chung, Claudia Lagranha, Yong Chen, Junhui Sun, Guang Tong, Steven C Hockman, Faiyaz Ahmad, Shervin G Esfahani, Dahae H Bae, Nazari Polidovitch, Jian Wu, Dong Keun Rhee, Beom Seob Lee, Marjan Gucek, Mathew P Daniels, Christine A Brantner, Peter H Backx, Elizabeth Murphy, Vincent C Manganiello
Although inhibition of cyclic nucleotide phosphodiesterase type 3 (PDE3) has been reported to protect rodent heart against ischemia/reperfusion (I/R) injury, neither the specific PDE3 isoform involved nor the underlying mechanisms have been identified. Targeted disruption of PDE3 subfamily B (PDE3B), but not of PDE3 subfamily A (PDE3A), protected mouse heart from I/R injury in vivo and in vitro, with reduced infarct size and improved cardiac function. The cardioprotective effect in PDE3B(-/-) heart was reversed by blocking cAMP-dependent PKA and by paxilline, an inhibitor of mitochondrial calcium-activated K channels, the opening of which is potentiated by cAMP/PKA signaling...
April 28, 2015: Proceedings of the National Academy of Sciences of the United States of America
Soma Ghosh, Ashish Kumar, Sudhir Chandna
Enrichment of tumour cells in G2/M phases in vitro is known to be associated with low-dose hyper-radiosensitivity (HRS). These cell cycle phases also involve reduced expression of adhesion protein connexin-43 (Cx43). Therefore, we investigated the role of Cx43 in HRS. Asynchronous or G2/M enriched tumour cells (U87, BMG-1, HeLa) and normal primary fibroblasts (HDFn) were γ-irradiated at varying doses, with an asynchronous group separately subjected to Cx43-knockdown prior to irradiation. Cx43 level, gap junctional activity, clonogenic cell survival, cell growth/viability, mitochondrial alterations and other apoptosis-regulating events were studied...
July 10, 2015: Cancer Letters
Mücella Kirca, Petra Kleinbongard, Daniel Soetkamp, Jacqueline Heger, Csaba Csonka, Péter Ferdinandy, Rainer Schulz
Connexin 43 (Cx43), which is highly expressed in the heart and especially in cardiomyocytes, interferes with the expression of nitric oxide synthase (NOS) isoforms. Conversely, Cx43 gene expression is down-regulated by nitric oxide derived from the inducible NOS. Thus, a complex interplay between Cx43 and NOS expression appears to exist. As cardiac mitochondria are supposed to contain a NOS, we now investigated the expression of NOS isoforms and the nitric oxide production rate in isolated mitochondria of wild-type and Cx43-deficient (Cx43(Cre-ER(T)/fl) ) mice hearts...
April 2015: Journal of Cellular and Molecular Medicine
Hu Shan, Jin Wei, Ming Zhang, Lin Lin, Rui Yan, Rong Zhang, Yan-He Zhu
Mitochondrial connexin 43 (Cx43) is important in cardioprotection by ischemic preconditioning; however, whether mitochondrial Cx43 is involved in mitochondrial dysfunction in the pathogenesis of dilated cardiomyopathy (DCM) remains to be elucidated. The present study was performed to investigate the changes in expression and the phosphorylation state of mitochondrial Cx43 in a rat model of DCM, and to determine whether the altered phosphorylation state of mitochondrial Cx43 was involved in mitochondrial dysfunction...
June 2015: Molecular Medicine Reports
Michela Pecoraro, Rosalinda Sorrentino, Silvia Franceschelli, Mariagiovanna Del Pizzo, Aldo Pinto, Ada Popolo
Doxorubicin is the highly effective anthracycline, but its clinical use is limited by cardiotoxicity and consequent dysfunction. It has been proposed that the etiology of this is related to mitochondrial dysfunction. Connexin 43 (Cx43), the principal protein building block of cardiac gap junctions and hemichannels, plays an important role in cardioprotection. Recent reports confirmed the presence of Cx43 in the mitochondria as well. In this study, the role of mitochondrial Cx43 was evaluated 3 or 6 h after Doxorubicin administration to the rat heart cell line H9c2...
October 2015: Cardiovascular Toxicology
Y Chang, T Yu, H Yang, Z Peng
Up to now, studies of exercise-induced cardiac arrhythmia have focused primarily on the working myocardium, with few studies examining to the cardiac conduction system where the rhythmic and synchronized contraction of the heart is initiated. To explore whether the cardiac conduction system is involved in the exercise-induced cardiac injury, we performed histological analysis of sinoatrial node, atrioventricular node and Purkinje fibers and tested the level of structural protein cardiac troponin T and Connexin 43 in Sprague Dawley rats following repeated exhaustive exercise...
January 2015: International Journal of Sports Medicine
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