Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Intercellular Junctions”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,027 records · Page 57Linked to original sources
PubMed1992

Differential extractability of calcium and pectic substances in different wall regions of epicotyl cells in young flax plants.

We applied the simultaneous use of a subtractive method and two imaging techniques (secondary ion mass spectrometry and electron microscopy after PATAg staining) to correlate the distribution of Ca2+ to pectic substances in cell walls of young flax plants. The calcium images were compared with the structural electron microscopy images. This suggests that the linkage of the pectic substances within the wall is mainly by calcium bridges in the intercellular junctions of most types of cells under study (epidermis, subepidermis, fiber layer, and endodermis) and in the outer part (close to the cuticle) of the wall of the epidermal cells. In the primary walls of the various types of cells under study and in the inner part (close to the cytoplasm) of the wall of the epidermal cells, the linkage of the pectic substances would be mainly by covalent bonds. In the middle lamellae of the various cells, and in the intercellular junctions within the cortical parenchyma, both types of linkages apparently coexist. The mechanism of "ionic condensation" may provide an interpretation for the chemical status of the Ca2+ ions which are associated with the pectic components solubilized in boiling water, and which do not seem to contribute to the linkage of these components within the wall.

Calcium↗
PubMed1999

Cell-cell contacts in the human cell line ECV304 exhibit both endothelial and epithelial characteristics.

Endothelial cells separate the intra- and extravascular space and regulate transport processes between these compartments. Since intercellular junctions are required for these specific cell functions, the cell-cell contacts in the permanent cell line ECV304 were systematically analyzed and compared with human umbilical vein endothelial cells (HUVECs) in primary culture and with the epithelial Madin Darby Canine Kidney (MDCK) cell line. Filter-grown ECV304 cells generate a distinct electrical resistance and a permeability barrier between cell culture compartments. Electron microscopy of ECV304 cells revealed lateral membrane interdigitations, typically found in endothelial cells in vivo, with direct membrane contact sites, which prevented the diffusion of lanthanum. By immunoblot and immunofluorescence analysis, the expression and cellular localization of the tight junction and adherens-type junction proteins occludin, ZO-1, symplekin, beta-catenin, and plakoglobin were analyzed. ECV304 cells display further characteristics of endothelial cells, including the expresssion of thrombomodulin and of the vitronectin receptor CD51, as well as the secretion of plasminogen activator inhibitor 1 (PAI-1) and endothelin. However, ECV304 cells also express proteins characteristically found in epithelial cells, including E-cadherin and the desmosomal proteins desmoplakin, desmocollin, and desmoglein; occasionally desmosomal structures can be identified by electron microscopy. In conclusion, ECV304 cells express many endothelial markers and form specialized intercellular junctions that display some epithelial features. Thus this reportedly endothelial-derived permanent human cell line may be dedifferentiated toward an epithelial phenotype.

Animals↗
PubMed1971

Electrical coupling between fat cells in newt fat body and mouse brown fat.

White fat from the newt, Triturus pyrrhogaster, fat body, and brown fat from the interscapular fat pad of newborn mice have been tested for the presence of low-resistance intercellular junctions. 42 pairs of amphibian fat cells and 15 pairs of mammalian brown fat cells were found to be "electrically coupled." In most of these cases intracellular deposition of a dye, Niagara Sky Blue: 6B, was used to supplement and confirm direct observations of impalements. Coupling was often difficult to find in both preparations, but the mechanical disturbance of the tissue during the preparative procedures may have uncoupled many cells. The fact that, in both types of fat, coupling was observed between cells separated by one or more other cells suggests that coupling may be more widespread in vivo. Electron microscopy (provided by Dr. J. -P. Revel and Mrs. K. Wolken) of the brown fat revealed frequent intercellular junctions resembling "gap junctions" but possibly lacking the substructure usually visible with colloidal lanthanum infiltration. The results are discussed in relation to current ideas about the exchange of regulatory molecules via low-resistance junctions and about the control of brown fat by hormones and nerves.

Adipose Tissue↗
PubMed1991

A study of modified lymphatics in the deep cortex of ruminant lymph nodes.

Ruminant lymph nodes, except when very small, were found to have a system of smooth-walled channels in the periphery of the 'deep cortical units' defined by Bélisle & Sainte-Marie (1981 a,b). Each channel originated with many 'blind' branches in the subnodular layer of the cortex and ended by joining a medullary sinus. The wall consisted of a continuous endothelial lining, a sometimes thin or discontinuous basement membrane without a basal lamina, and at least one layer of flattened reticular fibroblasts. The endothelium was higher than in most typical lymphatics, with a cytoplasmic fine structure similar to that of sinus-lining cells in the medullary sinuses. The intercellular junctions were generally long and elaborate. The lumen often contained opaque material, especially in the branches, as for initial lymphatics, as well as a few lymphocytes and an occasional nonlymphoid cell, but sinus macrophages were never seen. In some lymph nodes the lumen was crowded with lymphocytes. When small ferripolymaltose particles arrived in the node with the afferent lymph, many of them rapidly passed through the outer cortex and reached the lumen of the smooth-walled channels by way of the intercellular junctions of the endothelium. When colloidal carbon was introduced the same way, some of it also reached the channels where it accumulated in the basement membrane and in vesicles and vacuoles of the endothelium. These channels are interpreted as initial lymphatics of the same type as in other lymphoid organs rather than lymph node sinuses. They seem to play an important role for the exit of lymphocytes from the nodes and also for the passage of particulate material, including antigens, through those areas where recirculating lymphocytes arrive in the cortex.

Animals↗
PubMed1979

Structural aspects of the permeability of the microvascular endothelium.

This article reviews recent findings and current views concerning the structural aspects of microvascular permeability. The vascular endothelium is considered as a simple squamous epithelium which has acquired a remarkably high permeability to water and water soluble solutes (including macromolecules) through a characteristic process of differentiation of its cells. In terms of cellular structures, this differentiation involves an unusually large population of plasmalemmal vesicles. The evidence so far obtained indicates that these vesicles function as (1) mass-carriers of fluid and solutes across the endothelium and as (2) generators of transendothelial channels by concomitant fusion (followed by fission) with both domains (luminal and tissular) of the plasmalemma. The endothelial fenestrae of visceral capillaries are initially transendothelial channels subsequently collapsed to minimal length. The intercellular junctions of the endothelium are not detectably permeable to tracers of diam. greater than or equal to 18--20 A in capillaries, but are focally open to probes of 50--60 A diam. in postcapillary (pericytic) venules. A correlation is attempted between transendothelial channels (and fenestrae) and the pore systems postulated by the pore theory of capillary permeability. The channels appear to function as either small or large pores depending on the porosity of their associated diaphragms and on the size of local strictures along their pathway. Two main components are recognized in the analysis of capillary permeability: 1) a basic component comparable to that of other simple epithelia and involving transport across the plasmalemma and probably along the intercellular junctions (for molecules of diam. greater than or equal to 10 A); and a differentiated component which involves plasmalemmal vesicles and their derivatives (transendothelial channels and fenestrae). The postulated pores of the capillary endothelium are part of this differentiated component. The special situation found in postcapillary venules (focally open junctions) seems to be related to the role played by these vessels in inflammatory reactions.

Animals↗
PubMed2004

Endothelial cell-to-cell junctions: molecular organization and role in vascular homeostasis.

Intercellular junctions mediate adhesion and communication between adjoining endothelial and epithelial cells. In the endothelium, junctional complexes comprise tight junctions, adherens junctions, and gap junctions. The expression and organization of these complexes depend on the type of vessels and the permeability requirements of perfused organs. Gap junctions are communication structures, which allow the passage of small molecular weight solutes between neighboring cells. Tight junctions serve the major functional purpose of providing a "barrier" and a "fence" within the membrane, by regulating paracellular permeability and maintaining cell polarity. Adherens junctions play an important role in contact inhibition of endothelial cell growth, paracellular permeability to circulating leukocytes and solutes. In addition, they are required for a correct organization of new vessels in angiogenesis. Extensive research in the past decade has identified several molecular components of the tight and adherens junctions, including integral membrane and intracellular proteins. These proteins interact both among themselves and with other molecules. Here, we review the individual molecules of junctions and their complex network of interactions. We also emphasize how the molecular architectures and interactions may represent a mechanistic basis for the function and regulation of junctions, focusing on junction assembly and permeability regulation. Finally, we analyze in vivo studies and highlight information that specifically relates to the role of junctions in vascular endothelial cells.

Adherens Junctions↗
PubMed1991

Surface and subsurface structures of neuromasts in tadpoles of the crab-eating frog, Rana cancrivora.

Neuromast structure in Rana cancrivora larvae was observed by scanning and transmission electron microscopy. Neuromast units, each being composed of two or three neuromasts, are arranged in several well-defined lines in the head, body, and tail regions. The structure of neuromasts in these three regions is basically identical. The neuromast is composed of sensory, sustentacular, and mantle cells. The top of each neuromast has a hillocklike appearance, and is surrounded by four to six epidermal cells with tight intercellular junctions. Long kinocilia and many stereocilia occur in the apex of the neuromasts and are surrounded by numerous microvilli. Numerous granules are present on the apical portions of the mantle and the sustentacular cells. Four or five trapeziform mantle cells are connected closely with each other to form the shell of the neuromast. Large intercellular spaces occur between the mantle cells and the cells of the inner epidermal layers, and between the cells of the inner epidermal layer. Thus, at the apical parts of the neuromast intercellular junctions are tight and the intercellular spaces are more dilated in more basal areas. Morphologically the neuromasts of R. cancrivora larvae resemble those of generalized pond anurans, based on the grouping of Lannoo (Journal of Morphology 191:115-129, 1987a), although larvae of this species inhabit brackish water.

Animals↗
PubMed1979

Contractures and increase in internal longitudianl resistance of cow ventricular muscle induced by hypoxia.

This study was performed to determine whether hypoxia in glucose-free solutions can increase the electrical resistance of intercellular junctions in ventricular muscle. Internal longitudinal resistance (Ri), mechanical tension, and transmembrane action potentials were measured simultaneously in cow ventricular trabeculae. The mean control value of Ri was 265 +/- 38 omegacm (mean +/- SE) at 34 degrees C. After 1 hour of hypoxia in glucose-free Tyrode's solution, it had increased by 300 +/- 41% (n = 11, P less than 0.001). The rise in Ri was closely related to the increase in resting tension (contracture). These effects were more pronounced during a second exposure to hypoxia and were potentiated by application of epinephrine, by increasing extracellular calcium concentration, and by increasing frequency of stimulation. Addition of glucose (50 mM) provided some protection against hypoxia. It is inferred that the increase in Ri is entirely due to the increase in the resistance of intercellular junctions (electrical uncoupling). Intracellular calcium may be responsible for both the contracture and the uncoupling.

Animals↗
PubMed2005

Cx31 is assembled and trafficked to cell surface by ER-Golgi pathway and degraded by proteasomal or lysosomal pathways.

Gap junctions, consisting of connexins, allow the exchange of small molecules (less than 1 KD) between adjacent cells, thus providing a mechanism for synchronizing the responses of groups of cells to environmental stimuli. Connexin 31 is a member of the connexin family. Mutations on connexin 31 are associated with erythrokeratodermia variabilis, hearing impairment and peripheral neuropathy. However, the pathological mechanism for connexin 31 mutants in these diseases are still unknown. In this study, we analyzed the assembly, trafficking and metabolism of connexin 31 in HeLa cells stably expressing connexin 31. Calcein transfer assay showed that calcein transfer was inhibited when cells were treated with Brefeldin A or cytochalasin D, but not when treated with nocodazole or a-glycyrrhetinic acid, suggesting that Golgi apparatus and actin filaments, but not microtubules, are crucial to the trafficking and assembly of connexin 31, as well as the formation of gap junction intercellular communication by connexin 31. Additionally, a-glycyrrhetinic acid did not effectively inhibit gap junctional intercellular communication formed by connexin 31. Pulse-chase assay revealed that connexin 31 had a half-life of about 6 h. Moreover, Western blotting and fluorescent staining demonstrated that in HeLa cells stably expressing connexin 31, the amount of connexin 31 was significantly increased after these cells were treated with proteasomal or lysosomal inhibitors. These findings indicate that connexin 31 was rapidly renewed, and possibly degraded by both proteasomal and lysosomal pathways.

Brefeldin A↗
PubMed2005

Characterisation of adherens and tight junctional molecules in normal animal larynx; determining a suitable model for studying molecular abnormalities in human laryngopharyngeal reflux.

BACKGROUND: The disruption of intercellular junctions in the larynx is a pathological feature of laryngopharyngeal reflux (LPR). Good experimental models are necessary to gain greater insight into the molecular mechanisms and alterations that result from abnormal exposure of the laryngeal epithelium to acid refluxate. AIMS: To characterise laryngeal tissues from different species to determine the most suitable for use in experimental studies of LPR. METHODS: Human and non-human laryngeal tissues (mouse, rat, guinea pig, porcine, and rabbit) were studied. Histological characterisation was performed by light microscopy. The expression and subcellular localisation of adherens junctional molecules (E-cadherin and beta catenin) was evaluated by immunohistochemistry, and tight junction molecules (occludin and zonula occludens 1 (ZO-1)) by western blotting. The ultrastructural features of porcine and human tissue were assessed by electron microscopy. RESULTS: Porcine tissue revealed both respiratory-type and stratified squamous epithelium, as seen in the human larynx. The expression and subcellular localisation of the E-cadherin-catenin complex was detected in all species except mouse and rat. The pattern of ZO-1 and occludin expression was preserved in all species. CONCLUSION: The expression of intercellular junctional complexes in porcine epithelium is similar to that seen in humans. These results confirm the suitability of these species to study molecular mechanisms of LPR in an experimental system.

Adherens Junctions↗
PubMed1980

Ultrastructural aspects of mucinous (colloid) breast carcinoma.

Seven cases of mucinous (colloid) breast carcinoma were studied by electron microscopy. In addition to the predictably abundant mucosubstance production, the following observations merit elaboration: 1) absence of myoepithelial differentiation and basal lamina deposition, 2) notably developed cytoplasmic filamentous systems and relatively scarce lysosomes, 3) frequent and apparently well-developed intercellular junctions, and 4) a distinct paucity of vessels in the tumors' stroma. The rather favorable clinical prognosis of mucinous breast carcinoma despite the absence of myoepithelial differentiation and basal lamina deposition parallel observations made on medullary and tubular breast carcinomas, thus confirming that those parameters, however important, are not the sole determinants of an aggresive behavior. The conspicuous cytoplasmic filaments appear to be neither true myoepithelial filaments or tonfilaments. The peculiar arrangement of these contractile proteins and the suspected sarcity of lysosomal collagenases may be reflected in the rather low invasiveness of these carcinomas. Another factor that may impact favorably on the cohesiveness of these neoplastic cell clusters is the presence of abundant and well-developed intercellular junctions. We further speculate that the paucity of stromal vessels in these neoplasms may be the result of as yet unidentified factors that might inhibit angiogenesis.

Adenocarcinoma, Mucinous↗
PubMed2002

Activation of L-type calcium channels is required for gap junction-mediated intercellular calcium signaling in osteoblastic cells.

The propagation of mechanically induced intercellular calcium waves (ICW) among osteoblastic cells occurs both by activation of P2Y (purinergic) receptors by extracellular nucleotides, resulting in "fast" ICW, and by gap junctional communication in cells that express connexin43 (Cx43), resulting in "slow" ICW. Human osteoblastic cells transmit intercellular calcium signals by both of these mechanisms. In the current studies we have examined the mechanism of slow gap junction-dependent ICW in osteoblastic cells. In ROS rat osteoblastic cells, gap junction-dependent ICW were inhibited by removal of extracellular calcium, plasma membrane depolarization by high extracellular potassium, and the L-type voltage-operated calcium channel inhibitor, nifedipine. In contrast, all these treatments enhanced the spread of P2 receptor-mediated ICW in UMR rat osteoblastic cells. Using UMR cells transfected to express Cx43 (UMR/Cx43) we confirmed that nifedipine sensitivity of ICW required Cx43 expression. In human osteoblastic cells, gap junction-dependent ICW also required activation of L-type calcium channels and influx of extracellular calcium.

Animals↗
PubMed1981

Periarterial macrophage sheaths (ellipsoids) in cat spleen--an electron microscope study.

Periarterial macrophage sheaths (PAMS), a term we introduce to replace "ellipsoids," surround arterial capillaries in the red pulp of the spleen and are major sites for clearance of blood-borne particles. PAMS and their arterial capillaries in cat spleens in various states of congestion and contraction were studied by transmission electron microscopy. Thorotrast, a colloidal suspension of thorium dioxide, was injected to label macrophages. A PAMS consisted of a fine meshwork of reticular cells and reticular fibers which held macrophages and formed a cylindrical sheath around an arterial capillary lying in its longitudinal axis. Some PAMS were spongy due to loosening of cell associations by plasma infiltration; others were tightly compressed. Blood cells were both free in the interstices of the PAMS and attached to macrophages. Reticular cells formed a closely applied but incomplete layer adventitial to the arterial capillary and extended branches which contributed to the meshwork. Small villous processes on the major branches of reticular cells approached each other, sometimes forming intercellular junctions, and fit into complementary indentations in the surfaces of macrophages and endothelial cells. Thin filaments within reticular cells filled the villous processes and formed a border beneath the plasmalemma; intermediate filaments ran through the centers of the branches. Reticular fibers lay between reticular cells. Basement membrane fabricated of the same material as reticular fibers lay between the endothelium and reticular cells. Macrophages contained Thorotrast and abundant debris of phagocytized cells and were joined by extensive interdigitation of micropseudopodia. Endothelial cells were long rods which lay parallel and were joined along their bases by interdigitating lateral processes. Intercellular junctions were present at some points, but at others lateral processes were everted to form open interendothelial slits through which blood cells could pass. Endothelial cells possessed great numbers of randomly oriented intermediate filaments and small patches of thin filaments scattered along the basal plasmalemma and in lateral processes. Thin filaments may function to attach cells to one another and to the basement membrane and may assist in closing interendothelial slits. We believe that the endothelium responds to changes in arterial blood pressure and blood flow. It stretches to allow dilatation and recoils, probably due to the intermediate filaments, squeezing blood cells through interendothelial slits.

Animals↗
PubMed1990

Pathogenesis of hemorrhage induced by bilitoxin, a hemorrhagic toxin isolated from the venom of the common cantil (Agkistrodon bilineatus bilineatus).

The pathogenesis of hemorrhage induced by the i.m. injection of the hemorrhagic toxin, bilitoxin, was studied using light and electron microscopy. White mice were injected with sublethal doses of the toxin, and tissue samples were obtained at 5 and 30 min, and 1, 3 and 24 hr after the injection. There was a good correlation between amount of toxin injected and amount of hemorrhage observed. Microscopically, hemorrhage was visible in all parts of the connective tissue surrounding muscle cells just 5 min after injection and fibrin was present both intravascularly and extravascularly. At later time periods the hemorrhage was more extensive and there was more fibrin. Many vessels were plugged with platelets. At 30 min after the injection, muscle cells appeared to be damaged having either delta lesions or disrupted myofibrils. Electron microscopy revealed damaged capillaries with ruptured endothelial cells, disrupted basal lamina and intact intercellular junctions. Thus, this hemorrhagic toxin acts rapidly to disrupt the capillary endothelium without damaging the intercellular junctions, and it also appears to damage skeletal muscle cells.

Animals↗
PubMed2006

Role of aPKC isoforms and their binding partners Par3 and Par6 in epidermal barrier formation.

The skin water barrier, essential for terrestrial life, is formed by a multilayered stratifying epithelium, which shows a polarized distribution of both differentiation and intercellular junction markers. Recently, several reports showed the crucial importance of tight junctions for the in vivo water barrier function of the skin. In simple epithelial cells, intercellular junction formation is closely coupled to the establishment of polarity. However, if and how polarity proteins contribute to epidermal differentiation and junction formation is not yet known. Here, we have characterized the localization and isoform expression of the polarity protein atypical PKC (aPKC) and its binding partners Par3 and Par6 in epidermis and primary keratinocytes of mice. Their distribution is only partially overlapping in the granular layer, the site of functional tight junctions, suggesting that next to a common Par3/Par6/aPKC function they also may have functions independent of each other. Both aPKCzeta and aPKCiota/lambda, are expressed in the epidermis but only aPKCiota/lambda showed a strong enrichment in the junctions, suggesting that this aPKC isoform is important for epidermal tight junction function. Indeed, inhibition of aPKC function showed that endogenous aPKC is crucial for in vitro barrier function and this required the presence of both the Par3 and Par6 binding sites.

Adaptor Proteins, Signal Transducing↗
PubMed2000

Coordinated reassembly of the basement membrane and junctional proteins during corneal epithelial wound healing.

PURPOSE: To characterize changes in the localizations of the basement membrane protein laminin-1 and of adhesion proteins of intercellular junctions during wound healing after epithelial ablation in the rat cornea. METHODS: Epithelial ablation was performed with an excimer laser. Rats were killed immediately, 12 hours, 24 hours, 3 days, or 4 weeks after ablation, and corneal cryosections were subjected to two-color immunofluorescence staining with antibodies to laminin-1 and antibodies to connexin43 for gap junctions, desmoglein 1 or 2 (desmoglein 1 + 2) for desmosomes, or E-cadherin for adherens junctions. Sections were also stained with antibodies to occludin for examination of tight junctions. RESULTS: Laminin-1 was detected in the basement membrane, connexin43 in the basal cell layer, desmoglein 1 + 2 in the wing cell layer, E-cadherin in all cell layers, and occludin in the wing and superficial cell layers of the intact corneal epithelium. Laminin-1 immunostaining was not detected at the leading edge of migrating epithelial cells until 24 hours after ablation. Expression of connexin43 and desmoglein 1 + 2 coincided with the reappearance of laminin-1, whereas that of E-cadherin and occludin was apparent regardless of the absence or presence of laminin-1. Epithelial remodeling was complete after 4 weeks. The basement membrane was re-established, and the expression patterns for all the adhesion proteins were identical with those characteristic of the intact cornea. CONCLUSIONS: Actively migrating epithelial cells no longer manifested gap junctions and desmosomes in the wounded area with no basement membrane. Re-establishment of the basement membrane coincided with reassembly of these intercellular junctions, suggesting that the presence of the basement membrane may be required for their reformation in the rat cornea.

Animals↗
PubMed2002

Implication of direct host-tumor intercellular interactions in non-immune host resistance to neoplastic growth.

The hallmark of cancer as a disease is impaired homeostasis, which in normal tissue is maintained by the network of direct intercellular contacts. The cell-cell interaction machinery consists of intercellular junctions of various types, each of which has a role in the control of cell growth, differentiation, and motility. In cancer, the function of intercellular junctions is altered, often at quite advanced stages of tumor progression, while proper intercellular interactions between normal and tumor cells may control and even suppress, otherwise, aberrant growth and behavior of neoplastic cells. This type of host resistance to neoplastic growth implies a homotypic functional partnership between tumor cells and their normal host counterparts and, thus, is to a certain extent complementary to immune defense against tumorigenesis, which is effective only when tumor cells became 'foreign' for the host. Functional interactions between host and tumor cells could be lost at different stages of tumorigenesis through a range of mechanisms. In some cases, host-tumor interactions may be impaired reversibly, which in turn gives rise to the possibility of restoring this component of host defense against cancer by correctional interventions. This review highlights the role that direct intercellular host-tumor interactions may play in natural host resistance against neoplastic growth, with an emphasis on the underlying mechanisms of both their function and impairment.

Animals↗
PubMed2003

The expression of the tumor suppressor gene connexin 26 is not mediated by methylation in human esophageal cancer cells.

Gap junctional intercellular communication is thought to play an important role in cell differentiation and tissue homeostasis. Gap junctional intercellular communication is mediated by intercellular channels connecting adjacent cells and composed of connexin (Cx) proteins. Until now, approximately 20 different Cx have been characterized in mammals, and they are expressed in a tissue-specific manner. The downregulation of Cx expression is often observed in tumors and transformed cell lines and is believed to contribute to the loss of proliferating control. Connexin 26 (Cx26) is a Cx constitutively expressed in the normal epithelial esophageal tissue. In the majority of esophageal tumors, Cx26 expression is low or totally absent. CpG island hypermethylation is known to be associated with gene silencing in cancer. Because the promoter and exon 1 region of Cx26 are rich in CpG dinucleotides, we examined whether the loss of Cx26 expression in human esophageal TE cell lines was related to the hypermethylation of this region. We analyzed several TE cell lines derived from different human esophageal carcinomas and exhibiting different levels of Cx26 expression by using methylation-sensitive restriction digestion and Southern blot analysis. We did not find any correlation between the Cx26 expression and the methylation level of the promoter region of the Cx26 gene. Our results suggest that methylation was probably not involved as a primary mechanism of Cx26 regulation in human esophageal cancer cell lines.

Connexin 26↗