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PubMed1980

Effects of estrogen and androgen on the ultrastructure of secretory granules and intercellular junctions in regressed canine prostate.

Epithelial cells in the prostate of the castrated or hypophysectomized dog were studied by thin-section and freeze-fracture electron microscopy to determine in vivo responses to estradiol-17 beta 17-cyclopentylpropionate (ECP) and testosterone cyclopentylpropionate (TCP). Particular attention was given to changes in specific organelles and intercellular junctions that might reflect hormone action. The few secretory granules that remain in the regressed epithelium (vestigial granules) serve as markers of prior androgen responsiveness. Pharmacologic doses of ECP caused regressed glandular cells to acquire a novel phenotype. Characteristic features of these estrogen-modified glandular (EMG) cells are newly formed secretory granules and tonofilament bundles that coexist with vestigial granules, thus demonstrating bipotentiality of response. Glandular cell-tight junctions appear unaltered by the endocrine manipulations. Although EMG cells have squamous cell features, tight junctions remain intact. Desmosomes in the canine prostate are dimorphic and are classified 70F and 100F according to the width of the filaments that converge on the dense plaques. In intact dogs, 100F desmosomes are associated with basal-reserve cells, whereas only the 70F variety is found between glandular cells. TCP treatment does not alter this distribution. Following ECP administration, both 70F and 100F desmosomes are present between EMG cells. The coexistence of newly formed secretory granules and tonofilaments of 100F desmosomes in the same EMG cell represents estrogen-induced bidirectional differentiation. Our findings indicate that androgens and estrogens are individually capable of controlling the expression of secretory granules and desmosomes. In intact animals, male and female sex hormones may act in concert to direct epithelial cell differentiation of the prostate.

Androgens↗

PubMed2000

Intercellular junctions between palisade nerve endings and outer root sheath cells of rat vellus hairs.

Hair follicles have a longitudinal set of sensory nerve endings called palisade nerve endings (PN). We examined the junctional structures between the PN and outer root sheath (ORS) cells of hair follicles in the rat external ear. Transmission electron microscopy of serial thin sections showed that the processes of the ORS cells penetrated the basal lamina of the hair follicle, forming intercellular junctions with the PN (PN-ORS junctions). Two types of junctions were found: junctions between nerve endings and ORS cells (N-ORS junctions) and those between Schwann cell processes and ORS cells (S-ORS junctions). The N-ORS junctions had two subtypes: 1) a short process or small eminence of the ORS cell was attached to the nerve ending (type I); or 2) a process of the ORS cell was invaginated into the nerve ending (type II). The S-ORS junctions also had two subtypes: 1) a short process or small eminence of the ORS cell was abutted on the Schwann cell process (type I); or 2) a process of the ORS cell was invaginated into the Schwann cell process (type II). Vesicles, coated pits, coated vesicles, and endosomes were sometimes seen in nerve endings, Schwann cells, and ORS cells near the junctions. Computer-aided reconstruction of the serial thin sections displayed the three-dimensional structure of these junctions. These results suggested that the PN-ORS junctions provided direct relationships between the PN and ORS in at least four different patterns. The discovery of these junctions shows the PN-ORS relationship to be closer than previously realized. We speculate that these junctions may have roles in attachment of the PN to the ORS, contributing to increases in the sensitivity of the PN, and in chemical signaling between the PN and ORS.

Animals↗

PubMed1996

Focal adhesion kinase pp125FAK is associated with both intercellular junctions and matrix adhesion sites in vivo.

Previous studies have characterized pp125FAK as a focal adhesion (FA)-associated non-receptor tyrosine kinase. However, there are few data available on the expression and localization of this kinase in tissues. In this study we show that in human tissues the highest expression of pp125FAK is found in some developing epithelia, where pp125FAK is associated with either intercellular junctions or with sites of adhesion to the basement membrane, whereas the same adult tissues show only a faint reactivity. Connective tissue cells do not show any reactivity for pp125FAK in vivo, but developing arterial smooth muscle expresses pp125FAK at high levels. The expression pattern in malignant tissues is variable, but most carcinomas do not express this kinase. In primary cultures of human amnion epithelial cells pp125FAK first becomes associated with the polarized adhesion lamellae, but is subsequently translocated to the forming adherens junctions (AJs). Later upon culturing pp125FAK becomes associated with prominent FAs, as in cultured cell lines. Taken together, our results suggest that the association of pp125FAK with FAs in cultured cells is principally due to a process of adaptation, whereas in vivo pp125FAK mainly functions as a regulatory component of intercellular AJs and cell-matrix adhesions of developing epithelia and also in developing arterial smooth muscle.

Adult↗

PubMed2004

17beta-estradiol reduces the effect of metabolic inhibition on gap junction intercellular communication in rat cardiomyocytes via the estrogen receptor.

The effects of 17beta-estradiol (E2) on gap junction intercellular communication (GJIC) were assessed by Lucifer yellow dye coupling in cultured neonatal rat cardiomyocytes after metabolic inhibition (MI) using potassium cyanide and sodium iodoacetate. MI significantly reduced dye coupling of cardiomyocytes to 8.5% +/- 0.6% of control levels, and pretreatment with E2, but not its inactive isomer 17alpha-estradiol, dose-dependently (EC(50) = 0.41 microM) increased the dye coupling up to 76% +/- 15% of control levels. The effect of E2 on MI-induced dye uncoupling was abolished by tamoxifen, a potent estrogen receptor (ER) antagonist. The ligand, E2-BSA-FITC, labeled the cardiomyocyte surface, whereas BSA-FITC did not, suggesting the presence of membrane-associated E2 receptors. Double immunofluorescence microscopy showed that MI-induced the accumulation of non-phosphorylated Cx43 at the gap junction and that this was prevented by E2 pretreatment. Labeling of Lucifer yellow-microinjected cardiomyocytes with antibodies specific for Ser368-phosphorylated Cx43 (Ser368Cx43) or non-phosphorylated Cx43 confirmed that E2 reduced the MI-induced inhibition of dye coupling and accumulation of non-phosphorylated Cx43 concomitant with the reappearance of Ser368Cx43 at the gap junction. MI caused a decrease in Ser368Cx43 protein levels, and pretreatment with E2 significantly increased the levels of Ser368Cx43. Inhibition of protein kinase C (PKC) with chelerythrine blocked the E2-induced increase of Ser368Cx43 levels in MI-treated cardiomyocytes. These results suggest that E2 attenuates the inhibitory effect of MI on GJIC in cardiomyocytes by affecting the phosphorylation of Cx43, possibly mediated by activation of PKC via a membrane-associated signaling mechanism.

Alkaloids↗

PubMed1994

Gap junctional intercellular communication of cultured rat liver parenchymal cells is stabilized by epithelial cells and their isolated plasma membranes.

The gap junctional intercellular communication (GJIC) determined by measuring dye coupling with Lucifer yellow, decreased within 3 d from 66% to 28% in monocultures of rat liver parenchymal cells. Coculturing of the parenchymal cells with a nonparenchymal epithelial cell line from rat liver resulted in increased and stabilized intercellular communication (83% after 3 d). The presence of isolated plasma membrane vesicles of the nonparenchymal epithelial cells also stabilized the intercellular communication between the liver parenchymal cells (70% after 3 d). When liver parenchymal cells were cocultured with a rat liver fibroblast cell line the gap junctional communication between the parenchymal cells was not stabilized (43% after 3 d), and isolated plasma membrane vesicles of the fibroblast were also unable to support the GJIC in parenchymal cells (35% after 3 d). It is concluded that plasma membrane constituents of the nonparenchymal epithelial cells were responsible for the stabilization of the GJIC between parenchymal cells. A heterotypic gap junctional communication between parenchymal and nonparenchymal cells was not observed.

Animals↗

PubMed2006

[Effects of resveratrol on growth inhibition and gap-junctional intercellular communication of HepG2 cells].

OBJECTIVE: To investigate the effects of the resveratrol on proliferation and gap-junctional intercellular communication (GJIC) in human liver cancer cell line HepG2. METHODS: MTT assay was used to observe the effects of resveratrol on HepG2 cell growth, and the distribution of cell cycles was detected with flow cytometry (FCM). The effects of resveratrol on GJIC of HepG2 cells labeled with 5'-CFDA/AM was examined with fluorescence redistribution after photobleaching (FRAP) and confocal microscope. RESULTS: The results of MTT assay indicated that the proliferation of HepG2 cells was significantly inhibited by resveratrol in a time- and dose-dependent manner. Resveratrol could arrest HepG2 cell growth in S phase, inhibit DNA synthesis and induce cell apoptosis. Furthermore, the levels of GJIC increased sharply after resveratrol treatment of the cells. CONCLUSION: Resveratrol is capable of inhibiting HepG2 cell proliferation, causing cell growth arrest at S phase and inducing cell apoptosis. Increased GJIC level contributes to the effect of resveratrol in HepG2 cell proliferation inhibition and its cancer chemopreventive activity.

Antineoplastic Agents, Phytogenic↗

PubMed1997

The role of gap junctional intercellular communication (GJIC) disorders in experimental and human carcinogenesis.

There is a growing body of evidence supporting the etiologic implication of gap junctional intercellular communication disorders in carcinogenesis. Substantial progress has recently been made both in molecular biology of gap junction and in the field of cancer research. They provide new insights and conceptions of gap junctional disorders in tumor pathology. Modern understanding of the structure, function and regulation of gap junctions, as well as putative mechanisms of its disorders in human and experimental carcinogenesis are discussed in this review with particular emphasis on fast-moving aspects of this problem.

Animals↗

PubMed2004

Nitric oxide-mediated regulation of connexin43 expression and gap junctional intercellular communication in mesangial cells.

This study investigated a potential role of nitric oxide (NO) in the regulation of gap junctional intercellular communication (GJIC). Incubation of mesangial cells (MC) with NO donor S-nitroso-N-acetylpenicillamine (SNAP) enhanced both basal and 8-bromo-cAMP-stimulated GJIC as well as expression of gap junction protein connexin43 (Cx43). This potentiating action of SNAP on Cx43 expression was mimicked by two other NO donors and significantly blocked by soluble guanylate cyclase inhibitor 1H-[1,2,4]oxadiazolo[4,3,-alpha]quinoxalin-1-1. Guanosine 3',5'-cyclic monophosphate (cGMP) analogue 8-bromo-cGMP exerted an effect similar to NO, whereas another cGMP analogue, 8-pCPT-cGMP, which selectively activates cGMP-dependent kinase without affecting cGMP-inhibited phosphodiesterase (PDE3), had no effect. Moreover, the synergistic action of NO on Cx43 expression was completely prevented by protein kinase A inhibitor H89 but not by cGMP-dependent kinase inhibitor Rp-8-Br-PET-cGMP. These results suggested a possible involvement of NO-cAMP interaction via cGMP-mediated inhibition of PDE3. Indeed, PDE3 inhibitor cilostamide caused potentiation of 8-bromo-cAMP-elicited elevations of Cx43 expression that is similar to the effect of SNAP, and an elevation of intracellular cAMP was detected in SNAP-treated cells. With the use of genetically engineered reporter MC that express secreted alkaline phosphatase under the control of the cAMP response element, significant potentiation of cAMP-elicited activation of cAMP response element by SNAP was found. This effect was abrogated in the presence of PDE3 inhibitor cilostamide. Taken together, the results suggest that NO is involved in the control of GJIC and Cx43 expression. This effect of NO is due to activation of protein kinase A via cGMP-dependent inhibition of PDE3 activity.

3',5'-Cyclic-AMP Phosphodiesterases↗

PubMed1983

Intercellular junctions in the human fetal membranes. A freeze-fracture study.

Freeze-fracture replicas of the human reflected and placental amnion and chorion laeve at term were studied in order to give a systematic survey of the nature and extension of the intercellular junctions in the fetal membranes. No differences could be detected between the reflected and placental amniotic epithelium. In both the replicas never displayed plasma membrane differentiations typical of occluding junctions, while communicating junctions were occasionally and desmosomes frequently seen. In the chorionic trophoblast maculae occludentes, communicating junctions and desmosomes were regularly encountered. It is assumed that the maculae occludentes are remnants of occluding junctions which early in gestation possibly seal off the chorionic cavity; it appears improbable that they contribute significantly to the permeability properties of the chorionic trophoblast, since it is known from previous ultrastructural studies that large open intercellular channels cross the chorionic trophoblast. Thus the absence of occluding junctions, which could act as effective permeability barriers, in both epithelial components of the fetal membranes suggests that the factors able to influence the amniotic fluid turnover or the paraplacental protein exchange are the geometrical relationships and physico-chemical properties of the intercellular channels in the amniotic epithelium and chorionic trophoblast. In addition, communicating junctions were present between fibroblasts in the chorion laeve but not in the amnion, possibly indicating differences in the functional state of these cells and/or their extracellular microenvironments.

Amnion↗

PubMed2002

Irsogladine malate up-regulates gap junctional intercellular communication between pancreatic cancer cells via PKA pathway.

INTRODUCTION: Gap junctions (GJs) are intercellular channels that aid communication between coupling cells and may play a critical role in cell differentiation and growth. Connexins (Cxs) are structural proteins of GJs. Though several reports have demonstrated that Cx expression decreases in various malignant tumors, a pancreatic cancer cell line, PANC-1, was reported to express Cx43 mRNA. It is known that irsogladine malate (IM) can up-regulate gap junctional intercellular communication (GJIC). We examined the effects of IM on GJ between pancreatic cancer cells (PC cells) and the mechanism of GJ up-regulation. METHODOLOGY: GJIC between PC cells (PANC-1) was evaluated by dye transfer methods. The expression of Cx43 was estimated by Western blot analysis with immunoprecipitation sample and immunohistochemical analysis. Intracellular cAMP level was estimated by enzyme-linked immunoassay. RESULTS: IM increased cell coupling in a dose-dependent manner (0M-10 ). Western blot analysis of Cx43 revealed that PANC-1 cells expressed Cx43 protein. Treatment with IM was found to move localization of Cx43 immunoreactive spots from the cytoplasm to boundary lesions with neighboring cells, but no major change was seen in the phosphorylation state of Cx43. Intracellular cAMP level was increased by IM. The PKA inhibitor H-89 and adenylyl cyclase inhibitor SQ22536 inhibited the effects of IM. CONCLUSION: These results suggest that IM up-regulates GJIC between PC cells via regulation of the PKA pathway. It also suggests a useful adjuvant of IM to pancreatic cancer therapy.

Animals↗

PubMed1992

Electron microscope observations on the formation of primitive villi in rat small intestine with special reference to intercellular junctions.

Formation and fusion of intraepithelial cavities have long been considered an essential process in the histogenesis of the intestinal mucosa. By electron microscope observation of thin sections and freeze-fracture replicas of the small intestine of rat fetuses, we first demonstrated the initial steps in the formation of intraepithelial cavities: A focal tight junction (macula occludens) was formed in the abluminal part of the epithelium, after which the membrane of an intracellular cavity was fused with that of the focal tight junction to form an intercellular (intraepithelial) cavity enclosed by a zonula occludens. The present study also revealed that gap junctions appeared and enlarged simultaneously with the formation of primitive villi and differentiation of absorptive cells. These gap junctions gradually came to be confined in the epithelium of intervillous regions where proliferation and differentiation of epithelial cells took place. Absorptive cells in villi rarely had gap junctions. These results suggest that tight and gap junctions play important roles in the histogenesis of the intestinal mucosa, and in the proliferation and differentiation of epithelial cells.

Animals↗

PubMed1989

Synergistic inhibition of metabolic cooperation by oleic acid or 12-0-tetradecanoylphorbol-13-acetate and dichlorodiphenyltrichlorethane (DDT) in Chinese hamster V79 cells: implication of a role for protein kinase C in the regulation of gap junctional intercellular communication.

The effects of TPA and/or DDT and oleic acid and/or DDT on gap junction-mediated intercellular communication (i.e. metabolic cooperation) between Chinese hamster V79 cells was examined. Addition of TPA, DDT or oleic acid alone to cocultures of 6-thioguanine-resistant (6-TGR) and 6-thioguanine-sensitive (6-TGS) V79 cells significantly increased the recovery of 6-TGR cells indicating inhibition of metabolic cooperation. In the presence of TPA and DDT or oleic acid and DDT the observed recovery of 6-TGR cells was significantly greater than the expected (calculated) additive 6-TGR cell recovery. No synergistic increases in 6-TGR cell recovery were observed when co-cultures of V79 cells were exposed to dieldrin and DDT. These results indicate that TPA and DDT or oleic acid and DDT can act synergistically to inhibit metabolic cooperation. These data suggest a role for protein kinase C in the regulation of gap junction-mediated intercellular communication.

Animals↗

PubMed1996

Inhibition of gap junctional intercellular communication in normal human breast epithelial cells after treatment with pesticides, PCBs, and PBBs, alone or in mixtures.

Chemical pollutants in the Great Lakes have found their way through the food chain into humans because of their environmental persistence and lipophilicity. Some epidemiological studies have claimed an association between metabolites of 2,2-bis(p-chlorophenyl)-1,1,1-trichloroethane (DDT), polychlorinated biphenyls (PCBs), and polybrominated biphenyls (PBBs) and breast cancer, but others have reported no such association. We examined various halogenated hydrocarbons for their capacity to inhibit gap junctional intercellular communication (GJIC) in normal human breast epithelial cells (HBEC) when given as single compounds or as mixtures. The scrape-loading/dye transfer and fluorescent redistribution after photobleaching techniques were used to measure GJIC; immunostaining and Western and Northern analyses were performed on connexin 43 (Cx43) gap junction protein and message to determine how halogenated hydrocarbons might affect GJIC. DDT, dieldrin, and toxaphene inhibited GJIC in a dose-responsive manner after 90 min treatments. Dieldrin suppressed GJIC within 30 min with no recovery after 24 hr. Inhibition of GJIC by DDT and toxaphene was partially restored after 12 hr and fully restored after 24 hr. Several PCB and PBB congeners inhibited GJIC in a dose-responsive and time-dependent manner, but GJIC was almost restored to control values 24 hr after exposure. The highest concentrations of the individual chemicals that did not inhibit GJIC was determined, and mixtures containing two of these chemicals were tested for their ability to inhibit GJIC. Significant inhibition of GJIC was observed when cells were treated with a mixture of DDT and 2,4,5-hexachlorobiphenyl (2,4,5-HCB), dieldrin and 2,4,5-HCB, or dieldrin and 2,4,5-hexabromobiphenyl (2,4,5-HBB). These results indicate that halogenated hydrocarbons, alone or in specific combinations, can alter GJIC at the post-translational level. These results are consistent with the hypothesis that DDT, dieldrin, toxaphene, 2,3,4-HCB, 2,4,5-HCB, and 2,4,5-HBB could have tumor-promoting potential in human breast tissue.

Breast↗

PubMed2004

Intercellular junctions between odontoblasts as the transmitters of low charge electric current.

The aim of the work was to demonstrate structures responsible for the conduction of pain impulses with regard to tight junctions after transmission of small charges of electric current. For the experiment, freshly extracted (for orthodontic reasons) teeth were used. Immediately after extraction, low charges of electric current were passed through the teeth and the teeth were fixed. Teeth pulps were prepared for TEM studies. The obtained results were compared to those in a control group. In electron microscopic pictures, intercellular junctions are visible irrespective of the value of the current applied on the approximal surfaces of the cells (between the odontoblasts or between the odontoblasts and the neural fibres) as short callosities of plasmolemma.

Electrophysiology↗

PubMed2005

[Effects of phytoestrogens on gap junctional intercellular communication].

OBJECTIVE: To observe effects of phytoestrogens quercetin (QC), Genistein (GEN), coumestrol (COM), and enterolactone (ENL) on gap junctional intercellular communication (GJIC) in HaCaT cells. METHODS: HaCaT cells were exposed to QC, GEN, COM, and ENL at 0.1, 1.0, 10.0 and 100.0 micromol/L for 24 hours. The effects of phytoestrogens on GJIC were determined by fluorescence redistribution after photobleaching (FRAP) technique of using a laser scanning confocal microscope (LSCM). RESULTS: QC did not affect the GJIC at 0.1-10.0 micromol/L, whereas, GEN, COM, and ENL exhibited inhibition on the GJIC in some extent at 0.1-10.0 micromol/L without showing significant cytotoxicity. The ratio of fluorescence recovery were between 31.77% to 37.06%, which were significantly decreased compared the vehicle control (44.74%). CONCLUSION: The phytoestrogens GEN, COM, and ENL, but not QC, could inhibit the GJIC function in HaCaT cells at concentrations could be reached in human serum in some instance, indicating they could, under certain conditions, be cancer promoters. Therefore, it should be prudent to use these chemicals as pharmaceuticals or dietary supplements.

Cell Communication↗

PubMed2007

Rat mast cells communicate with fibroblasts via gap junction intercellular communications.

Usually mast cells (MCs) modulate other cellular activities through the release of their cytoplasmic granules. Recently, gap junctional intercellular communication (GJIC) between an established human MC cell line (HMC-1) co-cultured with human dermal fibroblasts in fibroblast populated collagen lattices (FPCLs), enhanced the rate and degree of FPCL contraction. However, HMC-1 cells were unable to generate GJIC with human neonatal fibroblasts in monolayer culture. Here freshly isolated rat peritoneal MCs are co-cultured with fibroblasts in collagen lattices and in monolayer culture in vitro and introduced into rat polyvinyl alcohol (PVA) sponge implants in vivo. Co-cultured MC-FPCL contracted faster and to a greater degree. Loading Calcein AM green fluorescent dye into red fluorescent Dil tagged MC generates MC-paratroopers. When MC-paratroopers form GJIC with fibroblasts, some green dye is passed into the fibroblast, while the MC-paratrooper retains both its red and green fluorescence. MC-paratroopers passed green fluorescent dye into both human and rat dermal fibroblasts in monolayer culture. In rats 7-day-old subcutaneous PVA sponge implants, which received an injection of MC-paratroopers, exhibited auto-fluorescent green fibroblasts, when harvested 24 h later. MC-paratroopers pretreated with a long-acting GJIC inhibitor prior to their introduction into PVA sponge implants, failed to pass dye into fibroblasts. It is proposed that GJIC between granulation tissue fibroblasts and MCs can modulate some aspects of wound repair and fibrosis.

Animals↗

PubMed1994

Altered homologous and heterologous gap-junctional intercellular communication in primary human liver tumors associated with aberrant protein localization but not gene mutation of connexin 32.

Gap-junctional intercellular communication (GJIC) in 20 primary human liver tumors with different degrees of malignancy has been studied at the functional and molecular levels. When GJIC capacity was determined by dye-transfer assay performed directly with freshly removed tumor tissue, significant reduction was found in all samples, regardless of their morphology. In addition, a selective lack of GJIC between tumor and surrounding non-tumorous cells was observed in some cases, probably due to the physical separation between them resulting from encapsulation of tumors. There was, however, no essential change in the level of expression of the major liver gap-junction protein, connexin (cx) 32, in liver tumors as measured by Northern and Western blot analyses. Immunohistochemical study revealed aberrant localization of cx 32 in the majority of malignant liver tumors. Instead of cytoplasmic membrane localization at intercellular contacts, cx 32 was detected mainly either intracytoplasmically or in plasma membrane free from contact with other cells. We did not detect any mutation in the coding sequence of the cx 32 gene from any of the human liver tumors we tested. Thus it is likely that the aberrant localization of cx 32 in tumor cells is due to disruption of the mechanisms for establishment of this protein into gap-junction plaques, rather than to structural abnormality of the cx 32 protein itself. Another member of the connexin family, cx 43, not detectable in non-tumorigenic hepatocytes, was expressed in several tumors, especially in invasive areas, but was detected in only a few tumor cells and was localized intracytoplasmically, suggesting that cx 43 protein is not involved in GJIC in the tumors.

Adult↗

PubMed2004

Tunicamycin preserves intercellular junctions, cytoarchitecture, and cell-substratum interactions in ATP-depleted epithelial cells.

Pretreatment with the nucleoside antibiotic tunicamycin was found to protect cultured renal epithelial cells in the face of ATP-depletion, in large part by preserving junctional and cellular architecture. Tunicamycin pretreatment of Madin-Darby canine kidney cells not only preserved E-cadherin staining at the plasma membrane, but also inhibited ATP-depletion-mediated E-cadherin degradation. Electron microscopic analysis, together with the preservation of the staining patterns of the tight junction marker ZO-1, the apical/microvillar marker gp135, and basolateral marker Na/K-ATPase suggested that tunicamycin preserved the junctional complex and the polarized epithelial cell phenotype. Tunicamycin pretreatment also prevented reductions in the filamentous actin content of the cells, as well as preserving Golgi architecture. Moreover, a quantitative measure of cell adhesion demonstrated that tunicamycin pretreatment resulted in a fivefold increase in attachment of cells to the substratum (77% versus 16%). Thus, pretreatment with tunicamycin protects polarized epithelial cells from ischemic injury through the preservation of epithelial cell architecture, intercellular junctions, and cell-substratum interactions in the setting of intracellular ATP-depletion.

Adenosine Triphosphate↗