Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “intercellular communication”

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 469 records · Page 26Linked to original sources
PubMed2005

Expression of connexin 43 and gap junctional intercellular communication in the cumulus-oocyte complex in sheep.

To evaluate the effects of FSH, LH and/or cAMP on expression of connexin 43 (Cx43) in the ovine cumulus-oocyte complex (COC) and gap junctional intercellular communication (GJIC) of cumulus cells, two experiments were carried out. In experiment 1, Cx43 was immunodetected in the COC, before or after maturation, obtained from non-treated or FSH-treated ewes. The expression of Cx43 in the COC was greater (P < 0.01) on day 16 than on day 15 of the estrous cycle. In vivo FSH treatment decreased (P < 0.02) Cx43 expression on day 16 but not on day 15 of the estrous cycle. In experiment 2, intact COCs or isolated cumulus cells obtained from small and large follicles from FSH-treated ewes were cultured with or without FSH, LH or cAMP agonist and evaluated for GJIC by laser cytometry. For large follicles, the basal rate of GJIC was greater (P < 0.01) for cumulus cells in intact COCs than for isolated cumulus cells. FSH increased (P < 0.04) GJIC in cumulus cells in intact COCs and tended to increase (P < 0.1) GJIC in isolated cumulus cells from small follicles but decreased (P < 0.01) GJIC in cumulus cells in intact COCs from large follicles. LH also increased (P < 0.01) GJIC in isolated cumulus cells from small follicles but decreased GJIC in intact COCs (P < 0.01) and isolated cumulus cells (P < 0.02) from large follicles. cAMP increased (P < 0.01) the GJIC in both intact COCs and cumulus cells from small and large follicles. These results indicate that day of estrous cycle, stage of maturation and duration of FSH treatment affect expression of Cx43 in ovine COCs. In intact COCs, GJIC in cumulus cells was enhanced, probably due to the presence of the oocyte. In addition, the effects of FSH and LH, but not cAMP, on GJIC of cumulus cells depended on the stage of follicular development and on the presence of the oocyte.

Animals↗
PubMed1988

[Intercellular communication and Tumor Invasion in the Petri Dish]

Malignant tumor cells are characterized by their ability to invade and destroy normal tissues, whereas benign tumor cells grow locally and, therefore, can be treated with more success. Tumor cell invasion proceeds the formation of metastases, which account for the high mortality of cancer patients. We investigated whether tumor cells which communicate via trans-membrane channels (gap junctions) with each other as well as with normal cells can more easily invade normal tissues than non-communicating tumor cells. Five tumor cell lines were cultured as monolayers and investigated with histological methods for gap junction formation and with electrophysiological methods for intercellular communication. Tumor cells were tested with an in vitro invasion model: spheroidal cell aggregates of normal and of malignant cells were confronted in petri dishes and co-cultured for varying time spans. Thin sections revealed that only tumor cells with gap junctions can actively invade aggregates of normal cells. Tumor cells without gap junctions are unable to invade the normal tissue: they may, however, destroy the normal cells by a completely different mechanism which may be a result of particular culture conditions.

Journal Article↗
PubMed1998

Inhibitory effect of pentachlorophenol on gap junctional intercellular communication in rat liver epithelial cells in vitro.

To understand the initiating/promoting actions of pentachlorophenol (PCP), a non-mutagenic hepatocarcinogen, and its metabolite, tetrachlorohydroquinone (TCHQ), we investigated the effects of each chemical on gap junctional intercellular communication (GJIC) in rat liver epithelial cells (WB cells) by the scrape-loading and dye transfer method. After treatment with PCP, the GJIC was initially inhibited at 4 h but was restored in 6-8 h, followed by a second phase of inhibition between 16 and 24 h. Both the first and second inhibitions were concentration-dependent and were restored by 2-4 h after removal of PCP. The phosphorylation state of connexin 43 (CX43) and its localization on the plasma membrane were unchanged up to 24 h after treatment; however, this was accompanied by a decrease in the CX43 protein level. No inhibitory effect was apparent on the GJIC of cells treated with TCHQ. These results suggest that PCP may play a critical role of promoting activity via non-mutagenic mechanisms.

Animals↗
PubMedDate not supplied

Defective gap junctional intercellular communication in lung cancer: loss of an important mediator of tissue homeostasis and phenotypic regulation.

Gap junctions provide direct pathways for the exchange of molecules and ions between neighboring cells, a process known as gap junctional intercellular communication (GJIC). This GJIC is important for homeostasis and regulation of mitosis, differentiation, and apoptosis. Gap junctions are present in lung airway and alveolar epithelial cells and, in addition to the above roles, might coordinate ciliary beating and surfactant secretion. GJIC is decreased in human and mouse lung carcinoma cells because of reduced expression of the gap junction protein, connexin43 (Cx43), and defects in signal transduction pathways that mediate Cx43 function. This reduced GJIC is important in the behavior of lung carcinoma cells because forced expression of Cx43 in lung carcinoma cells inhibits their growth and tumorigenicity. In this report, we summarize our studies on the role of GJIC in lung neoplasia.

Animals↗
PubMed1993

Heterologous gap junctional intercellular communication in normal and morphologically transformed colonies of Syrian hamster embryo cells.

A study was made of whether normal and morphologically transformed colonies in the Syrian hamster embryo (SHE) cell transformation assay performed heterologous gap junctional intercellular communication (GJIC). Two compounds, 12-O-tetradecanoylphorbol-13-acetate (TPA) and Na-orthovanadate (vanadate), which induce high frequencies of morphological transformation in SHE cells, have been employed. Three approaches were used to study the possibility of heterologous GJIC. (i) Morphologically transformed colonies (induced by TPA) partially overlapping with normal colonies were selected. Cells in the border area were micro-injected with the fluorescent dye Lucifer yellow to determine whether the dye spread to cells belonging to the other colony. This approach proved to be unsuccessful due to an inability to pinpoint which cells belonged to which colony. (ii) X-irradiated, non-dividing feeder cells are easily recognized by their large size. Feeder cells in contact with normal or TPA-transformed colonies were injected with Lucifer yellow. The dye was found to spread to most of the contacting cells, irrespective of whether they belonged to a normal or morphologically transformed colony. (iii) TPA- and vanadate-exposed colonies were labelled by endocytosis of Lucifer yellow overnight. This resulted in a punctate fluorescent pattern. Unlabelled, previously unexposed cells were seeded onto the dishes and incubated for 3.5-7 h. The ability to perform heterologous GJIC between the newly seeded cells and labelled colony cells was investigated. Both normal and transformed colonies were found to be able to communicate with the newly seeded cells. Thus, the present results indicate that selective communication is not a general property of morphologically transformed SHE cell colonies.

Animals↗
PubMed1995

Inhibition of gap junctional intercellular communication between primary human smooth muscle cells by tumor necrosis factor alpha.

Tumor necrosis factor alpha (TNF alpha), a pleiotrophic cytokine present in atherosclerotic lesions, caused a dose-dependent and persistent reduction in gap junctional intercellular communication (GJIC) between primary human smooth muscle cells in vitro. A continuous presence of TNF alpha was required for this persistent inhibition. Pretreatment of smooth muscle cells with ascorbic acid, alpha-tocopherol or glutathione prevented this inhibition of GJIC by TNF alpha. The persistent blockage of GJIC by continuous exposure to TNF alpha suggests that TNF alpha may share some mechanistic similarities with exogenous tumor promoters. Furthermore, this reduction in GJIC by TNF alpha may provide an additional link between the processes of atherosclerosis and carcinogenesis. The protection afforded by antioxidant compounds suggests a role for active oxygen species in the promotion stage of atherosclerosis.

Antioxidants↗
PubMedDate not supplied

The role of gap junctional intercellular communication in neoplasia.

Gap junctions are comprised of proteinaceous, plasma membrane channels that link the interiors of adjacent cells and permit cells to directly exchange small (< 1,000 Daltons) molecules and ions. This exchange, termed gap junctional intercellular communication (GJIC), appears to be involved in growth regulation. Growth controlling factors may pass between cells through the junctions. The loss of gap junctions or impairment of their permeability has been observed in many neoplastic cells and cells treated with growth promoting carcinogens and other agents. The loss of GJIC appears to be an important event in the conversion of a normal cell into a neoplastic one. On the other hand, the restoration of GJIC in neoplastic cells by transfection with gap junction protein (connexin) cyclic deoxyribonucleic acids (cDNAs) or by stimulating endogenous connexin gene expression has led to the reversal of the neoplastic phenotype. The biology of gap junctions and their role in growth regulation and neoplasia are reviewed.

Animals↗
PubMed1998

Regulation of connexin-43 gap junctional intercellular communication by mitogen-activated protein kinase.

Activation of the Ras/Raf/mitogen-activated protein kinase kinase/mitogen-activated protein (MAP) kinase signaling cascade is initiated by activation of growth factor receptors and regulates many cellular events, including cell cycle control. Our previous studies suggested that the connexin-43 gap junction protein may be a target of activated MAP kinase and that MAP kinase may regulate connexin-43 function. We identified the sites of MAP kinase phosphorylation in in vitro studies as the consensus MAP kinase recognition sites in the cytoplasmic carboxyl tail of connexin-43, Ser255, Ser279, and Ser282. In this study, we demonstrate that activation of MAP kinase by ligand-induced activation of the epidermal growth factor (EGF) or lysophosphatidic acid receptors or by pervanadate-induced inhibition of tyrosine phosphatases results in increased phosphorylation on connexin-43. EGF and lysophosphatidic acid-induced phosphorylation on connexin-43 and the down-regulation of gap junctional communication in EGF-treated cells were blocked by a specific mitogen-activated protein kinase kinase inhibitor (PD98059) that prevented activation of MAP kinase. These studies confirm that connexin-43 is a MAP kinase substrate in vivo and that phosphorylation on Ser255, Ser279, and/or Ser282 initiates the down-regulation of gap junctional communication. Studies with connexin-43 mutants suggest that MAP kinase phosphorylation at one or more of the tandem Ser279/Ser282 sites is sufficient to disrupt gap junctional intercellular communication.

Animals↗
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↗
PubMed2003

[Effects of lovastatin on proliferation and gap junctional intercellular communication of human breast cancer cell MCF-7].

BACKGROUND & OBJECTIVE: Lovastatin,an inhibitor of endogenous cholesterol biosynthesis,has been widely used in the clinical treatment of hypercholesterolemia.Recently,lovastatin has been paid more attention for its wide-range effects on human cancer cells; however,the detail mechanisms of its anti-cancer effects are not yet understood. This study was designed to investigate the effects of lovastatin on proliferation and gap junctional intercellular communication (GJIC) of MCF-7 human breast cancer cells. METHODS: After treated with lovastatin at dosages of 4,8,16 micromol/L for 1-3 days,the cell differentiation was examined with nitroblue tetrazolium (NBT) reduction test;the proliferation and distribution of cell cycles were examined with flow cytometry (FCM). Meanwhile,GJIC of MCF-7 cells was observed using the scrape-loading and dye transfer(SLDT) technique. RESULTS: Lovastatin could inhibit the proliferation of MCF-7 cells significantly and 75.80 percent of cells were inhibited after treated with 16 micromol/L lovastatin for 72 hours (P< 0.05). Meanwhile, lovastatin could arrest MCF-7 cells in the G(0)/G(1) phase of cell cycle and 80 percent of cells were arrested in G(0)/G(1) phase after treated with lovastatin for 72 hours. Furthermore, lovastatin could induce the differentiation of MCF-7 cells (P< 0.01) and up-regulate GJIC in MCF-7 cells. After treated with 16 micromol/L lovastatin for 72 hours, transfer of LY fluorescence could reach 4-5 rows of cells from the scraped line. However, apoptosis in MCF-7 cells was not obvious. All these effects of lovastatin were in a dose-and time-dependent manner. CONCLUSION: It suggests that lovastatin has the capabilities of inhibiting proliferation, arresting MCF-7 cells at G(0)/G(1) phase of cell cycle and inducing differentiation. These effects of lovastatin maybe correlate with lovastatin promoting GJIC function in MCF-7 cells.

Antineoplastic Agents↗
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↗
PubMed1997

A characterization of permolybdate and its effect on cellular tyrosine phosphorylation, gap junctional intercellular communication and phosphorylation status of the gap junction protein, connexin43.

Biological and analytical characterizations of permolybdate (a mixture of H2O2 and molybdate) were done. Molybdate (10 mM) and molybdenum(V) chloride (3 mM) did not affect gap junctional intercellular communication (GJIC), phosphorylation status of connexin43 (Cx43) or cellular tyrosine phosphorylation in early passage hamster embryonic cells (mainly fibroblast-like). High concentrations of H2O2 (3-10 mM) affected some of the parameters. Acidified permolybdate was clearly more stable than the unadjusted permolybdate. The maximum biological potency of acidified permolybdate was found at a molar ratio of 2:1 (H2O2:molybdate). The mixtures of molybdenum(V) chloride and H2O2 gave a maximum effect at 4:1 molar ratio (H2O2:molybdenum(V)). This can be explained by decomposition of H2O2 and by the generation of less biologically active compounds. Spectrophotometric analyses of the mixtures corroborated the biological results. The Mo(V) electron spin resonance spectrum disappeared upon addition of H2O2 to Mo(V) solutions, and no spectrum appeared when H2O2 was mixed with Mo(VI). Thus, permolybdate is probably diperoxomolybdate, a Mo(VI) compound. Regardless of the parent metal salt, the H2O2/metal salt mixtures showed concentration-dependent biphasic responses with an initial decrease in GJIC followed by an increase. A dissociation between alteration in Cx43 phosphorylation status and GJIC was obtained under certain conditions. The biological activities of permolybdate were only partially mimicked by phenylarsine oxide, an alternative protein tyrosine phosphatase inhibitor.

Animals↗
PubMed1994

Nongenotoxic effects of polycyclic aromatic hydrocarbons and their oxygenation by-products on the intercellular communication of rat liver epithelial cells.

Since polycyclic aromatic hydrocarbons (PAHs) are known to have epigenetic effects, we evaluated the effect of the parent chemical and the ozonated products on in vitro cell to cell communication bioassays which measures a nongenotoxic event. The scrape loading/dye transfer (SL/DT) technique was used to determine the effect of the following PAHs on gap-junction intercellular communication (GJIC): fluorene, 1-methyl-fluorene, fluoranthene, anthracene, 9-methyl-anthracene, phenanthrene, pyrene, benzo(a)pyrene, and benzo(e)pyrene. The methylated PAHs were more inhibitory to GJIC than the unmethylated counterparts. Fluoranthene, which has an additional ring added to fluorene, was more effective in inhibiting GJIC than fluorene. The three-ringed PAHs were also more inhibitory than the four- and five-ringed PAHs. A time-course study of fluoranthene and of pyrene resulted in maximal inhibition occurring within 30 min of incubation with the cells. The cells recovered from the inhibition within 1 hr after fluoranthene and pyrene were removed from the cell culture medium. Pyene, vbenzo(a)pyrene, fluorene, and fluoranthene were ozonated until the parent compound was completely eliminated as determined by reverse-phase high-pressure liquid chromatography (RP-HPLC). An increased level of inhibition of GJIC was observed for the ozonated mixtures of by-products of pyrene, fluoranthene, and benzo(a)pyrene, but not for fluorene, as monitored with the SL/DT technique. The products of the ozonated pyrene mixture were fractionated and collected by RP-HPLC. Each fraction was found to be inhibitory to GJIC as monitored by fluorescence recovery after photobleaching. In conclusion, current treatment technologies, such as ozonation or biologically based oxidations and methylations, do not necessarily eliminate toxicity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1996

Inhibition of gap junctional intercellular communication by barbiturates in long-term primary cultured rat hepatocytes is correlated with liver tumour promoting activity.

Rodent liver tumor formation can be promoted by certain barbiturates and this may involve their ability to inhibit hepatocyte gap junctional intercellular communication (GJIC). In order to address the mechanisms and specificity of action of barbiturates on hepatocyte gap junctions, we have compared the effects of liver tumor-promoting barbiturates (phenobarbital, sodium barbital and amobarbital: PB, SB and AB, respectively) and a non-liver tumor-promoting barbiturate (barbituric acid: BA) on primary cultured rat hepatocyte GJIC and connexin32 (Cx32) expression after short (1-24 h) and long (2-14 days) treatment. GJIC was evaluated by fluorescent dye microinjection (dye-coupling); Cx32 expression was monitored by Northern blot, Western blot and immunohistochemistry. Both parameters were maintained at high levels over 14 days by coculture of the cells with WB-F344 rat liver epithelial cells in the presence of dexamethasone. Treatment with PB (2 mM) for 1 h sharply reduced dye-coupling from approximately 90-30%, but the cells fully recovered by 24 h. No inhibition was seen with the other barbiturates over this 1-day treatment period. Longer treatments (2-14 days) with the promoters PB, SB and AB, however, gradually reduced hepatocyte dye-coupling to approximately 30-50%. The non-promoter, BA, did not affect hepatocyte GJIC. These decreases in hepatocyte dye-coupling occurred without changes in Cx32 or gap junction expression. Dye-coupling of WB-F344 cells and expression of their predominant gap junction protein, connexin43 (Cx43), were also not affected. Thus, the inhibition of GJIC was specific to liver tumor promoting barbiturates in hepatocytes, was time-dependent and was not due to altered Cx32 expression.

Animals↗
PubMed2001

Intercellular communication between Sertoli cells and Leydig cells in the absence of follicle-stimulating hormone-receptor signaling.

Effective interactions among the various compartments of the testis are necessary to sustain efficiency of the spermatogenic process. To study the intercellular communication between the Sertoli and Leydig cells in the complete absence of FSH receptor signaling, we have examined several indices of Leydig cell function in FSH receptor knockout (FORKO) mice. The serum testosterone levels were reduced in the 3- to 4-mo-old adult FORKO males compared to wild-type mice despite no significant alteration in circulating LH levels. Treatment with ovine LH resulted in a dose-dependent increase in serum testosterone levels in all three genotypes (+/+, +/-, and -/-). However, the response in FORKO males was significantly reduced. Similarly, the total intratesticular testosterone per testis was also lower, but the intratesticular testosterone per milligram of testis was significantly elevated in the FORKO males. Western blot analysis revealed an apparent higher expression of the enzyme 3beta-hydroxysteroid dehydrogenase (3beta-HSD) as well as LH-receptor density in the testis of FORKO males. Immunohistochemistry also showed an increase in the intensity of 3beta-HSD staining in the testicular sections of FORKO males. Although LH receptor binding increased per unit weight in FORKO mice, the total LH binding remained the same in all genotypes. Taken together, the results of the present study suggest that, in the absence of FSH receptor signaling, the testicular milieu is altered to affect Leydig cell response to LH such that circulating testosterone is reduced in the adult mutant. Studies are currently under way to understand the mechanisms underlying this phenomenon.

3-Hydroxysteroid Dehydrogenases↗
PubMed2000

Cooperation of bcl-2 and myc in the neoplastic transformation of normal rat liver epithelial cells is related to the down-regulation of gap junction-mediated intercellular communication.

The objectives of this study were to isolate several rat liver epithelial cell clones containing the human bcl-2 and myc/bcl-2 genes in order to study their potential cooperative effect on neoplastic transformation and gap junction-mediated intercellular communication (GJIC) and to test the hypothesis that the loss of GJIC leads to tumorigenesis. Using anchorage-independent growth as a surrogate marker for neoplastic transformation, we transfected both normal rat liver epithelial cells, WB-F344, and a WB-F344 cell line overexpressing v-myc with human bcl-2 cDNA. Those cell lines that only expressed v-myc or human bcl-2 were unable to form colonies in soft agar. However, those cell lines that overexpressed both v-myc and human bcl-2 showed varying ability to form colonies in soft agar, which did not correlate with their human bcl-2 expression level. In order to test if there was a correlation between cell line growth in soft agar and the ability to communicate through gap junctions, we performed scrape load dye transfer and fluorescence recovery after photobleaching assays. Our results show that v-myc and human bcl-2 can cooperate in the transformation of normal cells, but the degree to which the cells are transformed is dependent on the cells' ability to communicate through gap junctions.

Animals↗
PubMed2004

Peroxiredoxin 6 is upregulated in bovine oocytes and cumulus cells during in vitro maturation: role of intercellular communication.

Peroxiredoxins are peroxidases involved in antioxidant defense and intracellular signaling. Expression of transcripts coding for peroxiredoxin 6 (PRDX6) has been previously described to be upregulated in oocytes after in vitro maturation, a period during which general transcription decreases dramatically in oocytes. The aim of the present work was to evaluate PRDX6 regulation in bovine cumulus-oocyte complexes in relation to maturation and intercellular communication. PRDX6 expression was analyzed by reverse transcription-PCR and Western blotting in oocytes and cumulus cells before and after in vitro maturation. PRDX6 was found to be upregulated at the mRNA and protein levels in both cell types after maturation. The effect of paracrine and gap junctional communication on PRDX6 expression was then assessed by culturing cumulus clusters in the presence or absence of denuded oocytes. While PRDX6 upregulation in oocytes required intact cumulus-oocyte junctions, the presence of denuded oocytes was necessary but sufficient for the upregulation to occur in cumulus cells. Finally, the influence of recombinant mouse growth differentiation factor-9 (GDF-9) on PRDX6 expression in cumulus cells was studied. GDF-9 induced cumulus expansion and PRDX6 upregulation in bovine cumulus clusters. Altogether, our data suggest that PRDX6 upregulation in cumulus-oocyte complexes during in vitro maturation is mutually regulated by both cell types: PRDX6 upregulation in oocytes would require gap junctions with cumulus cells, while upregulation in cumulus would depend on secretion of oocyte paracrine factor(s) with GDF-9 being a likely candidate.

Animals↗
PubMed2000

Preventive effect of epicatechin and ginsenoside Rb(2) on the inhibition of gap junctional intercellular communication by TPA and H(2)O(2).

The anticarcinogenic effects of epicatechin (EC) and ginsenoside Rb(2) (Rb(2)), which are major components of green tea and Korea ginseng, respectively, were investigated using a model system of gap junctional intercellular communication (GJIC) in WB-F344 rat liver epithelial cells. 12-O-tetradecanoylphorbol-13-acetate (TPA) and hydrogen peroxide, known as cancer promoters, inhibited GJIC in the epithelial cells as determined by the scrape loading/dye transfer assay, fluorescence redistribution assay after photobleaching, and immunofluorescent staining of connexin 43 using a laser confocal microscope. The inhibition of GJIC by TPA and H(2)O(2) was prevented with treatment of Rb(2) or EC. The effect of EC on GJIC was stronger in TPA-treated cells than in H(2)O(2)-treated cells, while the effect of Rb(2) was opposite to that of EC. EC, at the concentration of 27.8 microg/ml, prevented the TPA-induced GJIC inhibition by about 60%. Rb(2,) at the concentration of 277 microg/ml, recovered the H(2)O(2)-induced GJIC inhibition by about 60%. These results suggest that Rb(2) and EC may prevent human cancers by preventing the down-regulation of GJIC during the cancer promotion phase and that the anticancer effect of green tea and Korea ginseng may come from the major respective components, EC and Rb(2).

Animals↗