scholarly journals Oxidized‐Phospholipids Alter Connexin Expression and Gap Junction Organization at the Myoendothelial Junction

2006 ◽  
Vol 20 (4) ◽  
Author(s):  
Brant E Isakson ◽  
Gerhard Kronke ◽  
Alexandra Kadl ◽  
Brian R Duling ◽  
Norbert Leitinger
Keyword(s):  
Gap Junction ◽  
Oxidized Phospholipids ◽  
Connexin Expression

Multiple mechanisms are responsible for altered expression of gap junction genes during oncogenesis in rat liver

1994 ◽  
Vol 107 (1) ◽  
pp. 83-95
Author(s):  
M.J. Neveu ◽  
J.R. Hully ◽  
K.L. Babcock ◽  
E.L. Hertzberg ◽  
B.J. Nicholson ◽  
...  
Keyword(s):  
Gap Junction ◽  
Cellular Localization ◽  
Molecular Mechanisms ◽  
Northern Blotting ◽  
Mrna Abundance ◽  
Common Mechanism ◽  
Cx43 Expression ◽  
Bile Duct Proliferation ◽  
Altered Expression ◽  
Connexin Expression

Although several abnormalities in gap junction (GJ) structure and/or function have been described in neoplasms, the molecular mechanisms responsible for many of the alterations remain unknown. The identification of a family of GJ proteins, termed connexins, prompted this study of connexin32 (Cx32), connexin26 (Cx26) and connexin43 (Cx43) expression during rat hepatocarcinogenesis. Using antibody, cDNA and cRNA probes, we investigated connexin mRNA and protein expression in preneoplastic and neoplastic rat livers. In normal liver, Cx32 is expressed in hepatocytes throughout the hepatic acinus, Cx26 is restricted to periportal hepatocytes, and Cx43 is expressed by mesothelial cells forming Glisson's capsule. Most preneoplastic altered hepatic foci generated by diethylnitrosamine (DEN) initiation and either phenobarbital (PB) or 2,3,7,8-dichlorodibenzo-p-dioxin (TCDD) promotion exhibited decreased Cx32 or increased Cx26 staining. Foci from either protocol failed to display Cx43 immunoreactivity. In the majority of PB-promoted foci, Cx32 immunoreactivity decreased independently of changes in mRNA abundance. Continuous thymidine labeling, following cessation of PB promotion, showed that downregulation of Cx32 staining is reversible in foci that are promoter-dependent for growth, but irreversible in lesions that are promoter-independent for growth. Hepatic neoplasms from rats initiated with DEN and promoted with PB or TCDD also displayed modified connexin expression. While all 24 neoplasms studied were deficient in normal punctate Cx32 and Cx26 staining, altered cellular localization of these proteins was apparent in some tumors. Immunoblotting of crude tissue extracts revealed that neoplasms with disordered Cx32 staining showed immunoreactive bands with altered electrophoretic mobility. These observations show that hepatomas may downregulate Cx32 expression through changes in the primary structure of Cx32 or by post-translational modifications. Northern blotting of total tumor mRNAs failed to demonstrate consistent changes in the abundance of Cx32, Cx26 or Cx43 transcripts. Some tumors expressed steady-state transcripts without observable immunoreactivity, indicating that some hepatomas downregulate connexin immunoreactivity independently of mRNA abundance. Increased levels of Cx43 mRNA and protein were found in several neoplasms, but immunostaining was always localized to nonparenchymal cells. Areas of bile duct proliferation and cholangiomas displayed Cx43 staining, whereas, cholangiocarcinomas were deficient in immunoreactivity. These findings show that alterations in the expression of connexins, by either downregulation or differential induction, represent common modifications during hepatocarcinogenesis. Although our results imply that connexins represent useful markers for the boundary between tumor promotion and progression, preneoplastic and neoplastic rat hepatocytes fail to use a common mechanism to modify connexin expression.

scholarly journals Connexin expression and gap junction communication compartments in the developing mouse limb

1992 ◽  
Vol 195 (3) ◽  
pp. 153-161 ◽  
Author(s):  
Dale W. Laird ◽  
S. Barbara Yancey ◽  
Lakshmi Bugga ◽  
Jean-Paul Revel
Keyword(s):  
Gap Junction ◽  
Connexin Expression ◽  
Gap Junction Communication ◽  
Mouse Limb

Connexin expression and gap-junction-mediated cell interactions in an in vitro model of haemopoietic stroma

2004 ◽  
Vol 316 (1) ◽  
pp. 65-76 ◽  
Author(s):  
Sandra P. Hurtado ◽  
Alex Balduino ◽  
Estev�o C. A. B�di ◽  
M�rcia C. El-Cheikh ◽  
Antonio C. Campos de Carvalho ◽  
...  
Keyword(s):  
Gap Junction ◽  
In Vitro Model ◽  
Cell Interactions ◽  
Connexin Expression ◽  
Vitro Model

scholarly journals Age-related Alteration of Gap Junction Distribution and Connexin Expression in Rat Aortic Endothelium

2000 ◽  
Vol 48 (10) ◽  
pp. 1377-1389 ◽  
Author(s):  
Hung-I Yeh ◽  
Hao-Min Chang ◽  
Wen-Wei Lu ◽  
Yi-Nan Lee ◽  
Yu-Shien Ko ◽  
...  
Keyword(s):  
Gap Junction ◽  
Connexin Expression ◽  
Aortic Endothelium ◽  
Age Related

Changes in lens connexin expression lead to increased gap junctional voltage dependence and conductance

1995 ◽  
Vol 269 (3) ◽  
pp. C590-C600 ◽  
Author(s):  
P. J. Donaldson ◽  
Y. Dong ◽  
M. Roos ◽  
C. Green ◽  
D. A. Goodenough ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Gap Junction ◽  
Voltage Dependence ◽  
Expression Patterns ◽  
Fiber Cell ◽  
Lens Epithelial Cells ◽  
Connexin Expression ◽  
Fiber Cells ◽  
Gap Junctional ◽  
Mouse Lens

The differentiation of mouse lens epithelial cells into fiber cells is a useful model for studying the changes of the electrical properties of gap junction (cell-to-cell) channels that are induced by an alteration in connexin expression patterns. In this model, cuboidal lens epithelial cells differentiate into elongated fiber cells, and the expression of connexin43 (Cx43) in the epithelial cells is replaced with the production of high levels of Cx50 and Cx46 in the fiber cells. We now report a new procedure to isolate mouse lens fiber cell pairs suitable for double whole cell patch-clamp analysis. Analysis was also performed for fiberlike cell pairs differentiated from epithelial cells in culture. Voltage dependence and unitary conductance of fiber cell gap junction channels were determined and compared with the corresponding values previously measured for the channels joining lens epithelial cells and for lens connexin channels formed in Xenopus oocyte pairs. Our results support a differentiation-induced shift toward stronger gap junctional voltage dependence and larger unitary conductances in the fiber cells. Our data further reflect a balanced functional contribution of Cx50 and Cx46 in the fiber cell-to-cell channels rather than a predominance of a single connexin.

Sharing signals: connecting lung epithelial cells with gap junction channels

2002 ◽  
Vol 283 (5) ◽  
pp. L875-L893 ◽  
Author(s):  
Michael Koval
Keyword(s):  
Epithelial Cells ◽  
Gap Junctions ◽  
Gap Junction ◽  
Alveolar Epithelial Cells ◽  
Lung Epithelial Cells ◽  
Cell Phenotype ◽  
Connexin Expression ◽  
Gap Junction Channels ◽  
Alveolar Epithelial ◽  
Junctional Communication

Gap junction channels enable the direct flow of signaling molecules and metabolites between cells. Alveolar epithelial cells show great variability in the expression of gap junction proteins (connexins) as a function of cell phenotype and cell state. Differential connexin expression and control by alveolar epithelial cells have the potential to enable these cells to regulate the extent of intercellular coupling in response to cell stress and to regulate surfactant secretion. However, defining the precise signals transmitted through gap junction channels and the cross talk between gap junctions and other signaling pathways has proven difficult. Insights from what is known about roles for gap junctions in other systems in the context of the connexin expression pattern by lung cells can be used to predict potential roles for gap junctional communication between alveolar epithelial cells.

Gap Junction Remodeling in Skin Repair Following Wounding and Disease

Physiology ◽  
2013 ◽  
Vol 28 (3) ◽  
pp. 190-198 ◽  
Author(s):  
Jared M. Churko ◽  
Dale W. Laird
Keyword(s):  
Wound Healing ◽  
Gap Junction ◽  
Present Review ◽  
Gain Of Function ◽  
Skin Development ◽  
Connexin Expression ◽  
Skin Repair ◽  
Therapeutic Value ◽  
Cellular Phenotypes

In the present review, we provide an overview of connexin expression during skin development and remodeling in wound healing, and reflect on how loss- or gain-of-function connexin mutations may change cellular phenotypes and lead to diseases of the skin. We also consider the therapeutic value of targeting connexins in wound healing.

scholarly journals Gap Junction Localization and Connexin Expression in Cytochemically Identified Endothelial Cells of Arterial Tissue

1997 ◽  
Vol 45 (4) ◽  
pp. 539-550 ◽  
Author(s):  
Hung-I Yeh ◽  
Emmanuel Dupont ◽  
Steven Coppen ◽  
Stephen Rothery ◽  
Nicholas J. Severs
Keyword(s):  
Endothelial Cells ◽  
Coronary Artery ◽  
Gap Junctions ◽  
Gap Junction ◽  
Vascular Endothelial Cells ◽  
Rat Aorta ◽  
Arterial System ◽  
Connexin Expression ◽  
Arterial Tissue ◽  
Surrounding Areas

Vascular endothelial cells interact with one another via gap junctions, but information on the precise connexin make-up of endothelial gap junctions in intact arterial tissue is limited. One factor contributing to this lack of information is that standard immunocytochemical methodologies applied to arterial sections do not readily permit unequivocal localization of connexin immunolabeling to endothelium. Here we introduce a method for multiple labeling with specific endothelial cell markers and one or more connexin-specific antibodies which overcomes this limitation. Applying this method to localize connexins 43, 40, and 37 by confocal microscopy, we show that the three connexin types have quite distinctive labeling patterns in different vessels. Whereas endothelial cells of rat aorta and coronary artery characteristically show extensive, prominent connexin40, and heterogeneous scattered connexin37, the former, unlike the latter, also has abundant connexin43. The relative lack of connexin43 in coronary artery endothelium was confirmed in both rat and human using three alternative antibodies. In the aorta, connexins43 and 40 commonly co-localize to the same junctional plaque. Even within a given type of endothelium, zonal variation in connexin expression was apparent. In rat endocardium, a zone just below the mitral valve region is marked by expression of greater quantities of connexin43 than surrounding areas. These results are consistent with the idea that differential expression of connexins may contribute to modulation of endothelial gap junction function in different segments and subzones of the arterial system.

scholarly journals Remodeling of Cardiac Gap Junctional Cell–Cell Coupling

Cells ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 2422
Author(s):  
Stefan Dhein ◽  
Aida Salameh
Keyword(s):  
Gap Junctions ◽  
Gap Junction ◽  
Conduction System ◽  
Cell Coupling ◽  
Connexin Expression ◽  
Gap Junction Channels ◽  
Developmental States ◽  
Gap Junction Channel ◽  
Arrhythmogenic Substrate ◽  
Cell Cell

The heart works as a functional syncytium, which is realized via cell-cell coupling maintained by gap junction channels. These channels connect two adjacent cells, so that action potentials can be transferred. Each cell contributes a hexameric hemichannel (=connexon), formed by protein subuntis named connexins. These hemichannels dock to each other and form the gap junction channel. This channel works as a low ohmic resistor also allowing the passage of small molecules up to 1000 Dalton. Connexins are a protein family comprising of 21 isoforms in humans. In the heart, the main isoforms are Cx43 (the 43 kDa connexin; ubiquitous), Cx40 (mostly in atrium and specific conduction system), and Cx45 (in early developmental states, in the conduction system, and between fibroblasts and cardiomyocytes). These gap junction channels are mainly located at the polar region of the cardiomyocytes and thus contribute to the anisotropic pattern of cardiac electrical conductivity. While in the beginning the cell–cell coupling was considered to be static, similar to an anatomically defined structure, we have learned in the past decades that gap junctions are also subject to cardiac remodeling processes in cardiac disease such as atrial fibrillation, myocardial infarction, or cardiomyopathy. The underlying remodeling processes include the modulation of connexin expression by e.g., angiotensin, endothelin, or catecholamines, as well as the modulation of the localization of the gap junctions e.g., by the direction and strength of local mechanical forces. A reduction in connexin expression can result in a reduced conduction velocity. The alteration of gap junction localization has been shown to result in altered pathways of conduction and altered anisotropy. In particular, it can produce or contribute to non-uniformity of anisotropy, and thereby can pre-form an arrhythmogenic substrate. Interestingly, these remodeling processes seem to be susceptible to certain pharmacological treatment.

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