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PubMed1999

Gap junction intercellular communication mediates the competitive cell proliferation disadvantage of irradiated mouse preimplantation embryos in aggregation chimeras.

Gap junction intercellular communication (GJIC) is thought to play a role in the growth modulation that occurs within cell populations. An example of heterologous growth inhibition (competitive cell proliferation disadvantage) occurs within mouse aggregation chimeras comprised of irradiated and nonirradiated cleavage-stage embryos. The goal of this investigation was to test the hypothesis that GJIC participates in the competitive cell proliferation disadvantage that is expressed by the irradiated embryo in aggregation chimeras. Specifically, we tested the capacity of the GJIC inhibitor 18 alpha-glycyrrhetinic acid (AGA) to inhibit competitive cell proliferation disadvantage in heterologous aggregation chimeras that were comprised of one embryo that was irradiated with 1.0 Gy of (137)Cs gamma rays and then paired with one nonirradiated embryo. We found that AGA successfully inhibited fluorescent dye transfer between irradiated and nonirradiated embryos in heterologous chimeras. Chronic exposure to AGA prevented competitive cell proliferation disadvantage in these radiation chimeras, while exposure to AGA for the first 15 h of culture (prior to gap junction development) did not prevent competitive cell proliferation disadvantage. An unexpected observation was the apparent lack of any effect of inhibiting GJIC by exposure to AGA on blastocyst formation and cell number allocation in the two principal stem cell lineages of the preimplantation mammalian embryo, trophectoderm and inner cell mass.

Animals↗
PubMed1994

[Studies on the gap junctional intercellular communication of human nasopharyngeal carcinoma cells and effect of RII].

To evaluate the effects of gap junctional intercellular communication (GJIC) on the growth, invasion and metastasis of tumor, human nasopharyngeal carcinoma (HNPC) parent cell line (CNE-2Z) and its variants (L2, H2, L4) with different invasive and metastatic potential were examined in vitro. Only a few intermediate junction (IJ) but no gap junction (GJ) structures were observed under EM. The parent line cells showed marked GJIC, while its variants lacked this function by SLDT technique. It was further shown that L2 cell line (variant with high invasive potential) had lower concentration of cytosolic free calcium ([Ca2+]i) compared to H2, L4 cell lines (variants with medium and low invasive potential, respectively). It reflected that some correlation may exist between [Ca2+]i level and the invasive potential of HNPC cell lines. The effect of RII on GJIC of HNPC was also investigated. After 3-7 ds of RII (0.0001 mol/L) treatment, there was no change in the number of GJs. The GJIC function of CNE-2Z weakened and then disappeared finally with prolonged RII treatment. The level of [Ca2+]i in HNPC cells apparently fell after 6h of RII treatment, and rose to original level with persistent RII treatment. Whether the fluctuating of [Ca2+]i level relates the inhibitory effect of RII treatment. Treatment on the growth and invasion needs to be further studied.

Calcium↗
PubMed2003

Reduced gap junctional intercellular communication and altered biological effects in mouse osteoblast and rat liver oval cell lines transfected with dominant-negative connexin 43.

Gap junctional intercellular communication (GJIC) maintains normal growth and differentiation of cells in a tissue. The intercellular molecules traversing gap junctions are largely unknown, but the molecular weight (MW) cutoff is normally 1200 Da. No differences in dye transfer were observed in normal or vector controls of WB-F344 rat liver epithelial or mouse osteoblastic MC3T3-E1 cells with either Lucifer Yellow (LY) with a MW of 457 Da (LY-457) or LY with a MW of 649 Da (LY-649). Transfection of a dominant negative-connexin 43 (Cx43) gene decreased GJIC (>50%) when LY-649 was used, however, normal GJIC was observed in both cell lines when LY-457 was used. Therefore, the MW cut off in these clones was considerably less than the wild type. The dominant negative clones of the MC3T3-E1 cells exhibited over 90% less alkaline phosphatase (ALPase) activity and calcium deposition after the induction of differentiation. Similarly, dominant negative Cx43 inhibited gene expression of ALPase and bone sialoprotein but not osteocalcin in MC3T3-E1. WB-F344 cells normally exhibit a biphasic response to 12-O-tetradecanoylphorbol-13-acetate (TPA) where inhibition of GJIC recovers after 2 h, but the dominant negative clones showed no recovery from inhibition of GJIC by TPA. Dominant negative Cx43 also inhibited the formation of network-like structures by WB-F344 cells on Matrigel. These results demonstrate that the dominant negative gene transfected into cell types containing the wild-type connexins result in diminished channel sizes, thus allowing the determination of whether distinct biological endpoints, i.e., differentiation, are dependent upon either small or high MW intercellular signals.

Animals↗
PubMed2003

Modulation of homologous gap junctional intercellular communication of human dermal fibroblasts via a paracrine factor(s) generated by squamous tumor cells.

Loss of gap junctional intercellular communication (GJIC) is a characteristic of cancer cells. Since a coordinated interaction of epithelial tumor cells with stromal cells is a prerequisite for tumor invasion and metastasis, the present study was designed to test the hypothesis that skin-derived tumor cells may modulate homologous and heterologous GJIC. While homologous GJIC of human dermal fibroblasts as well as epidermal keratinocytes was detected, no communication was measured between SCL-1 cells derived from squamous cell carcinoma of human skin. Interestingly, co-cultures of dermal fibroblasts and SCL-1 tumor cells in serum-containing medium resulted in a 52-70% lowering of the number of communicating fibroblasts. Furthermore, incubation of confluent fibroblast cultures with serum-free supernatant fractions (20-30 kDa) from tumor cells, termed the 20/30 fraction, lowered the homologous gap junction communication of fibroblasts by >90%. This novel aspect of down-regulated homologous GJIC of dermal fibroblasts, which is reversible, was neither mediated by alteration of the expression of connexin43, the major gap junctional protein of dermal fibroblasts, nor by aberrant localization of connexin43 in the plasma membrane. Furthermore, post-translational modifications of connexins, such as phosphorylation, was not measured by mobility shift studies. Tumor cell-mediated GJIC down-regulation between fibroblasts was suppressed using EGTA-containing serum-free tumor cell-derived supernatants suggesting that calcium ions (Ca2+) might mediate the transduction of this effect. The involvement of Ca2+ in down-regulation of homologous GJIC of fibroblasts was supported by an increase in fluorescence intensity of the intracellular calcium-sensitive indicator Fura-2 upon treatment of fibroblasts with the active 20/30 fraction. In conclusion, these data establish homologous GJIC of (stromal) fibroblasts as a parameter modulated by a paracrine acting factor(s) of epithelial tumor cells during tumor-stroma interaction of skin cells.

Base Sequence↗
PubMed1993

Endogenous and exogenous modulation of gap junctional intercellular communication: toxicological and pharmacological implications.

During the evolution of single-celled organisms to multicellular metazoans, a family of highly conserved genes coding for proteins (connexins), which as hexameric units (connexins), has evolved to form intercellular channels (gap junctions). These gap junctions allow ions and small molecular weight molecules to flow between coupled cells, thereby facilitating synchronization of electrotonic or metabolic cooperation. Control of cell proliferation, cell differentiation and adaptive responses of differentiated cells have been speculated to be biological roles of gap junctions. The regulation of these gap junctions can occur at the transcriptional, translational and posttranslational levels. Transient downregulation by endogenous or exogenous chemicals can bring about adaptive or maladaptive consequences depending on circumstances. Stable abnormal regulation of gap junction function has been associated with the activation of several oncogenes. Several tumor suppressor genes have also been associated with the up-regulation of gap junction function. Since gap junctions exist in all organs of the multi-cellular organisms, the dysfunction of these gap junctions by various toxic chemicals which have cell type/tissue/organ specificity could bring about very distinct clinical consequences, such as embryo lethality or teratogenesis, reproductive dysfunction in the gonads, neurotoxicity of the CNS system, hyperplasia of the skin, and tumor promotion of initiated tissue. Understanding how many non-mutagenic chemicals might alter normal gap junction function should form the basis of "epigenetic" toxicology. On the other hand, restoring normal gap junction function to cells which have dysfunctional intercellular communication could be the basis for a new approach for therapeutic pharmaceuticals.

Animals↗
PubMed1996

Upregulation of gap junctional intercellular communication in immortalized gonadotropin-releasing hormone neurons by stimulation of the cyclic AMP pathway.

Increased gap junctional intercellular communication induced by agents that stimulate the adenylyl cyclase/cAMP pathway was observed in the GnRH-secreting neuronal cell line, GT1-7, and possible underlying mechanisms were examined. A 24-hour treatment of GT1-7 neurons with 100 microM dibutyryl cAMP + 100 microM IBMX or with 2 microM forskolin increased by greater than 2-fold the percentage of cells that were dye coupled, using the noninvasive dye coupling assay, fluorescent recovery after photobleaching (FRAP). Longer treatment times (48 h) and higher concentrations of dibutyryl cAMP (500 microM) did not further increase the percentage of dye-coupled cells, while there was no increase in dye coupling observed between untreated cells and cells treated for 2 h or less. The increase in dye coupling induced by dibutyryl cAMP/IBMX was inhibited by octanol or dieldrin, agents known to block gap junction-mediated intercellular coupling in other cell types. Western blot analysis of total protein or membrane protein-enriched extracts revealed no apparent difference in the cellular levels of connexin 26, a connexin subtype previously shown to be expressed by GT1-7 cells, between untreated cells and cells treated for 24 h with dibutyryl cAMP/IBMX or forskolin. In addition, expression of connexin 32 or 43 protein before or after treatment was not detected. On the other hand, a dramatic increase in both the number of neurites and neurites that immunostained positive for connexin 26 was observed in dibutyryl cAMP/IBMX-treated cells. We hypothesize that the observed increase in dye coupling between GT1-7 neurons following stimulation of the adenylyl cyclase/cAMP pathway results from an augmentation of cell-cell contacts due to an increased number of neurites containing gap junctional plaques, possibly through an effect on cellular differentiation.

1-Methyl-3-isobutylxanthine↗
PubMed1987

Development of intercellular communication during the epithelial reorganization of a renal cell line (LLC-PK1).

Junctional permeability determinations after microinjection of the fluorescent tracer, Lucifer Yellow CH, show that the cells in confluent monolayers of the renal epithelial cell lines LLC-PK1 and A6 are interconnected by intercellular junctions. This cell-to-cell communication network permits the fluorescent dye to diffuse from the microinjected cell into multiple adjacent neighboring cells. Cell-to-cell diffusion of the fluorescent dye was not observed at pH 6.0. Full recovery occurred, however, when the pH of the extracellular medium was adjusted to 7.4. To provide a sensitive index of the averaged efficacy of junctional communication, we measured the number of cells that survived ouabain treatment in a 50% mixture of wild and ouabain-resistant mutant LLC-PK1 cells. Electron probe microanalysis in uncoupled cells showed that ouabain treatment produced two populations of cells, with totally different intracellular Na+ and K+ content. Under this condition, only 50% of the population survived after 48 h of treatment. When ouabain treatment was initiated 24 h after plating, however, 100% survival was observed, and the cells contained uniform intracellular Na+ and K+ concentration. This finding is consistent with the theory that this protective effect is mediated through the presence of the functional communicating intercellular junctions. When ouabain was applied at different times after plating, full protection is reached by 2 h. The early development of cell-to-cell communication, which precedes the development of the occluding junctions and several transport systems by several hours, is consistent with the involvement of the intercellular junctions in the synchronization of the polarization process.

Cell Communication↗
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↗
PubMed1997

Differential dose-dependent effects of alpha-, beta-carotenes and lycopene on gap-junctional intercellular communication in rat liver in vivo.

In order to examine the relevance of alteration of gap-junctional intercellular communication (GJIC) to chemopreventive activity against carcinogenesis, the effects of alpha- and beta-carotene as well as lycopene, typical chemopreventive carotenoids, on cell coupling via gap junctions in rat liver in vivo were studied using a direct functional dye-transfer technique. We found that all three test compounds given at a dose of 50 mg/kg-body weight (b.w.) daily, 5 times by gavage, inhibited GJIC, while similar treatment with 5 mg/kg b.w. caused enhancement, especially in the beta-carotene- and lycopene-treated groups. At the dose level of 0.5 mg/kg b.w., the three compounds had no effect. The findings show that all three agents differentially modulate GJIC depending on the dose, with beneficial effects on cell communication only detected at the one dose. The result suggests that determination of the dose of chemicals to be used is crucial for human intervention studies.

Animals↗
PubMed1999

Further evidence for the selective disruption of intercellular communication by heptanol.

The lack of selective gap junctional uncoupling agents has hampered evaluation of the contribution of intercellular communication to pharmacomechanical coupling and vascular contractility. Thus we further explored the utility and selectivity of heptanol as a gap junctional uncoupling agent in isolated rat aortic rings. Fifty-two aortic rings were obtained from 15 rats and were precontracted to approximately 75% of maximum with phenylephrine (PE). When contraction achieved steady state (approximately 5 min), a single concentration of heptanol (200 microM) was added to each aortic ring at 1- to 3-min intervals for up to 42 min post-PE addition. At early time points (5-10 min after PE), heptanol elicited an approximately 50% loss of tension (i.e., relaxation). At subsequent time points post-PE, a gradual and time-dependent decrease in the magnitude of the heptanol-induced relaxation was observed until, after approximately 40 min, addition of heptanol was associated with little, if any, detectable relaxation. Linear regression analysis of the magnitude of the heptanol-induced relaxation vs. the square root of the elapsed time interval (from addition of PE) revealed a highly significant negative correlation (P < 0.001, R = 0.81). Studies conducted on KCl-precontracted aortic rings revealed no detectable heptanol-induced relaxation after development of the steady-state KCl-induced contraction. These data extend our previous observations to further document the potential utility of heptanol as a "relatively selective" uncoupling agent.

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↗
PubMed1984

Lack of intercellular communication between chemically transformed and surrounding nontransformed BALB/c 3T3 cells.

In order to study the possible role of intercellular communication in the process of in vitro cell transformation, the communicating capacity of BALB/c 3T3 cells transformed by 20-methylcholanthrene was investigated using a dye transfer method. Morphologically transformed foci, detectable 4 to 5 weeks after treatment with 20-methylcholanthrene (1.0 microgram/ml), are clearly distinguishable under the phase-contrast microscope from surrounding nontransformed monolayer cells; therefore, a tracer dye can be injected into individual cells, and gap-junctional communication between and among transformed and nontransformed can be studied directly. When fluorescent Lucifer Yellow CH was microinjected into a cell within the transformed focus, the dye was transferred to other transformed cells but not to cells in the adjacent nontransformed area, although they were in physical contact. Similarly, dye injected into a nontransformed cell was transferred to neighboring nontransformed cells but not to cells in an adjacent transformed focus. These results indicate that when BALB/c 3T3 cells are transformed by 20-methylcholanthrene they can no longer communicate with surrounding normal cells, although they maintain the ability to communicate with other transformed cells in the focus. These results suggest that loss of the ability to communicate with surrounding nontransformed cells may be one of the important determinants of induction and expression of the final malignant transformation.

Animals↗
PubMed1989

Dynamics of intercellular communication and differentiation in a rapidly developing mammalian airway epithelium.

A considerable body of data suggests that gap junctions represent channels that facilitate intercellular communication, thereby modulating growth and development. However, direct quantitative evidence supporting such a structure/function relationship is limited. This study has identified a new model in the rapidly developing tracheal epithelium of infant ferrets wherein gap junction prevalence and intercellular transfer of a fluorescent, low molecular weight dye, epithelial cell incorporation of tritiated thymidine, and progressive ciliation of the epithelium have been characterized. This developmental pattern provides favorable conditions for the study of relationships between gap junctions, intercellular translocation of chemical signals, and cell growth and differentiation in a mammalian airway epithelium with a minimum of experimental intervention.

Animals↗
PubMed1997

Flavonoids (apigenin, tangeretin) counteract tumor promoter-induced inhibition of intercellular communication of rat liver epithelial cells.

We have shown previously that two flavonoids, apigenin and tangeretin, enhance gap junctional intercellular communication (GJIC) in rat liver epithelial cells, named REL cells. Here, we show that these two flavones also antagonize the inhibition of GJIC induced by tumor promoters like 12-O-tetradecanoyl-phorbol-acetate (TPA) and 3,5,di-tertio-butyl-4-hydroxytoluene (BHT). Their preventive effect is rapid. It does not seem to involve any change of the amount of the connexin expressed in REL cells, connexin 43 (Cx 43), and in its phosphorylation state. Other flavonoids tested including naringenin, myricetin, catechin and chrysin did not enhance GJIC nor counteract TPA-induced inhibition of GJIC.

Animals↗
PubMed2003

Recovery of gap junctional intercellular communication after phorbol ester treatment requires proteasomal degradation of protein kinase C.

Reversible down-regulation of gap junctional intercellular communication (GJIC) is proposed to be an important cellular mechanism in tumor promotion. Gap junction function is modified by a variety of tumor promoters, including the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA). Treatment of cells with TPA results in the activation and subsequent depletion of the TPA-responsive protein kinase C (PKC) isoforms. TPA-induced degradation of the PKC isoforms alpha, delta and epsilon was recently shown to occur via the ubiquitin-proteasome pathway. In the present study we investigated the role of the proteasome in the TPA-induced modification of GJIC in IAR20 rat liver epithelial cells. TPA exposure of IAR20 cells induced hyperphosphorylation of gap junction protein connexin43 and inhibition of GJIC. Prolonged TPA treatment induced down-regulation of PKCalpha, delta and epsilon and a reduction in the total PKC activity, which was associated with recovery of GJIC. Co-treatment of IAR20 cells with TPA and the proteasomal inhibitor MG132 suppressed down-regulation of PKCalpha, delta and epsilon and caused prolonged PKC activity. Under these conditions, the recovery of GJIC was blocked. The general PKC inhibitor GF109203X reversed the effect of MG132, indicating that the prolonged TPA-induced inhibition of GJIC caused by MG132 was due to the prolonged PKC activity. These results indicate that proteasomal degradation of PKC is one mechanism by which the recovery of GJIC after TPA treatment is regulated.

Animals↗
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↗
PubMed1991

[Frequency coding in intercellular communication based on a generalized chronopharmacology].

An important function of biological rhythms is to support the frequency encoding of intercellular communications. Two examples of this phenomenon are discussed, namely, communication by cyclic AMP pulses in the slime mold Dictyostelium, and the pulsatile secretion of gonadotropic hormones. The existence of an optimal frequency of stimulation in these two systems possesses clinical implications, as attested by the use of pulsatile hormonal therapies in endocrinology. More generally, the pulsatile administration of some drugs, at the appropriate frequency, could maximize their physiological effect. Such a generalized chronopharmacology would take into account the kinetic characteristics of desensitization and resensitization in target cells, and would not be limited to the sole consideration of circadian rhythms within the organism.

Animals↗
PubMed1990

TPA-induced inhibition of gap junctional intercellular communication is not mediated through free radicals.

The present investigation was designed to determine whether the inhibition of gap junction-mediated intercellular communication (GJIC) induced by TPA (12-O-tetradecanoylphorbol-13-acetate) in rat liver epithelial (WB-F344) cells in vitro is mediated through free radical production. As assessed by fluorescence redistribution after photobleaching (FRAP) analysis, GJIC was significantly inhibited in cells treated for 1 hr with either 10 ng/ml TPA or 500 microM hydrogen peroxide (H2O2). Addition of 1000 U/ml catalase or 25 microM N',N'-diphenyl-p-phenylenediamine (DPPD) to TPA-treated cells did not alleviate the TPA-induced inhibition of GJIC. However, the concurrent addition of 1000 U/ml catalase to the culture medium prevented the H2O2 inhibition of GJIC. 2'-7'-dichlorofluorescein-mediated fluorescence, a measure of free radical production utilizing the Meridian ACAS 470 interactive laser cytometer, was not significantly increased in WB-F344 cells treated with 10 and 100 ng/ml TPA when compared to control cells. However, polymorphonuclear leukocytes (PMNs) treated for 10 min with 100 ng/ml TPA showed a substantial oxidative burst, as did WB-F344 cells treated for 1 hr with 500 microM H2O2. The concurrent addition of 1000 U/ml catalase to the culture medium attenuated H2O2-mediated free radical production in both PMNs and WB-F344 cells. Data from this study do not support a role for free radicals in the TPA-induced inhibition of GJIC in WB-F344 cells.

Animals↗