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PubMed1988

Intercellular junctions in the follicular envelope of the teleost, Brachydanio rerio.

The nature and distribution of intercellular junctions in the outer ovarian epithelium (serosa, mesothelium), endothelium, and follicle cells of the teleost oocyte-follicle complex were investigated by freeze-fracture electron microscopy. Tight-junctions were common between outer squamous epithelial cells, sometimes closely associated with intercalated foci of communicating junctions. The tight junctions consisted of one to several sealing strands which possessed focal discontinuities. In addition, the strands existed as loops or as short, free-ending elements; a condition that could indicate lability in their assembly or disassembly. The presence of free-ending strands could also mean that the structure serves for attachment as well as involved in the formation of occluding zonules. The free ends of some bars comprising the tight junctional strands are enlarged slightly. In outer ovarian epithelial or serosal cells, as is the case for mammalian mesothelium described by others, clusters of particles comprising communicating (gap) junctions are often intercalated within or are located in close proximity to tight junctional strands. In freeze-cleaved replicas, the outer squamous epithelial (serosal) cells contained a multitude of micropinocytotic pits (caveolae) and vesicles. Capillary endothelium also contains tight junctional components which are often closely associated with communicating junctions. Tight junctions also exist between follicle cells, but their structure changes during oocyte growth. Communicating junctions between follicle cells tend to be focal in distribution and not closely associated with tight junctions.

Animals↗
PubMed2003

Gap junctional intercellular communication and cellular response to heat stress.

Gap junctional intercellular communication (GJIC) is essential in the maintenance of tissue homeostasis and has been implicated in tumor suppression. Recent studies have indicated that GJIC is also involved in cellular stress responses to low dose ionizing radiation, UV light and hydrogen peroxide. However, the contribution of GJIC to the heat stress response has not yet been elucidated. We here demonstrate a potential link between GJIC and the heat stress response. First, we investigated whether the abolition of GJIC by lindane affects heat sensitivity in normal human cells. Lindane potentiated cell killing by heat shock at 43 degrees C, whereas little or no cytotoxicity was observed at 37 degrees C. Nuclear translocation of heat shock protein 72 (HSP72) was interrupted by lindane, although its induction was not affected. These results indicate that lindane exacerbates hyperthermic lethality via disrupted nuclear translocation of HSP72 protein. Second, we assessed whether heat shock alters GJIC and phosphorylation of gap junction connexin (Cx) proteins in normal human cells. Persistent heat treatment augmented Cx43 phosphorylation in a heat- and time-dependent fashion and this phosphorylation was recovered after heat shock. GJIC was also disturbed by heat shock. These results indicate that heat shock augments Cx43 phosphorylation leading to GJIC abrogation. Our present results imply that GJIC contributes to protection against heat stress and that loss of GJIC function during carcinogenesis exacerbates hyperthermic lethality.

Cell Communication↗
PubMed2000

Taurine preserves gap junctional intercellular communication in rat hepatocytes under oxidative stress.

Gap junctional intercellular communication (GJIC) between hepatocytes is important for the maintenance of differentiated liver functions. Taurine is known to be cytoprotective, and is used clinically to improve liver functions. We evaluated the effect of taurine on GJIC in hepatocyte doublets under oxidative stress. Hepatocyte doublets were isolated from female Wistar rats, using a collagenase perfusion technique, and cultured in Leibovitz-15 medium containing fetal bovine serum (10%). H2O2 (2 mM) and/or taurine (0.1-1 mM) were added 2 h after inoculation, and the culture was incubated for 3 h. Fluorescent dye (Lucifer Yellow CH) coupling between adjacent cells was evaluated by microinjection. The distribution and quantity of connexin 32 (Cx32) in hepatocytes were detected using indirect immunofluorescence analysis and Western blotting. Steady state mRNA levels of Cx32 were detected by Northern blotting. The percentage of dye coupling 5 h after inoculation was 88 +/- 6.3% in the control. however, this was decreased to almost half the control value by H2O2. Taurine prevented the decrease caused by H2O2 in a dose-dependent manner. Immunofluorescence analysis for Cx32 demonstrated numerous punctate fluorescent spots along the intercellular plasma membrane in controls, which were significantly decreased by H2O2. Taurine prevented the decrease of Cx32. Western blot analysis also showed the decrease of Cx32 protein levels by H2O2 treatment, which decrease was prevented by taurine. Interestingly, H2O2 and/or taurine treatments did not affect Cx32 mRNA levels. Our findings indicated that H2O2 treatment decreased GJIC between hepatocytes, most likely due to augmenting the degradation of Cx32 proteins, whereas taurine prevented this process. This effect of taurine is beneficial for the preservation of differentiated functions in the liver under oxidative stress.

Animals↗
PubMed1991

Molecular mechanisms of TPA-mediated inhibition of gap-junctional intercellular communication: evidence for action on the assembly or function but not the expression of connexin 43 in rat liver epithelial cells.

We found that a rat liver epithelial cell line (IAR 20) expresses connexin 43, the major cardiac gap-junction protein, but not connexin 26 or connexin 32, major liver gap-junction proteins. The effects of TPA on connexin 43 expression in IAR 20 were investigated using northern blot analysis, western blot analysis, and an immunofluorescence technique. Gap-junctional intercellular communication (GJIC) in this cell line decreased within 60 min of 12-O-tetradecanoylphorbol-13-acetate (TPA) treatment and recovered after 24 h. The number of immunofluorescence spots of connexin 43 on IAR 20 was closely related to the change in GJIC induced by TPA. However, TPA did not change the level of mRNA measured by northern blot analysis. Moreover, connexin 43 protein expression analyzed by western blotting suggests that connexin 43 proteins were still present in TPA-treated cells at a similar level. These results suggest that GJIC of these rat liver epithelial cells was mediated by connexin 43 protein and that TPA inhibited GJIC by inhibiting posttranslational processing of connexin 43 proteins, e.g., localization or assembly.

Animals↗
PubMed1998

Cooperative effects of v-myc and c-Ha-ras oncogenes on gap junctional intercellular communication and tumorigenicity in rat liver epithelial cells.

The objective of this study was to isolate and partially characterize several rat liver epithelial cell clones containing myc, ras and myc/ras oncogenes in order to study their roles in apoptosis and to test the hypothesis that gap junctional intercellular communication is necessary for apoptosis in solid tissues and that the loss of junctional communication leads to tumorigenesis. The co-transfection of the myc and ras oncogenes in the normal rat liver epithelial cell line (WB-F344) resulted in a loss of functional channels and normal growth regulation; cell-cell communication was significantly decreased and tumorigenicity determined in adult male F344 rats was induced. We examined cell growth properties, gap junctional intercellular communication (GJIC), using the scrape-loading-dye transfer and fluorescence-redistribution-after-photobleaching assays, and tumorigenicity in a series of normal and v-myc-, c-Ha-ras- and v-myc/c-Ha-ras-transfected WB-F344 cell lines. The c-Ha-ras- and the v-myc/c-Ha-ras-transduced cell lines appeared distinctly different from the other lines, having spindle-shaped morphology, shorter generation time and contact insensitivity. On the other hand, the normal WB-F344 cell line and the v-myc-transduced cell line showed excellent GJIC. Moreover, the c-Ha-ras-transduced cell lines displayed decreasing levels of GJIC associated with their increasing tumorigenicity. The v-myc/c-Ha-ras-transformed cell lines showed the lowest levels of GJIC and were also the most tumorigenic. These findings suggest that the reduction of GJIC in c-Ha-ras- and v-myc/c-Ha-ras-transformed WB-F344 cells is linked to their tumorigenic potential. These cell lines should provide valuable tools to study the role of GJIC in apoptosis during tumorigenesis.

Animals↗
PubMed2004

Role of transglutaminase 1 in stabilisation of intercellular junctions of the vascular endothelium.

Microvascular endothelial monolayers from mouse myocardium (MyEnd) cultured for up to 5 days postconfluency became increasingly resistant to various barrier-compromising stimuli such as low extracellular Ca(2+) and treatment with the Ca(2+) ionophore A23187 and with the actin depolymerising compound cytochalasin D. In contrast, microvascular endothelial monolayers from mouse lung microvessels (PulmEnd) remained sensitive to these conditions during the entire culture period which corresponds to the well-known in vivo sensitivity of the lung microvasculature to Ca(2+) depletion and cytochalasin D treatment. One molecular difference between pulmonary and myocardial endothelial cells was found to be transglutaminase 1 (TGase1) which is strongly expressed in myocardial endothelial cells but is absent from pulmonary endothelial cells. Resistance of MyEnd cells to barrier-breaking conditions correlated strongly with translocation of TGase1 to intercellular junctions. Simultaneous inhibition of intracellular and extracellular TGase activity by monodansylcadaverine (MDC) strongly weakened barrier properties of MyEnd monolayers, whereas inhibition of extracellular TGases by the membrane-impermeable active site-directed TGase inhibitor R281 did not reduce barrier properties. Weakening of barrier properties could be also induced in MyEnd cells by downregulation of TGase1 expression using RNAi-based gene silencing. These findings suggest that crosslinking activity of intracellular TGase1 at intercellular junctions may play a role in controlling barrier properties of endothelial monolayers.

Animals↗
PubMed1998

Downregulation of connexin32 protein and gap-junctional intercellular communication by cytokine-mediated acute-phase response in immortalized mouse hepatocytes.

In the present study, we have analyzed the direct effects of cytokines, which mediate the acute-phase response in liver, on connexin expression and gap-junctional intercellular communication in immortalized MHSV12 mouse hepatocytes. When these cells were stimulated for 24 h with interleukin 1 and interleukin 6, the amount of connexin26 (Cx26) mRNA increased together with beta-fibrinogen mRNA, as expected for this positive acute-phase gene. In contrast, connexin32 (Cx32) mRNA expression was not affected under these conditions. Indirect immunfluorescence revealed a drastic decrease in Cx32 signals, whereas slightly more Cx26 signals were found. Stronger stimulation with interleukin 1 and tumor necrosis factor alpha gave a dose-dependent increase in steady state levels of Cx26 and beta-fibrinogen mRNA, but no further change in Cx32 mRNA level was seen. However, when Cx32 protein was analyzed on immunoblots, we found a 5-fold decrease in expression even at low cytokine doses that did not affect Cx32 mRNA expression. Under these conditions, cell to cell transfer of Lucifer yellow, microinjected into immortalized hepatocytes, was decreased by 70%, suggesting that intercellular communication through Cx32 channels was partially inhibited earlier than other genetic alterations characteristic of the acute-phase response. Thus, the major hepatic gap junction protein was largely downregulated at the beginning of the experimental inflammatory reaction, but about 30% of gap-junctional intercellular communication was maintained. This suggests that, during the acute-phase response, the second hepatic Cx26 protein may compensate in part for the downregulation of the Cx32 protein.

Acute-Phase Reaction↗
PubMed2003

Suppression of gap junctional intercellular communication via 5' CpG island methylation in promoter region of E-cadherin gene in endometrial cancer cells.

Previously, we demonstrated that connexins (Cxs) showed aberrant localization and expression in most endometrial hyperplasia and carcinoma samples, indicating that during endometrial carcinogenesis, loss of gap junctional intercellular communication (GJIC) may occur at relatively early stages. In the present study, we focused on the correlations between GJIC and the expression of the E-cadherin and its 5' CpG island methylation in endometrial cancer cells and tissues to investigate their roles in the carcinogenesis and tumor progression of endometrial cancer. In this study, three of the 10 cell lines investigated, Ishikawa, RL-952 and KLE, in which both Cxs and E-cadherin mRNA were expressed, exhibited GJIC by scrape-loading/dye transfer. On the other hand, the other seven cell lines, in which either or both Cxs and E-cadherin mRNA were negative or weakly expressed, did not show GJIC. HEC-50, HEC-1B and HEC-108, in which Cxs were positively expressed but E-cadherin was negatively expressed, showed cytoplasmic localization of Cxs by immunohistochemistry. All five lines, which showed the weak expression of E-cadherin, had E-cadherin 5' CpG island methylation. By immunohistochemistry of 56 endometrial carcinomas, 13 of 27 methylated samples showed weak expression of Cx26 and the other 14 showed diffuse localization in cytoplasm. On the other hand, of 29 unmethylated samples, two showed cell-cell localization, 25 weak expression and two diffuse localization. Furthermore, E-cadherin expression was revealed to be drastically down-regulated by E-cadherin antisense oligonucleotides that post-transcriptionally down-regulated E-cadherin expression and in the cell, the localization of Cxs were changed from the cell-cell borders to the cytoplasm, and GJIC also decreased. The results indicated that 5' CpG island methylation, which caused loss of E-cadherin expression, indirectly caused the suppression of GJIC by aberrant localization of Cxs in endometrial carcinoma cells.

Adenocarcinoma↗
PubMed1990

Inhibition of hepatocyte gap junctional intercellular communication by endosulfan, chlordane and heptachlor.

The cyclodiene pesticides endosulfan, chlordane and heptachlor have been reported to be non-genotoxic rodent hepatocarcinogens. These three compounds and several metabolites of endosulfan (endosulfan sulfate, endosulfan ether and endosulfan lactone) were examined for their effects on gap junctional intercellular communication (GJIC) in primary cultured male F344 rat hepatocytes and B6C3F1 mouse hepatocytes. GJIC was evaluated by Lucifer Yellow CH dye-coupling. Endosulfan and endosulfan sulfate inhibited rat and mouse hepatocyte GJIC in a dose-responsive manner (50-200 microM) after 4 h treatment. Endosulfan ether inhibited rat hepatocyte GJIC only at 200 microM and had no effect on mouse hepatocytes. Endosulfan lactone did not affect rat or mouse hepatocyte GJIC. Chlordane and heptachlor inhibited both mouse and rat hepatocyte GJIC at concentrations of 50-200 microM. The inhibition of GJIC by the cyclodienes showed similar dose-response relationships and kinetics of onset of inhibition and reversibility for both mouse and rat hepatocytes. Concomitant treatment of the cells with inhibitors of cytochrome P450 monooxygenases (SKF-525A, piperonyl butoxide or carbon monoxide) did not alter the inhibition of GJIC by the cyclodienes, suggesting that cytochrome P450 metabolism was not involved in the inhibitory mechanism. Dibutyryl cyclic AMP (0.5 mM), however, decreased the inhibition of GJIC by the cyclodienes and may indicate that these compounds inhibit intercellular communication through a cAMP-dependent process. The inhibition of mouse and rat hepatocyte GJIC by the cyclodienes correlated with previous reports indicating that these compounds are non-genotoxic rodent liver carcinogens.

Animals↗
PubMed1984

Intercellular junctions of methylcholanthrene-induced rat skin basocellular and squamous carcinomas.

The occurrence of different intercellular junctions in epithelial rat skin tumours induced by methylcholanthrene was investigated using thin sections and freeze-fracture replicas examined by electron microscopy. Tumours which appeared first were basal cell carcinomas. Later, different tumours of hair follicle and of sebaceous gland origin were formed. Finally, in the majority of tumours a squamous component evolved. Metastases developed from the squamous carcinomas exclusively. Desmosomes and gap junctions were detected in basal cell carcinomas whereas, in squamous carcinomas, tight junctions were also seen. While all three types of junction were found in the primary squamous tumours, the tumour metastases in lymph nodes and lungs contained only desmosomes.

Animals↗
PubMed2006

Herpes simplex virus-type 2 infectivity and agents that block gap junctional intercellular communication.

In rat liver epithelial (WB) cells, the protein kinase C inhibitor H7 blocked gap junctional intercellular communication (GJIC) and reduced virus infectivity. Octanol, 18-beta-glycyrrhetinic acid, and staurosporine, agents that reduce GJIC, had no effect upon virus infectivity. Previous studies demonstrated that herpes simplex virus-type 2 (HSV-2) infection was accompanied by attenuated GJIC. Of agents tested, only H7 reduced plaque forming unit (pfu) ability in a dose-dependent manner with 100% plaque reduction at 40 microM without evidence of cytotoxicity. Dye transfer indicated that H7 decreased GJIC, although Western blotting revealed that it did not alter phosphorylation of the gap junction protein, connexin 43 (Cx43). Using indirect immunofluorescence, Cx43 was found to localize in membrane plaques in uninfected cells and H7 did not alter this distribution. However, Cx43 was lost from the membrane at 24h in both H7-treated and untreated cells infected with HSV-2. Viral infection increased serine phosphorylation, particularly in the nuclear region, and this effect was reduced following H7 treatment. Thus, H7 attenuated both GJIC and infectivity of HSV-2 in WB cells but the anti-viral effects were due to reduced nuclear protein phosphorylation rather than alterations in phosphorylation or localization of Cx43.

Animals↗
PubMed1991

[Effects of tumor promoting herb Wikstroemia chamaedaphne extract on V79 cells and WB liver cells: I. Correlation between cellular growth and gap junctional intercellular communication].

A Chinese herb, wikstroemia Chamaedaphen (WC) extract, recently has been shown to be a potential tumor promoting agent on uterine cervical carcinoma induced by HSV-2 or MCA in mice. To determine whether the tumor promoting effects of WC extract were mediated through inhibition of gap junctional intercellular communication (GJIC) with relation to cellular growth, experiments were conducted on Chinese hamster V79 cells and rat WB liver cells by utilization of SLDT method for GJIC detection and cell growth curve examination, 3H-TdR incorporation, mitotic index (MI) and Flow Cytometry (FCM) methods. TPA was used for comparative purpose. WC extract inhibited GJIC and stimulated cell growth in a dose (2-200 micrograms/ml) and time (0-72 hr)-dependent manner in both cell lines. Both WC extract and TPA treatments increased V79 cell growth rate. The average cell doubling-time was decreased from 36.5 hr in control V79 cells to 28.2 hr in WC extract (10 micrograms/ml) and 20.9 hr in TPA (50 ng/ml) treatment by the 3rd day. Stimulating effect of both drugs on DNA synthesis of V79 cells was demonstrated. The results of FCM and MI indicated that the cell number of M-phase cells was increased after drug treatment. It is suggested that (1) tumor promoting effect of WC extract might be mediated through inhibition of GJIC: (2) inhibition of GJIC is closely correlated with increased cell growth rate and entry of cell division cycle.

Animals↗
PubMed1993

Gap junctional intercellular communication of primary and asbestos-associated malignant human mesothelial cells.

We examined gap junctional intercellular communication (GJIC) of primary human mesothelial cells and cell lines of asbestos-associated human pleural mesotheliomas, and the effect of asbestos and other mineral fibres on these cells. In homologous cultures, the GJIC capacity of six out of seven tumour cell lines was markedly less than for primary mesothelial cells. This defect in GJIC appeared not to be at the expression level of mRNA and protein of the gene encoding the 43 kDa gap junction protein. In heterologous cocultures of tumour cells and primary mesothelial cells, however, 80-90% of the tumour cell/normal cell contacts were functional. Exposure of primary mesothelial cells to TPA, a phorbol ester tumour promoter, resulted in marked inhibition of GJIC, being an action common to numerous tumour promoters. Such an effect though was not observed with the carcinogenic mesothelioma-inducing mineral fibres chrysotile and amosite, neither with glass wool. These results suggest that a permanent defect in GJIC capacity is a common feature of human mesothelioma cells, but how mineral fibres are involved in the process of mesotheliomagenesis is still unclear.

Asbestos↗
PubMedDate not supplied

Intercellular junction formation between polymorphonuclear leukocytes, and between polymorphonuclear leukocytes and tumor cells.

Morphologic evidence of intercellular junctions was found between polymorphonuclear leukocytes (PMNs) and between PMNs and tumor cells. All these junctions displayed electron-dense plaques along the plasma membranes with linear spaces in between. These plaques were finely granular and devoid of filaments. Fine granules were also observed in some of these linear spaces. The significance of these morphologic findings is not known but may be elucidated by a correlative type of study.

Adenocarcinoma↗
PubMed1980

Intercellular junctions in the uterine epithelium of Salamandra salamandra (L.) (Amphibia, Urodela). A freeze-fracture study.

Intercellular junctions in the uterine epithelium of the ovoviviparous urodele Salamandra salamandra were studied in pregnant and non-pregnant females by freeze-fracture technique. Junctional complexes consist of zonulae occludentes (tight junctions) and numerous maculae adhaerentes (desmosomes); z. adhaerentes and nexuses (gap junctions) could not be identified. Tight junctions are of the "flexible" type exhibiting loosely interconnected fibrils. The fibrillary network appears stretched more often in pregnant females possibly due to the mechanical stress of pregnancy. The structure and occurrence of the junctions identified, especially that of the tight junctions, is discussed with regard to the functions of the uterus during pregnancy.

Animals↗
PubMed2000

Induction of gap junctional intercellular communication, connexin43 expression, and subsequent differentiation in human fetal neuronal cells by stimulation of the cyclic AMP pathway.

Expression of gap junction proteins and cell-cell communication was studied in the human neural-glial cell line, SVG, as a first step in defining whether the SVG cells could be used as a model system to study the role of gap junctions in neuronal precursor cells. SVG cells were found to express connexin43 protein that co-migrated with WB-F344 rat liver connexin43 and that reacted with connexin43-specific antibodies on Western blots. However, fluorescence recovery after photobleaching analysis of 5,6-carboxyfluorescein-loaded cells failed to show significant dye coupling. Agents that stimulate the adenylyl cyclase/cAMP pathway were used to induce gap junctional intercellular communication in the SVG cultures. A 24-48 h treatment of SVG cells with 5 microM forskolin or 5 microM forskolin + 200 microM 3-isobutyl-1-methylxanthine increased the percentage of dye-coupled cells from 5-65%, using the fluorescent recovery after photobleaching method. The increase in dye coupling induced by forskolin or forskolin + 3-isobutyl-1-methylxanthine was inhibited by octanol, which is known to block gap junction-mediated cell communication. Western blot analysis of total protein extracts revealed the appearance of a higher molecular weight connexin43 protein band after treatment of SVG cells with forskolin or forskolin + 3-isobutyl-1-methylxanthine, that was not observed in vehicle-treated controls. Alkaline phosphatase treatment of total protein extracts from forskolin or forskolin + 3-isobutyl-1-methylxanthine-treated cells reduced the higher molecular weight band to approximately 41,000 the same as observed in the control extracts. The alkaline phosphatase treatment demonstrates that the higher molecular weight band was due to a phosphorylation event stimulated by forskolin or the forskolin + 3-isobutyl-1-methylxanthine combination. In addition, treatment of the SVG cells with the forskolin or forskolin + 3-isobutyl-l-methylxanthine stimulated outgrowth of neurite-like processes from the cell body which immunostained positive for the connexin43 protein as well as protein markers for neurons and oligodendrocytes. We hypothesize that the SVG cells may represent a neuronal progenitor cell population that has the ability to differentiate when exposed to the appropriate signals.

1-Methyl-3-isobutylxanthine↗
PubMed1994

Two inhibitors of gap junctional intercellular communication, TPA and endosulfan: different effects on phosphorylation of connexin 43 in the rat liver epithelial cell line, IAR 20.

The skin tumour promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) and the chlorinated insecticide, endosulfan, are two potent inhibitors of gap junctional intercellular communication. In the present study the effects of TPA and endosulfan on cell communication have been investigated in IAR 20 rat liver epithelial cells, as well as the effects of these compounds on connexin 43 (cx43), the main gap junction protein in this cell line. The results clearly demonstrate that at non-toxic doses both compounds inhibited the cell communication by at least 90% within 5 min. The communication was partially restored after 4 h of TPA exposure and almost fully restored by 24 h, whereas in endosulfan-exposed cells the communication was completely down-regulated for the whole exposure-period of 24 h. Immunoblots of IAR 20 cell extracts indicated that TPA initially caused an increased phosphorylation of cx43. A normal phosphorylation pattern was observed after 4 h when the cell communication was restored. Immunoblot analysis after endosulfan-exposure showed a slightly increased phosphorylation of cx43 after 10 min treatment, gradually followed by dephosphorylation during the rest of the 24 h treatment period. Immunostaining of IAR 20 cells showed that both compounds caused a rapid disappearance of cx43 from the cell membrane. After 4 h of exposure immunofluorescent cx43-plaques started to reappear in the cell membrane, although less pronounced in endosulfan-treated cells. However, after 24 h of endosulfan-exposure a high number of cx43-spots was demonstrated. These results indicate that different mechanisms are responsible for the inhibition of gap junctional intercellular communication induced by TPA and by endosulfan, at least during the later part of the 24 h exposure-period. TPA causes a marked hyperphosphorylation of cx43, whereas endosulfan increases phosphorylation initially only slightly but longer exposure-periods lead to hypophosphorylation. Thus, phosphorylation as well as dephosphorylation seem to be important factors involved in the regulation of the function of cx43 in this cell line.

Animals↗
PubMed1982

Intercellular junctions of the hen parathyroid gland. A freeze-fracture study.

The fine structure of the intercellular junctions of the hen parathyroid gland was studied using freeze-fracture replicas and thin sections. In the conventional thin sections, desmosomes, intermediate junctions (maculae adherentes) and gap junctions were observed, and in the lanthanum-fixed sections, tight junctions (maculae occludentes) were demonstrated as well. In the freeze-fracture replicas, desmosomes, gap junctions, tight junctions and combination forms of gap and tight junctions occurred, but intermediate junctions were not identified. Junctional complexes (zonulae occludentes) were not encountered in any preparations. The gap junctions varied in size and shape; they ranged from irregularly shaped, minute assemblages of particles to large aggregations of a round or elliptic outline. Both the tight junctions and the combination forms of gap and tight junctions also exhibited a variety of shape and dimension, and, depending on the form of the tight junctional strands, they were classified into three types: type I consisted of a simple line of strands; type II consisted of a closed network of strands; and type III consisted of an open network of strands. The combination forms were more numerous than the typical tight junctions. The possible significance of these junctions is discussed in relation to the function of the parathyroid parenchymal cell.

Animals↗