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At least 19 recordsLinked to original sources
PubMed1997

Paracrine communication in the anterior pituitary as studied in reaggregate cell cultures.

The classical image of the endocrine system is that secretory function of a gland is regulated from outside that gland by other organs. Focused on the pituitary gland, hormone secretion by the anterior lobe is under control of peptides and biogenic amines produced by the hypothalamus. About a decade ago, our group launched the new idea that functioning of the anterior pituitary (AP) is also regulated from within, i.e., that the constituent cell types inter-communicate to control hormone secretion. Extensive in vitro research has now provided a body of evidence that paracrine communication plays an important role, not only in regulation of hormone secretion but also in development, growth, and differentiation of the AP [reviewed in Denef (1994) The Pituitary Gland, pp. 351-378]. It further revealed that crosstalk between the cells is mediated by local, paracrine, factors. The main objective of our research is to identify those factors, their actions and the producing and target cell type(s) in order to unravel the paracrine communication network that is functional in the AP. Equally important, we set the step towards in vivo examination of the results obtained in vitro using transgenic mice. In the present article, we will review the technology used, three examples of AP cell-to-cell interactions studied, and we will discuss the value of transgenic animal models in the study of AP paracrine communication.

Acetylcholine↗
PubMed1992

Paracrine communication regulates adrenocorticotropin secretion.

Local communication among cells of the anterior pituitary appears to play an important role in the regulation of ACTH secretion. Dissociated pituitary cells were plated as a monolayer at decreasing concentrations of cells (increasing the distance between cells and, thus, decreasing their potential interactions), and ACTH secretion was measured from individual corticotropes using a specific reverse hemolytic plaque assay. There was a critical intercell distance above which significant changes in the number of CRF-responsive corticotropes were observed. Provided that this critical distance was not exceeded the number of secretory corticotropes in response to CRF (10 nM) was relatively constant, thereby defining a fraction of corticotropes that was robustly CRF responsive. In contrast, when this critical distance between cells was exceeded, the number of CRF-responsive corticotropes progressively increased to almost double their original number, thereby defining a second fraction of CRF-responsive corticotropes that was previously repressed. These observations suggest the presence of a paracrine factor that profoundly inhibits CRF-stimulated ACTH secretion from a repressed fraction of corticotropes. Further independent studies confirmed and extended these observations. We identified the cellular source of the inhibitory factor as the robustly CRF-responsive fraction of corticotropes. Pituitary cells were identified by reverse hemolytic plaque assay and then destroyed using a laser photoablation procedure that did not compromise the remaining cells. The pituitary cells were separated by a distance at which the inhibitory factor was fully effective. Destruction of the cellular source of the paracrine inhibition would, therefore, allow secretion from the previously repressed fraction of corticotropes. Accordingly, when robustly CRF-responsive corticotropes were destroyed, a significant number of previously repressed corticotropes appeared in a second assay. Destruction of somatotropes or a cell adjacent to a robustly CRF-responsive corticotrope did not alter the number of CRF-stimulated corticotropes among the remaining cells. We conclude that a paracrine factor liberated by the robustly CRF-responsive corticotropes inhibits ACTH secretion from the repressed fraction of corticotropes. The robustly CRF-responsive corticotropes appear unresponsive to the effects of the factor, and the repressed corticotropes are unlikely to secrete it. A role of this paracrine communication is to hold corticotropes in reserve and, therefore, prevent the severe depletion of hormone. This form of paracrine communication may be a specialized adaption among cells where the physiological setting demands robust secretory responses to multiple stimuli. The experimental paradigms developed here may be extremely useful for 1) screening potential paracrine factors and 2) determining whether the secretion of the paracrine factor is regulated by adrenal or hypothalamic hormones.

Adrenocorticotropic Hormone↗
PubMed2005

Intrafollicular paracrine communication in the zebrafish ovary: the state of the art of an emerging model for the study of vertebrate folliculogenesis.

The development and function of vertebrate ovary are primarily controlled by the gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH), from the pituitary. However, most of the activities of FSH and LH are mediated or modulated by a variety of locally produced factors that form an intimate regulatory network within and between the follicles. As a top vertebrate model for genetic and developmental studies, the zebrafish has caught tremendous attention in the past two decades; however, its utility has quickly been extended to other areas including physiology. In the past few years, a variety of peptide growth factors have been identified and characterized in the zebrafish ovary including activin and epidermal growth factor (EGF), and lines of evidence point to the existence of an ovarian network of communication involving these factors. This article provides the state of the art of zebrafish as a model for analyzing ovarian development and its regulation.

Animals↗
PubMed2002

Paracrine communication between malignant and non-malignant prostate epithelial cells in culture alters growth rate, matrix protease secretion and in vitro invasion.

Epithelial cancer cell invasion is facilitated by stromal cells, immune cells, endothelial cells and other epithelial cells. We have used two human papilloma immortalized prostate cell lines, CA-HPV-10 from a carcinoma and PZ-HPV-7 cells from normal prostatic epithelium to study cell-cell influences on growth, gelatinase secretion, invasion and responses to TGFbeta1. We found that co-culture with CA-10 carcinoma cells stimulates proliferation of the PZ-7 epithelial line. TGFbeta1 inhibited growth of both lines, but while inhibitory effects on the CA-10 cells diminished after removal of the peptide, inhibition of PZ-7 was lasting. Interestingly, the TGFbeta-induced growth inhibition in PZ-7 cells could be partially reversed by co-culture with CA-10 cells. Co-culture with CA cells in a 3-chamber invasion assay also promoted invasion of PZ cells. CA-10 invasion was enhanced by co-culture with TGFbeta1-treated-PZ-7 cultures and this enhancement was associated with TGFbeta1-induced secretion of matrix metalloproteinase-9. Our observations suggest that interaction between prostate cancer cells and prostate epithelial cells may promote proliferation of the epithelial cell population and produce a paracrine source of MMP-9 which may facilitate early cancer cell invasion.

Cell Communication↗
PubMed2004

Directionally specific paracrine communication mediated by epithelial FGF9 to stromal FGFR3 in two-compartment premalignant prostate tumors.

Tissue homeostasis in normal prostate and two-compartment nonmalignant prostate tumors depends on harmonious two-way communications between epithelial and stromal compartments. Within the fibroblast growth factor (FGF) family, signaling to an epithelial cell-specific FGF receptor (FGFR) 2IIIb-heparan sulfate complex from stromal-specific FGF7 and FGF10 delivers directionally specific instruction from stroma to epithelium without autocrine interference. Using a two-compartment transplantable prostate tumor model in which survival of stromal cells in vivo depends on epithelial cells, we show that signaling from epithelial FGF9 to stromal FGFR3 potentially mediates epithelial-to-stromal communication that also is directionally specific. FGF9 mRNA was expressed exclusively in the epithelial cells derived from well-differentiated, two-compartment Dunning R3327 rat prostate tumors. In contrast, FGFR3 was expressed at functionally significant levels only in the derived stromal cells. Competition binding and immunoprecipitation assays revealed that FGF9 only bound to an FGFR on the stromal cells. FGF9 also failed to covalently cross-link to clonal lines of stromal cells devoid of FGFR3 that expressed FGFR1 and FGFR2IIIc. Furthermore, FGF9 specifically stimulated DNA synthesis in stromal cells expressing FGFR3. These results demonstrate a directionally specific paracrine signaling from epithelial FGF9 and stromal FGFR3. Similar to the FGF7/FGF10 to FGFR2IIIb signaling from the stroma to the epithelium, the directional specificity from epithelium to stroma appears set by a combination of cell-specific expression of isoforms and cell-context specificity of FGFR isotypes for FGF.

Animals↗
PubMed2002

Paracrine intercellular communication by a Ca2+- and SNARE-independent release of GABA and glutamate prior to synapse formation.

GABA and glutamate receptors are expressed in immature "silent" CA1 pyramidal neurons prior to synapse formation, but their function is unknown. We now report the presence of tonic, spontaneous, and evoked currents in embryonic and neonatal CA1 neurons mediated primarily by the activation of GABA(A) receptors. These currents are mediated by a nonconventional release of transmitters, as they persist in the presence of calcium channel blockers or botulinium toxin and are observed in Munc18-1-deficient mice in which vesicular release is abolished. This paracrine communication is modulated by glutamate but not GABA transporters, which do not operate during this period of life. Thus, a Ca(2+)- and SNARE-independent release of transmitters underlies a paracrine mode of communication before synapse formation.

Animals↗
PubMed2002

Paracrine mediators of endometrial matrix metalloproteinase expression: potential targets for progestin-based treatment of endometriosis.

The endometrial lining of the human uterus is a highly specialized, steroid-sensitive tissue. Throughout the reproductive years, the endometrium undergoes dramatic cycles of growth, differentiation, and breakdown under the influence of ovarian steroids. In response to changes in steroid exposure throughout the menstrual cycle, the endometrium produces an array of bioactive growth factors and other cytokines that are critical components of paracrine communication. For example, cell-cell communication via paracrine factors directs the expression of matrix metalloproteinases (MMPs), enzymes that mediate tissue remodeling during the menstrual cycle. The disease endometriosis is thought to occur as a consequence of retrograde menstruation, and MMPs appear to contribute to the establishment and progression of ectopic endometrial growth in the peritoneal cavity. Although the risk for developing endometriosis is linked to a woman's steroid exposure, locally produced paracrine factors can modify steroid action on multiple gene targets, including the MMPs. Estrogen-associated growth factors as well as inflammatory cytokines are potent stimulators of MMP expression and may contribute to the ability of endometrial fragments to invade the peritoneal surface and establish ectopic sites of growth. In contrast, paracrine factors associated with progesterone action during early pregnancy inhibit MMP expression and prevent ectopic endometrial growth in an experimental model. For example, locally produced retinoic acid and transforming growth factor-beta (TGF-beta) act in concert with progesterone to suppress MMPs, while enhancing expression of MMP inhibitors (TIMPs) during endometrial differentiation. Targeting pregnancy-associated factors that inhibit endometrial-specific MMP expression and action may enhance the effectiveness of progestin-related treatments for endometriosis.

Endometriosis↗
PubMed2005

ATP-dependent paracrine intercellular communication in cultured bovine corneal endothelial cells.

PURPOSE: Intercellular communication (IC) in nonexcitable cells is mediated through gap junctions and/or through the release of paracrine mediators. This study was conducted to investigate adenosine-5' triphosphate (ATP)-dependent paracrine IC in the propagation of Ca2+ waves in confluent monolayers of cultured bovine corneal endothelial cells (BCECs). METHODS: A Ca2+ wave was induced by point mechanical stimulation (PMS) of a single cell by indentation with a glass micropipette (approximately 1 microm tip) for <1 second. Dynamic changes in [Ca2+]i in the mechanically stimulated (MS) cell and in the neighboring (NB) cells were visualized with a confocal microscope, using a fluorescent dye. Normalized fluorescence (NF), calculated as the ratio of the average fluorescence of a cell to the average under resting conditions, was used as a measure of [Ca2+]i. Expression of P2Y receptors and ecto-adenosine triphosphatases (ATPases) was investigated by RT-PCR. ATP release in response to PMS was measured by luciferin-luciferase (LL) bioluminescence. RESULTS: BCECs subjected to PMS showed a transient [Ca2+]i increase. Under control conditions, the maximum NF in the MS cell occurred within 600 ms, and the fluorescence returned to baseline within 170 seconds. NB cells also presented a [Ca2+]i increase with a transient characterized by decreasing maximum NF and increasing latency as a function of the distance from the MS cell. These transients propagated as an intercellular Ca2+ wave to a distance of five or six NB cells away from the MS cell, covering areas (called active areas, AAs) up to 77,000 +/- 3,200 microm2 (N=21). The percentage of responsive cells (defined as cells showing maximum NF >1.1) decreased with increasing distance from the MS cell. The Ca2+ wave crossed cell-free lanes. Pretreatment of cells with the nonselective purinergic receptor antagonist suramin (200 microM), exogenous apyrases, which break down nucleotides (10 U/mL), or the PLC inhibitor U-73122 (10 microM) reduced the wave propagation, whereas the ecto-ATPase inhibitor ARL-67156 (100 microM) significantly enhanced it. ATP-dependent LL bioluminescence increased after PMS. RT-PCR showed mRNAs for P2Y1 and P2Y2 receptors and ecto-ATPases in BCECs. CONCLUSIONS: PMS of BCECs induces release of ATP and a concomitant intercellular Ca2+ wave, even in the absence of direct cell-cell contacts. The AA of the wave is modulated by agents that affect P2Y receptor activity. Thus, PMS-induced intercellular Ca2+ wave propagation in BCECs involves ATP-dependent paracrine IC.

Adenosine Triphosphatases↗
PubMedDate not supplied

Paracrine factors in adult rat testis gonadotrophin control of opioids and LHRH like peptide.

A paracrine regulation involves agents which are produced by one cell type and act on an other one within an organ. In rodent testis, local control mechanisms modulate the actions of the gonadotrophins according to local requirements. Two groups of peptides-opioids and testicular LHRH are defined as paracrine factors and in vivo they are both modified by HCG. In vitro, after HCG exposure, we first localized an opioid like material in Sertoli cells cytoplasma by immunohistochemistry. This material is detected in freeze dried homologous culture media using a dot immunobinding technique. With a longer HCG exposure, an LHRH like material is then visualized in the basal compartment of the Sertoli cells and it is detected in freeze dried homologous culture media by the same technical procedure than for opioid material. By adding synthetic enkephalins to culture medium, we obtain the same results as with the endogenous opioid material, excreted after HCG addition. If naloxone a potent opiate antagonist, is added to the culture medium previously to HCG or enkephalins, the Sertoli cells cytoplasma are no more immunoreactives with the anti-enkephalin serum and no LHRH material is neither visualized by immunohistochemical technique neither detected in culture media. We conclude that testicular opioids, synthetized by the Leydig cells and which have specific Sertoli cells receptors are one Leydig-Sertoli paracrine communication factor. One way of response to their receptor fixation is the synthesis and excretion by Sertoli cells of testicular LHRH. This one is known to act on Leydig cells via specific receptors and it is one Sertoli-Leydig cells paracrine communication factor.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2003

Interaction of bovine granulosa and theca cells in a novel serum-free co-culture system.

The objective of this study was to develop a defined culture system in which bovine follicular and granulosa cells are grown in close contact with each other and with the extracellular matrix (ECM) component laminin. Granulosa and theca cells from follicles 4-6 mm in diameter were cultured on either side of laminin-coated BioCoat cell culture inserts in a serum-free medium containing 10 ng insulin ml(-1) at plating densities of 10(5) and 3 x 10(5) cells per membrane side. The cells adopted a clumped arrangement, maintained steroidogenic activity for at least 7 days and demonstrated paracrine communication by increased steroidogenesis and enhanced cell survival compared with cells in mono-culture. Co-cultured theca cells secreted significantly more androstenedione compared with cells in mono-culture. Granulosa cell viability was doubled by co-culture with theca cells. Co-cultures at both cell plating densities were responsive to treatment with physiological combinations of either FSH, LH and LR3 insulin-like growth factor I (IGF-I) (treatment A) or FSH, LR3 IGF-I and androstenedione (treatment B). Significantly more androstenedione was secreted in the presence of treatment A compared with controls. In contrast, oestradiol secretion was increased only by treatment B. Progesterone secretion was unaffected by treatment and did not increase during culture. Co-cultures at the higher plating density demonstrated higher theca cell survival and better maintenance of the follicular cell phenotype. In conclusion, this novel co-culture system provides a unique model for the study of paracrine communication between ovarian somatic cells and cell-ECM interactions during follicle growth.

Androstenedione↗
PubMed2001

Cellular basis for paracrine regulation of ovarian follicle development.

Paracrine factors secreted by oocytes and somatic cells regulate many important aspects of early ovarian follicle development in mammals. From activation of dormant primordial follicles to selection of secondary follicles, locally acting factors have been identified that appear to exert important effects on the growth and differentiation of oocytes and granulosa cells. This article summarizes evidence to support a model for bi-directional paracrine communication that is based on developmental regulation of the delivery and reception of paracrine factors at the oocyte-granulosa cell interface. Transzonal projections that originate from granulosa cells and terminate at the oocyte plasma membrane provide a polarized means to orient the secretory organelles of somatic cells. Characterization of transzonal projections in follicles from normal and genetically modified mice reveals dynamic changes in the density and stability of transzonal projections. On the basis of new data analysing the orientation and cytoskeletal content of transzonal projections in mammalian oocytes, a model is proposed for regulation of paracrine growth factor secretion by follicle-stimulating hormone. These findings have immediate implications for ovarian hyperstimulation protocols and follicle culture models as related to the production of mammalian embryos by assisted reproductive technologies.

Animals↗
PubMed2003

Extracellular purines from cells of seminiferous tubules.

It has been long postulated that extracellular purines can modulate the function of the male reproductive system by interacting with different purinergic receptors of Sertoli and germinative cells. Many authors have described the biological changes induced by extracellular ATP and/or adenosine in these cells, and some hypothetical models for paracrine communication mediated by purines were proposed; however, the cellular source(s) of these molecules in seminiferous tubules remains unknown. In this study, we demonstrated for the first time that Sertoli cells are able to release ATP (0.3 nmol/mg protein) and adenosine (0.1 nmol/mg protein) in the extracellular medium, while germinative and myoid peritubular cells are able to secrete adenosine (0.02 and 0.37 nmol/mg protein, respectively). Indeed, all the three types of cells were able to release inosine at significant concentrations (about 0.4 nmol/mg protein). This differential secretion depending on the cellular type suggests that these molecules may be involved in the paracrine regulation and/or control of the maturation processes of these cells.

5'-Nucleotidase↗
PubMed2004

A paracrine signaling role for serotonin in rat taste buds: expression and localization of serotonin receptor subtypes.

Recent advances in peripheral taste physiology now suggest that the classic linear view of information processing within the taste bud is inadequate and that paracrine processing, although undemonstrated, may be an essential feature of peripheral gustatory transduction. Taste receptor cells (TRCs) express multiple neurotransmitters of unknown function that could potentially participate in a paracrine role. Serotonin is expressed in a subset of TRCs with afferent synapses; additionally, TRCs respond physiologically to serotonin. This study explored the expression and cellular localization of serotonin receptor subtypes in TRCs as a possible route of paracrine communication. RT-PCR was performed on RNA extracted from rat posterior taste buds with 14 prime sets representing 5-HT(1) through 5-HT(7) receptor subtype families. Data suggest that 5-HT(1A) and 5-HT(3) receptors are expressed in taste buds. Immunocytochemistry with a 5-HT(1A)-specific antibody demonstrated that subsets of TRCs were immunopositive for 5-HT(1A). With the use of double-labeling, serotonin- and 5-HT(1A)-immunopositive cells were observed exclusively in nonoverlapping populations. On the other hand, 5-HT(3)-immunopositive taste receptor cells were not observed. This observation, combined with other data, suggests 5-HT(3) is expressed in postsynaptic neural elements within the bud. We hypothesize that 5-HT release from TRCs activates postsynaptic 5-HT(3) receptors on afferent nerve fibers and, via a paracrine route, inhibits neighboring TRCs via 5-HT(1A) receptors. The ole of the 5-HT(1A)-expressing TRC within the taste bud remains to be explored.

Animals↗
PubMed1998

Role of the subchondral vascular system in endochondral ossification: endothelial cells specifically derepress late differentiation in resting chondrocytes in vitro.

Endochondral ossification in growth plates proceeds through several consecutive steps of late cartilage differentiation leading to chondrocyte hypertrophy, vascular invasion, and, eventually, to replacement of the tissue by bone. It is well established that the subchondral vascular system is pivotal in the regulation of this process. Cells of subchondral blood vessels act as a source of vascular invasion and, in addition, release factors influencing growth and differentiation of chondrocytes in the avascular growth plate. To elucidate the paracrine contribution of endothelial cells we studied the hypertrophic development of resting chondrocytes from the caudal third of chick embryo sterna in co-culture with endothelial cells. The design of the experiments prevented cell-to-cell contact but allowed paracrine communication between endothelial cells and chondrocytes. Under these conditions, chondrocytes rapidly became hypertrophied in vitro and expressed the stage-specific markers collagen X and alkaline phosphatase. This development also required signaling by thyroid hormone in synergy. Conditioned media could replace the endothelial cells, indicating that diffusible factors mediated this process. By contrast, smooth muscle cells, fibroblasts, or hypertrophic chondrocytes did not secrete this activity, suggesting that the factors were specific for endothelial cells. We conclude that endochondral ossification is under the control of a mutual communication between chondrocytes and endothelial cells. A finely tuned balance between chondrocyte-derived signals repressing cartilage maturation and endothelial signals promoting late differentiation of chondrocytes is essential for normal endochondral ossification during development, growth, and repair of bone. A dysregulation of this balance in permanent joint cartilage also may be responsible for the initiation of pathological cartilage degeneration in joint diseases.

Alkaline Phosphatase↗
PubMed2005

Catalytically inactive human cathepsin D triggers fibroblast invasive growth.

The aspartyl-protease cathepsin D (cath-D) is overexpressed and hypersecreted by epithelial breast cancer cells and stimulates their proliferation. As tumor epithelial-fibroblast cell interactions are important events in cancer progression, we investigated whether cath-D overexpression affects also fibroblast behavior. We demonstrate a requirement of cath-D for fibroblast invasive growth using a three-dimensional (3D) coculture assay with cancer cells secreting or not pro-cath-D. Ectopic expression of cath-D in cath-D-deficient fibroblasts stimulates 3D outgrowth that is associated with a significant increase in fibroblast proliferation, survival, motility, and invasive capacity, accompanied by activation of the ras-MAPK pathway. Interestingly, all these stimulatory effects on fibroblasts are independent of cath-D proteolytic activity. Finally, we show that pro-cath-D secreted by cancer cells is captured by fibroblasts and partially mimics effects of transfected cath-D. We conclude that cath-D is crucial for fibroblast invasive outgrowth and could act as a key paracrine communicator between cancer and stromal cells, independently of its catalytic activity.

Animals↗
PubMed1999

Transforming growth factor-beta regulates Kit ligand expression in rat ovarian surface epithelial cells.

In preparation for ovulation, paracrine communication between the preovulatory follicle and overlying theca/stromal cells and ovarian surface epithelium (OSE) must take place to facilitate the degradative and apoptotic events associated with ovulation. Kit tyrosine kinase receptors and their ligand, kit ligand (KL) are expressed within ovarian follicles, and ligand-induced receptor activation appears to account for some of the cell - cell interactions important for oocyte development. We investigated the expression of Kit receptors and KL in OSE cells and the possibility that modulation of their expression could affect OSE cell activity. KL mRNA and protein were detected in the OSE cell layer of rat ovaries, and primary cultures of rat OSE as well as the immortalized rat OSE cell line, ROSE 199, expressed KL, but not Kit receptors. Both primary and immortalized OSE cells preferentially expressed KL-1, rather than KL-2, transcripts, suggesting that these cells produce predominantly the soluble form of KL. Activation of the cAMP signalling pathway using dibutyryl cAMP decreased proliferation of ROSE 199 cells and elicited a threefold increase in KL expression. TGF-beta similarly inhibited ROSE 199 cell proliferation, but strongly inhibited dibutyryl cAMP-induced KL expression, indicating that changes in KL expression were not directly associated with OSE cell proliferation. The expression of mostly soluble KL in the surface epithelium suggests that this cytokine may be acting in a paracrine fashion, perhaps interacting with nearby Kit receptor-bearing theca cells.

Animals↗
PubMed1993

Cellular communication in the circadian clock, the suprachiasmatic nucleus.

The hypothalamic suprachiasmatic nucleus functions as the circadian clock in the mammalian brain. Communication between the cells of the suprachiasmatic nucleus is likely to be responsible for the generation and accuracy of this biological clock. Communication between many cells of the brain is mediated by action potentials that pass down the axon and cause release of neurotransmitters at the neuronal synaptic junction. Additional mechanisms of cellular communication appear to operate in the suprachiasmatic nucleus. Several lines of evidence point to multiple modes of cellular communication: these include the continuing operation of the clock after Na(+)-mediated action potentials have been blocked, the orchestrated metabolic rhythms of suprachiasmatic nucleus cells prior to synaptogenesis, the entrainment of fetal to maternal rhythms, and the rapid recovery of function after suprachiasmatic nucleus transplants into arrhythmic rodents. Possible alternative means of intercellular communication in the suprachiasmatic nucleus are examined, including calcium spikes in presynaptic dendrites, ephaptic interaction, paracrine communication, glial mediation, and gap junctions. This paper identifies and examines some of the unanswered questions related to intercellular communication of suprachiasmatic nucleus cells.

Action Potentials↗