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PubMed1987

[Hypothesis of mediation pathology in surgery (4)].

The mediation pathology concept takes account to a large extent, though by no means exhaustively, of that horizontal language between peripheral cells, based on locally produced hormone-like substances and aimed at covering extremely short distances. This brings us well and truly into the paracrine domain of intercellular communication, whereby an exchange of messages takes place between adjacent cells via the interstitial spaces. Alongside this short-range communication network, there also exists a long-range network, involving above all the blood stream both as an intermediary and as mediation terrain. To the mediatory processes partakes the neuro-endocrine system, albeit it is not the predominant one as it was classically thought. There are other actors on the mediation stage: oxygen radical plays an important role.

Cell Communication↗
PubMed1997

[Immunological aspects of endometriosis].

The effect of adherence process on Fallopian tubes and ovaries in late stages endometriosis is clear, but it is more important to understand pathophysiologic mechanism of infertility in minimal, mild endometriosis. Although the etiology of endometriosis is unknown, components of the immune system may be involved and play a central role in the pathogenesis of the disease by immunologically altering the peritoneal microenvironment. Increased number and activity of leucocyte subpopulations in the peritoneal fluid result in cytotoxic effects that exert adverse influence on spermatozoa, oocyte, germ cell interaction, and early embryo development, while cytokine and growth factor secretion stimulates or promotes cellular proliferation of endometriotic tissue in an "immunological tolerance" environment. The immunological aspects of endometriosis, including autocrine or paracrine pathways of intercellular communication, are reviewed.

Adolescent↗
PubMed1998

Direct action of serotonin on prolactin, growth hormone, corticotropin and luteinizing hormone release in cocultures of anterior and posterior pituitary lobes: autocrine and/or paracrine action of vasoactive intestinal peptide.

There is extensive evidence that serotonin (5-HT) is implicated in the neuroendocrine control regulating the secretion of several anterior pituitary hormones. It has also been reported that the posterior pituitary is necessary for prolactin (PRL) response to 5-HT as well as to suckling, in which 5-HT implication has been demonstrated. As we have previously shown that vasoactive intestinal peptide (VIP) mediates through an autocrine or paracrine action the PRL release induced by insulin-like growth factor I, thyrotropin-releasing hormone (TRH) and dopamine withdrawal, the aim of the present work was to determine whether 5-HT has a direct action on pituitary secretion and to study the possible role of pituitary VIP in this situation. Cells from the anterior pituitary lobe (AP) were cultured either alone or together with cells from the posterior pituitary lobe (PP). As melanotropes from PP express glucocorticoid receptors in vitro, both AP cultures and cocultures of AP/PP cells were incubated in the presence or absence of corticosterone (0.1 microg/ml), thus designing four experimental conditions. Then both AP and mixed cultures were incubated with 5-HT (100 nM) for 20, 45 and 180. The release of PRL, growth hormone (GH), corticotropin (ACTH) and luteinizing hormone (LH) was stimulated by 5-HT, but only in cocultures of AP/PP cells preincubated with corticosterone, whereas follicle-stimulating hormone and thyroid-stimulating hormone release was not modified. As AP cultures did not show any response to 5-HT, both in the presence or absence of corticosterone, and as melanotropes are the main cellular type present in the PP cultures, we studied the response of alpha-melanocyte-stimulating hormone (alphaMSH) to 5-HT in PP cells cultured with or without corticosterone. Serotonin did not modify alphaMSH release either in the absence or the presence of corticosterone. VIP release was also stimulated by 5-HT in the cocultures, and the time response profile was only similar to that of PRL. In order to study whether pituitary VIP is implicated in 5-HT action, cocultures preincubated with corticosterone were incubated in the presence of 5-HT, a VIP-receptor antagonist (VIP-At) or simultaneously with 5-HT plus VIP-At. PRL response to 5-HT was abolished by the simultaneous presence of VIP-At, whereas GH, ACTH and LH response remained unchanged. These data demostrate that: (1) 5-HT stimulates the secretion of PRL, GH, ACTH, LH and VIP acting directly at pituitary level on PP, probably by releasing an unidentified mediator from melanotropes; (2) glucocorticoids make the response of AP cells to 5-HT possible due to the presence of PP cells in the coculture; (3) PRL response to 5-HT is mediated through an autocrine and/or paracrine action of VIP.

Adrenocorticotropic Hormone↗
PubMed1994

Paracrine Ca2+ signaling in vitro: serotonin-mediated cell-cell communication in mast cell/smooth muscle cocultures.

Mast cells are tissue-resident immune cells that are capable of signaling many different cell types in vascularized tissue including epithelia and smooth muscle. We have developed an in vitro coculture system in which secretion of serotonin by a mucosal mast cell line (RBL-2H3) can be studied at a single cell level by measuring Ca2+ transients in fura-2 loaded mast cells and serotonin-sensitive A7r5 smooth muscle cells using fluorescence video microscopy and digital image processing. A7r5 cells elevate intracellular Ca2+ via 5HT2 receptors in response to bath-applied serotonin with an ED50 for serotonin of 550nM. Crosslinking IgE receptors with antigen caused Ca2+ transients in the mucosal mast cells. Ca2+ responses in the smooth muscle were detected approximately 30-240 sec after the initiation of the mast cell Ca2+ responses. Smooth muscle Ca2+ responses were dependent on preloading mast cells with serotonin and were blocked by the 5HT2 antagonist ketanserin. The timing and magnitude of the smooth muscle responses indicated that secretion from mast cells can lead to local concentrations of serotonin in the range of 300 nM within 1 min of antigen stimulation. This coculture technique has allowed the first direct demonstration of serotonin-mediated signaling between immune cells and vascular elements.

Animals↗
PubMed1999

Paracrine regulation of distinct trophoblast functions in vitro by placental macrophages.

In view of the accumulating evidence for paracrine mechanisms regulating trophoblast function, we tested the hypothesis that placental macrophages affect trophoblast activity in a paracrine fashion. Trophoblast was isolated from 17 term placentas (-IP). One aliquot of cells was further immunopurified (+IP) using an HLA class I antibody. This increased the proportion of trophoblast (+IP >97%; -IP approximately 70%) as identified by rigorous immunocytochemistry. Most (approximately 70%) non-trophoblast cells in -IP were macrophages. The cells were cultured for 5 days with a daily medium change. In addition, +IP cells from seven placentas were cultured with lipopolysaccharide (LPS)-stimulated or -unstimulated macrophage-conditioned media. The concentrations of lactate, trophoblast-specific hormones, human chorionic gonadotropin-beta (hCG-beta) and human placental lactogen (hPL), of several prostanoids and of endothelin-1 and angiotensin II were determined in the culture media. The accumulated amounts of substances released into the culture media, corrected for the greater proportion of trophoblast in +IP cultures, were on average two- to threefold higher (hCG-beta: 18-fold) in +IP than in -IP, with the exception of endothelin-1,2 (no change), angiotensin II (-70%) and 6-keto-prostaglandin-F1alpha (-40%). [3H]leucine incorporation into the trichloroacetic acid (TCA)-precipitable pool measured on day 5 was twofold higher in +IP than in -IP. Addition of conditioned media reverted these changes. The data demonstrate that placental macrophages in culture affect trophoblast biosynthetic activity in a paracrine fashion. We conclude that macrophages are important regulators of trophoblast activity.

Cell Communication↗
PubMed1993

Neuro-immunophysiology of colon function.

Neuroimmunophysiology involves direct communication between the mucosal immune system and the minibrain in the colon. Communication is chemical in nature (paracrine) and involves specialized sensing functions of the immune cells for specific antigens together with intelligent interpretation of the signals by the enteric nervous system. Immunoneural integration progresses sequentially starting with immune detection followed by signal transfer to enteric microcircuits followed by neural interpretation and then selection of a specific neural program of coordinated mucosal secretion and motor propulsion that acts to clear the antigenic threat from the colonic lumen. Histamine and serotonin are important chemical messages released from mucosal mast cells to act at specific receptor subtypes on neural elements of the enteric minibrain.

Animals↗
PubMed1994

A new communication system between hepatocytes and sinusoidal endothelial cells in liver through vascular endothelial growth factor and Flt tyrosine kinase receptor family (Flt-1 and KDR/Flk-1).

Hepatocyte Growth Factor (HGF)/Scatter Factor secreted from sinusoidal endothelial cells and Kupffer cells in liver activates the c-Met tyrosine kinase receptor expressed on hepatocytes. Here we report yet another possible communication system through a different ligand and tyrosine kinase receptor in an opposite direction. We isolated and determined the primary structure of the entire coding region of rat flt-1 (fms-like tyrosine kinase), a receptor for Vascular Endothelial Growth Factor (VEGF). Using rat flt-1 cDNA as a probe we found that the flt-1 mRNA was expressed at very high levels in sinusoidal endothelial cells in normal rat liver, but was hardly detectable in hepatocytes. The transcripts of another VEGF receptor KDR/Flk-1 structurally related to Flt-1 was also expressed specifically in sinusoidal endothelial cells. On the other hand, VEGF mRNA was expressed weakly in hepatocytes, but not in the nonparenchymal cell fraction. Furthermore, in an in vitro culture system, VEGF demonstrated a remarkably specific growth-stimulatory activity as well as maintenance activity on the sinusoidal endothelial cells. These results suggest that hepatocytes regulate the proliferation and survival of the sinusoidal endothelial cells in liver in a paracrine manner. Therefore two reciprocal communication systems, VEGF-Flt receptor family and HGF-Met receptor, may exist in hepatic tissue.

Amino Acid Sequence↗
PubMed1999

Pathophysiological role of the cytokine network in the anterior pituitary gland.

Recent evidence has demonstrated that cytokines and other growth factors act in the anterior pituitary gland. Using the traditional criteria employed to determine autocrine or paracrine functions our review shows that, in addition to their role as lymphocyte messengers, certain cytokines are autocrine or paracrine regulators of anterior pituitary function and growth. The cytokines known to regulate and/or be expressed in the anterior pituitary include the inflammatory cytokine family (IL-1 and its endogenous antagonist, IL-1ra; TNF-alpha, and IL-6), the Th1-cytokines (IL-2 and IFN-gamma), and other cytokines such as LIF, MIF, and TGF-beta. This review examines at the cellular, molecular, and physiological levels whether: (1) each cytokine alters some aspect of pituitary physiology; (2) receptors for the cytokine are expressed in the gland; and (3) the cytokine is produced in the anterior pituitary. Should physiological stimuli regulate pituitary cytokine production, this would constitute additional proof of their autocrine/paracrine role. In this context, we analyze in this review the current literature on the actions of cytokines known to regulate anterior pituitary hormone secretion, selecting the in vivo studies that support the direct action of the cytokine in the anterior pituitary. Further support for direct regulatory action is provided by in vitro studies, in explant cultures or pituitary cell lines. The cytokine receptors that have been demonstrated in the pituitary of several species are also discussed. The endogenous production of the homologous cytokines and the regulation of this expression are analyzed. The evidence indicating that cytokines also regulate the growth and proliferation of pituitary cells is reviewed. This action is particularly important since it suggests that intrinsically produced cytokines may play a role in the pathogenesis of pituitary adenomas. The complex cell to cell communication involved in the action of these factors is discussed.

Animals↗
PubMed1994

Production and secretion of adrenomedullin from vascular smooth muscle cells: augmented production by tumor necrosis factor-alpha.

In this study, we demonstrate production and secretion of adrenomedullin (AM) from cultured vascular smooth muscle cells (VSMCs). In addition to endothelial cells (ECs), we found immunoreactive (ir-) AM in culture media of rat and bovine VSMCs in the survey for AM-producing cells. Although the secretion level of ir-AM was at most 1/6 that of rat ECs, all the examined VSMCs were shown to produce AM. By gel filtration, reverse phase high-performance liquid chromatography, and biological characterization, ir-AM in the culture medium was identified to be rat AM of 50 residues. By RNA blot analysis, a positive band of AM mRNA was detected in cultured VSMC at an intensity 3-4 fold higher than that in adrenal gland. Gene expression and production of AM were markedly augmented by tumor necrosis factor-alpha. Based on these data as well as the presence of AM specific receptors on VSMCs, AM secreted from VSMC is deduced to function as an autocrine or paracrine regulator in vascular cell communication.

Adrenomedullin↗
PubMed1998

Morphological basis of the interactions between endocrine cell types in the pancreatic islets of the teleost, Blennius gattoruggine.

The endocrine pancreas of the teleost fish Blennius gattoruggine was studied by immunochemistry using both light and electron microscopy. Generally, one large Brockmann body, along with intermediate and small islets, was found. Cells immunoreactive (IR) to anti-insulin (B), anti-glucagon (A) anti-somatostatin (D) anti-pancreatic polypeptide and anti-PYY sera were detected with B cells located at the center of the islet and the other cell types forming a peripheral mantle. The B-cell cytoplasm showed rows of microtubules close to the secretory granules and perpendicular to the plasmalemma. The ultrathin section images revealed exocytotic and endocytotic features, and the presence of intercellular gap junctions between the plasmalemma of contiguous cells, suggesting intercellular routes of communication, e.g. via autocrine and/or paracrine mechanism. These features were observed in all of the cell types, and were abundant in D cells. D cells were particularly numerous in the islets and were disposed close to A and B cells, as observed in other teleost species. The most peripheral B cells, in closer contact with D cells than the central ones, appeared strongly immunolabeled, perhaps owing to the inhibitory action of somatostatin. Some D cells exhibited a long protrusion directed towards the center of the islet. In view of their cytological characteristics and their secretion, D cells might have an important role in the modulation of A and B-cell secretion in an endocrine and/or paracrine fashion.

Animals↗
PubMed1997

Interleukin-6 is an autocrine growth factor for folliculostellate-like TtT/GF mouse pituitary tumor cells.

Within the pituitary, folliculostellate (FS) cells are considered to regulate the intercellular communication between endocrine cells by paracrine mechanisms. One of the possible paracrine factors involved, could be interleukin-6 (IL-6) which is produced by these cells. Since IL-6 has been shown to be a growth factor of pituitary cells, we have determined whether IL-6 can also influence FS cell proliferation. To test this, a FS cell-like mouse pituitary cell line (TtT/GF cells) was used that exhibits most characteristics of normal FS cells. Under serum-free conditions the proliferation of TtT/GF cells is critically dependent on the initial seeding density: cells seeded at low density do not grow at all whereas cells seeded at high density proliferate with maximal doubling times of 34 hrs. Mouse IL-6 (mIL-6) stimulated only low density cell cultures in a dose and time dependent manner. For cells seeded at high density, exogenously added IL-6 may have failed to stimulate growth because of endogenously produced mIL-6. Conditioned medium from TtT/GF cells, in which mIL-6 concentrations up to 1017 pg/ml were measured, stimulated the proliferation of TtT/GF cells, indicating an autocrine growth stimulatory mechanism. A neutralizing mIL-6 antibody partially suppressed the growth of TtT/GF cells seeded at high density and partially reduced the growth stimulatory activity of TtT/GF conditioned medium. Thus, IL-6 is one but not the only factor that is involved in the autocrine growth stimulatory loop. The relevance of this mechanism for normal FS cells and its physiological consequence needs to be elucidated.

Animals↗
PubMed1997

Expression and function of endothelins, endothelin receptors, and endothelin converting enzyme in the porcine trachea.

Endothelins (ETs) can modulate the airway smooth muscle tone. Using simultaneous measurements of cytosolic Ca2+ concentration ([Ca2+]i) and tension as well as the reverse transcription polymerase chain reaction (RT-PCR), we examined ET systems in the porcine trachea. In the functional study, the application of ET-1, ET-3 or sarafotoxin S6c (S6c) caused increases in [Ca2+]i and tension, in a concentration-dependent manner. These ET ligands were found to increase the Ca2+ sensitivity of the myofilament of the tracheal smooth muscle cells (SMCs). The contractions induced by ET-1 (10(-7) M), an ET receptor (ET-R) non-selective agonist, were much greater than those induced by S6c, an ET(B)-R selective agonist. BQ-123 (10(-6) M), an ET(A)-R antagonist, inhibited the ET-1 induced contraction. These functional experiments suggested the presence of both functioning ET(A)- and ET(B)-Rs in tracheal SMCs. RT-PCR experiments revealed that the tracheal SMCs expressed both ET(A)-R and ET(B)-R mRNAs, while tracheal epithelial cells (EpCs) predominantly expressed ET(A)-R mRNA. The porcine tracheal SMCs and EpCs also expressed pre-pro ET-1 (ppET-1), ppET-3, and endothelin converting enzyme-1 (ECE-1) mRNAs. These results suggested that ETs induce contraction of porcine tracheal SMCs not only by increasing [Ca2+]i but also increasing the Ca2+ sensitivity of the myofilament and that ETs could potentially be the autocrine and/or paracrine transmitters to regulate the contraction in the porcine airway smooth muscle.

Animals↗
PubMed1997

Endometrial corticotropin-releasing hormone. Its potential autocrine and paracrine actions.

Corticotropin-releasing hormone (CRH) is expressed at several peripheral tissues including normal epithelial cells of human and rodent uterus. However, its biological role is unknown in both species. To clarify this role we studied the regulation of CRH promoter in endometrial cells. We performed homologous transfection experiments in Ishikawa cells, a human endometrial cell line, using a 0.9-kb fragment of the 5'-flanking region of human CRH gene coupled to luciferase. We found that the activity of the 5'-flanking region of the CRH gene is stimulated by cAMP and EGF and inhibited in a receptor-mediated, dose-dependent fashion by estradiol and dexamethasone. The antiglucocorticoid RU 486 acted as a glucocorticoid agonist suppressing CRH gene activation, whereas progesterone was devoid of any activity. Prostaglandin E2 and interleukins-1 and -6 stimulated CRH activation, and the prostanoid inhibitor indomethacin suppressed it, most probably by inhibiting endogenous prostaglandins. These findings suggest that endometrial CRH gene expression may be under the negative control of estrogens and glucocorticoids and under the positive control of PGE2, IL-1, and IL-6. Considering the involvement of CRH in proinflammatory phenomena, we postulate that endometrial CRH, in association with uterine prostanoids and cytokines, may participate in intrauterine inflammatory processes of early pregnancy, such as decidualization and blastocyst implantation.

Animals↗
PubMed1997

Macrophage migration inhibitory factor induces phagocytosis of foreign particles by macrophages in autocrine and paracrine fashion.

Exposure to foreign particles sometimes causes inflammatory reactions through production of cytokines and chemoattractants by phagocytic cells. In this study, we focused on macrophage migration inhibitory factor (MIF) to evaluate its pathophysiological role in the phagocytic process. Immunohistochemical analysis of human pseudosynovial tissues retrieved at revision of total hip arthroplasty showed that infiltrating mononuclear and multinuclear cells were positively stained by both an anti-CD68 antibody and anti-human MIF antibody. For in vitro study, MIF was released from murine macrophage-like cells (RAW 264.7) in response to phagocytosis of fluorescent-latex beads in a particle dose-dependent manner. Northern blot analysis showed marked elevation of the MIF mRNA level in the phagocytic macrophage-like cells. Moreover, pretreatment of RAW 264.7 cells with rat recombinant MIF increased the extent of phagocytosis by 1.6-fold compared with the control. Taken together, these results suggest that MIF plays an important role by activating macrophages in autocrine and paracrine fashion to phagocytose foreign particles.

Animals↗
PubMed1998

Characterization of inhibin/activin subunit, activin receptor, and follistatin messenger ribonucleic acid in human and mouse oocytes: evidence for activin's paracrine signaling from granulosa cells to oocytes.

Inhibin, activin, and follistatin (FS) are gonadal proteins that appear to have a role in regulating folliculogenesis through possible paracrine and/or autocrine interactions. To further examine the potential role of activin in oocyte-granulosa cell communication, we developed a sensitive reverse transcription-polymerase chain reaction protocol to analyze mRNA for the alpha, betaA, and betaB inhibin/activin subunits, FS, and the four activin receptor subtypes in individual human and mouse oocytes. The resulting expression pattern was further compared to that in human cumulus granulosa cells. Our results indicate that neither ssA nor betaB mRNA was detectable in any human or mouse oocyte, that alpha subunit was marginally present in some of the human oocytes, and that FS mRNA was detectable in human but not mouse oocytes. On the other hand, inhibin/activin subunit and FS mRNAs were abundantly expressed in cumulus cells. In addition, mRNAs for all four activin receptor subtypes (ActRIA, ActRIB, ActRIIA, and ActRIIB) were easily detectable in both oocytes and granulosa cells and appeared to be differentially expressed in oocytes during nuclear maturation. Finally, RNAs for both zona pellucida 3 and growth-differentiation factor-9, which were originally used as oocyte-specific markers, were detected in human but not mouse cumulus cells, although at lower levels than observed in oocytes. Taken together with previous studies, these results indicate that oocytes may be capable of responding to, but not synthesizing, activin.

Activin Receptors↗
PubMed1997

Paracrine and intracellular signaling mechanisms of calcium waves in cultured human uterine myocytes.

OBJECTIVE: To establish mechanisms of intercellular communication in human myometrium other than action potential propagation. METHODS: Monolayer cultured human myometrium was used as a model system. The calcium-sensitive fluorescent dye, calcium green-1, was used as a probe for the concentration of intracellular free calcium. Intercellular calcium waves were initiated by mechanical stimulation and observed with video spectrofluorimetry. This technique allowed initiation of calcium waves from a known location at a known time while simultaneously controlling the flow rate of the bathing solution across the surface of the cells. Intercellular calcium waves were observed at bath flow rates between 0 and 5.1 mL/minute through a 0.4 mL chamber. Experiments were performed using low calcium, high potassium bathing solutions to eliminate the possibility of action potential signaling. RESULTS: In still bathing solution, calcium waves radiated symmetrically from the site of initiation. With the bathing solution flowing, two mechanisms of intercellular calcium wave propagation were observed-one dependent on and one independent of the direction of bath flow. The calcium waves that were independent of bath flow used an intracellular mechanism for intercellular communication, were only observed within 100 microns of the site of wave initiation, and demonstrated mean (+/- standard deviation [SD]) wave speeds of 14.1 +/- 2.6 microns/second. The waves dependent on bath flow used an extracellular signaling mechanism, were observed at distances much greater than 100 microns, and exhibited downstream biasing. Mean (+/- SD) wave speeds of flow-dependent calcium waves were faster under flow conditions than still bath conditions (36.0 +/- 4.7 versus 6.2 +/- 1.3 microns/second; P < .001). By exposing the cells to flurbiprofen, a water soluble prostaglandin synthetase inhibitor, both types of calcium waves were inhibited. CONCLUSION: Human myocytes demonstrate paracrine and intracellular signaling mechanisms for intercellular communication that are distinctly different from action potential propagation.

Calcium↗
PubMed1995

Keratinocyte growth factor as a cytokine that mediates mesenchymal-epithelial interaction.

Keratinocyte growth factor (KGF) is a member of the heparin-binding fibroblast growth factor family (FGF-7) with a distinctive pattern of target-cell specificity. Studies performed in cell culture suggested that KGF was mitogenically active only on epithelial cells, though from a variety of tissues. In contrast, KGF was produced solely by cells of mesenchymal origin, leading to the hypothesis that it might function as a paracrine mediator of mesenchymal-epithelial communication. Biochemical analysis and molecular cloning established that the KGF receptor (KGFR) was a tyrosine kinase isoform encoded by the fgfr-2 gene. Many detailed investigations of KGF and KGFR expression in whole tissue and cell lines largely substantiated the pattern initially perceived in vitro of mesenchymal and epithelial distribution, respectively. Moreover, functional assays in organ culture and in vivo and analysis of agents regulating KGF expression reinforced the idea that KGF acts predominantly on epithelial cells. While the data do not implicate a KGF autocrine loop in neoplasia, paracrine sources of factor or ligand-independent signaling by the KGFR might contribute to malignancy. Alternatively, because of its differentiation-promoting effects, KGF may retard processes that culminate in uncontrolled cell growth.

Animals↗