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At least 127 records · Page 7Linked to original sources
PubMed1979

Topography of somatostatin cells in the stomach of the rat: possible functional significance.

Somatostatin cells in the stomach of the rat have a characteristic shape and distribution. In the antral mucosa they occur together with gastrin cells and enterochromaffin cells at the base of the glands. In the oxyntic mucosa they are scattered along the entire glands with some predominance in the zone of parietal cells. Throughout the gastric mucosa the somatostatin cells possess long and slender processes that emerge from the base of the cell and end in club-like swellings. Such processes appear to contact a certain proportion of neighbouring gastrin cells in the antral mucosa and parietal cells in the oxyntic mucosa. Exogenous somatostatin given by intravenous infusion to conscious rats counteracted the release of gastrin stimulated by feeding, elevated antral pH or vagal excitation. Gastrin causes parietal cells to secrete HCl and endocrine cells in the oxyntic mucosa to mobilise and synthesise histamine. Somatostatin is known to block the respone of the parietal cells to gastrin. In contrast, somatostatin did not block the response of the histamine-storing endocrine cells to gastrin, perhaps because these endocrine cells lack receptors to somatostatin. Conceivably, somatostatin in the gastric mucosa has a paracrine mode of action. The observations of the present study suggest that somatostatin may affect some, but not all of the various cell types in the stomach. Under physiological conditions this selectivity may be achieved in the following ways: 1) Communication may be based on direct cell-to-cell contact. 2) Only certain cell types are supplied with somatostatin receptors.

Animals↗
PubMed1988

[Factors regulating the differentiation of somatic cells of mammalian ovarian follicles].

Experimental data on regulation of the cytodifferentiation of theca and the granulosa cells in mammalian ovaries are reviewed, in addition to mechanisms of cooperative interactions of these cell types in steroidogenesis. Evidence is provided on the gonadotropin induced differentiation in the cultured ovarian somatic cells, and on a modifying effect exerted on this process by some central (prolactin, LH-RH, etc.) or local factors (steroids, growth factors, low-molecular fraction of follicular fluid, etc.). A possible physiological importance of endocrine and also of auto- and paracrine regulators of differentiation in growth processes and selection of the dominant follicle in the mammalian ovaries is discussed.

Animals↗
PubMed1994

The nitric oxide-cyclic GMP signal transduction system for intracellular and intercellular communication.

From our work and that of others, it is now quite apparent that the NO-cGMP system can function as an intracellular or intercellular signal transduction system (Murad et al., 1988, 1990; Murad, 1989a,b; Ishii et al., 1989, 1991). If a specific cell possesses both NO synthase and an isoform of guanylyl cyclase that is activatable with NO, then cGMP levels in that cell can be regulated by agents that alter NO synthase activity and NO formation (Fig. 1). NO, or a complex of NO which is liberated from the producing or donor cell, can also activate guanylyl cyclase in a neighboring or perhaps a distant cell to increase cGMP synthesis. In the latter scenario, NO or its carrier complex behaves as a paracrine substance, autacoid, or hormone. Interestingly, the liberated extracellular NO can also feed back and increase cGMP synthesis in the cell of origin. This is best demonstrated by the inhibitory effects of hemoglobin on agonist-induced cGMP accumulation in homogeneous cell culture systems where the hormone or agonist effects on cGMP are mediated by NO. Presumably, hemoglobin would not be permeable and could only trap or scavenge extracellular NO to account for its ability to decrease hormonally induced cGMP increases in homogeneous cell populations. There is no direct evidence that NO can act as an endocrine substance to increase cGMP synthesis in a distant target cell population. However, complexes or carrier states of NO that would liberate NO at a distant site could most certainly be viewed as endocrinological agents (hormones or autocoids). We suspect that appropriately designed experiments in the future will also support this role for NO as an endocrinological agent that can also function at a distance similar to classical hormones. Indeed, we believe that NO should be added to the list of agents that can function as a neurotransmitter, paracrine substance, and autacoid or hormone. It can also be viewed as an intracellular, as well as intercellular, messenger. To date, no substance has played such a diverse role in intracellular and intercellular signal transduction. Thus, NO appears to be a unique and simple molecule with diverse functions in signal transduction.

Amino Acid Oxidoreductases↗
PubMed1993

Growth factors and growth control of heterogeneous cell populations.

In an earlier work a model of the autocrine and paracrine pathways of tumor growth control was developed (Michelson and Leith. 1991. Autocrine and paracrine growth factors in tumor growth. Bull. math. Biol. 53, 639-656). The target population, a generic tumor, was modeled as a single, homogeneous population using the standard Verhulst equation of logistic growth. Mitogenic signals were represented by modifications to the Malthusian growth parameter and adaptational signals were represented by modifications to the carrying capacity. Three growth scenarios were described: (1) normal tissue wound healing, (2) unperturbed tumor growth, and (3) tumor growth in a radiation damaged environment, a phenomenon termed the Tumor Bed Effect (TBE). In this paper, we extend those results to include a "triad" of growth factor controls (autocrine, paracrine and endocrine) and heterogeneity of the target population. The heterogeneous factors in the model represent either intrinsic, epigenetic or environmental differences in both normally differentiating tissues and tumors. Three types of growth are modeled: (1) normal tissue differentiation or wound healing, assuming no communication between differentiated and undifferentiated cell compartments; (2) normal wound healing with feedback inhibition, due to signalling from the differentiated compartment; and (3) the development of hypoxia in a spherical tumor. The signal processing within the triad is discussed for each model and biologically reasonable constraints are defined for limits on growth control.

Animals↗
PubMed1989

Co-inoculation of tumorigenic rat prostate mesenchymal cells with non-tumorigenic epithelial cells results in the development of carcinosarcoma in syngeneic and athymic animals.

Co-inoculation of NbF-I and NbE-I s.c. into either adult male syngeneic rats or athymic nude mice induced the development of tumors that resembled carcinosarcoma on histopathologic evaluation. These tumors were composed of a mixture of adenocarcinoma and fibrosarcoma and were induced by the mixtures of NbF-I and NbE-I cells at a ratio ranging from 0.001 to 3.2; inoculation of NbF-I alone resulted in the development of fibrosarcoma. Flow-cytometric analysis showed that the epithelial cells subcloned from the carcinosarcoma had a DNA profile like that of their parental cell line and remained non-tumorigenic. When co-inoculated with the tumorigenic fibroblasts in syngeneic hosts, however, the subcloned epithelial cells again formed carcinosarcomas. Our results indicate that cell fusion between epithelial cells and fibroblasts is an unlikely explanation for tumorigenicity. We propose that prostatic fibroblasts exert a directive influence on their adjacent epithelial cells through a paracrine mechanism that determines epithelial growth and tumorigenicity in vivo.

Animals↗
PubMed1995

Ischaemia-induced expression of bFGF in normal skeletal muscle: a potential paracrine mechanism for mediating angiogenesis in ischaemic skeletal muscle.

To test the hypothesis that induction of endogenous bFGF can lead to angiogenesis in ischaemic skeletal muscle, we studied the expression of bFGF after transposition of a well-vascularized muscle flap onto an ischaemic hindlimb in the rabbit. The results indicated a marked induction of bFGF mRNA throughout the myoblasts of the well-perfused muscle flap but not the myoblasts of the ischaemic muscle. bFGF protein was detected in the muscle flap, particularly in the myoblasts located closest to a newly formed, adjacent interface, and in the interface itself. In contrast, bFGF expression was not induced after transposition of a well-perfused muscle flap onto healthy muscle tissue. These data provide evidence that the juxtaposition of ischaemic skeletal muscle with healthy mesenchymal tissue triggers an increased expression of bFGF in the myoblasts of the well-perfused muscle. This paracrine induction of bFGF, in turn, leads to increased angiogenesis and regeneration of the ischaemic skeletal muscle.

Animals↗
PubMed1989

The paracrine stimulation of MCF-7 cells by MDA-MB-231 cells: possible role in antiestrogen failure.

The influence of paracrine factors secreted by the hormone independent breast cancer cell line MDA-MB-231 on the growth of the hormone dependent breast cancer cell line MCF-7 was examined in the absence of estradiol and in the presence of inhibitory concentrations of antiestrogens. MDA-MB-231 cells were grown on transwell membranes and co-cultured with MCF-7 cells (50,000) plated in 6-well tissue culture dishes. Growth was maximally increased (80%) when MCF-7 cells were grown in the presence of 150,000 or more MDA-MB-231 cells for 4 days. The non-steroidal antiestrogens tamoxifen (10(-10) to 10(-6) M) and 4-hydroxytamoxifen (10(-11) to 10(-7) M), the steroidal antiestrogens ICI 164384 (10(-10) to 10(-6) M) and Ru39411 (10(-11) to 10(-7) M) all inhibited estradiol (10(-11) M) stimulated MCF-7 cell growth in a dose related manner when cultured for 4 days. However, the paracrine stimulation of MCF-7 cells produced by co-culture with 250,000 MDA-MB-231 cells was not inhibited by any of these antiestrogens. These data suggest that in heterogeneous tumors, paracrine factors from hormone independent cells may reverse the growth inhibitory action that antiestrogens have on estrogen-dependent breast cancer cell growth.

Breast Neoplasms↗
PubMed1993

A unique costimulatory pathway defined with T cell hybridomas specific for myelin basic protein: third party costimulators restrict antigenic responses in time and space.

Costimulatory signals regulate T cell responses to myelin basic protein (MBP) during induction of EAE in Lewis rats. However, the physiology of these costimulatory pathways has yet to be resolved. In this study, costimulatory pathways were defined by comparing MBP-stimulated IL-2 production by two types of T cell hybridoma (designated THYB-1 and THYB-2). THYB-1 hybrids required presentation of MBP/Ia complexes to stimulate IL-2 production, whereas THYB-2 hybrids also required the additional presence of costimulatory signals from radiosensitive (RS), nonadherent (NAdh) splenocytes (SPL). This study shows that allogeneic SPL, syngeneic B cells, or syngeneic T cells provided costimulatory signals to THYB-2 hybrids, although only syngeneic B cells were able to provide APC activity. Transduction of costimulatory signals did not occur across a microporous membrane but rather required close proximity of T cell hybrids with RS accessory cells. Simultaneous presence of costimulatory signals together with MHC-restricted antigen were required to initiate and maintain IL-2 production by THYB-2 hybrids. These findings support a model in which costimulatory molecules expressed by effector cells serve to restrict lymphokine production by T-helper cells. That is, THYB-2-like T-helper cells may mediate a paracrine pathway of IL-2 production that provides "help" to antigen-activated effector cell types that coexpress IL-2 receptors with appropriate costimulatory molecules.

Animals↗
PubMed1992

Molecular biology mechanisms in the radiation induction of pulmonary injury syndromes: interrelationship between the alveolar macrophage and the septal fibroblast.

Pulmonary fibrosis is a crippling, essentially lethal chronic disease due to an interplay of events following irradiation between the pneumonitic and fibrotic phases. In this series of experiments it is demonstrated that there is no latent period after irradiation, but an immediate intercellular communication system which springs into action to initiate recovery. Latency was only a function of our inability to uncover the molecular events that precede and underlie the clinical pathologic course of organ/tissue irradiation. Current advances in understanding the production of growth factors by different cells provides new insights to autocrine, paracrine and endocrine messages as a basis for understanding radiation pathophysiology as a progressive process that is amplified by other injurious events such as chemotoxicity. This is the first demonstrated release of trophic factors (cytokines) after in vivo irradiation that persists up to a month after exposure, suggesting that the persistence of a small incremental stimulus during a silent "latent" period can be the basis for the clinical pathologic expression of a late radiation effect, that is, pulmonary interstitial fibrosis.

Animals↗
PubMed1992

Prostate and bone fibroblasts induce human prostate cancer growth in vivo: implications for bidirectional tumor-stromal cell interaction in prostate carcinoma growth and metastasis.

Prostate cancer selectively metastasizes to the axial skeleton to produce osteoblastic lesions, which suggests that bidirectional paracrine interactions exist between prostate cancer and bone cells. To evaluate the role of tumor-stromal cell interaction and stromal-specific growth factors in prostate cancer growth and dissemination, we coinoculated nontumorigenic human prostate cancer cells (LNCaP) and various tissue-specific fibroblasts subcutaneously in athymic mice. LNCaP tumors were induced most consistently by human bone fibroblasts (62%), followed by two prostate fibroblast cell lines (31% and 17%), but not by lung, kidney, or embryonic 3T3 fibroblasts. Carcinomas formed preferentially in male hosts, demonstrating in vivo androgen sensitivity. Immunohistochemical and biochemical techniques confirmed the human prostate component of these tumors and were paralleled by elevations in serum prostate specific antigen. In vitro mitogenic assays revealed a two-to three-fold bidirectional stimulation between LNCaP and bone or prostate fibroblast conditioned media, but not lung, kidney, or 3T3 fibroblast conditioned media. A novel method developed to deliver concentrated bone or prostate fibroblast conditioned media in vivo using a slowly absorbed matrix (gelfoam) also induced tumor formation, emphasizing the importance of fibroblast growth factors in LNCaP tumor formation. Northern analysis identified the stromal compartment as the primary source of extracellular matrix (collagen, fibronectin), while only LNCaP cells expressed transforming growth factor alpha. Although LNCaP and stromal cells express basic fibroblast growth factor (bFGF), the bidirectional paracrine-mediated mitogenic activity between these cells is not inhibited by anti-bFGF antibodies, suggesting that other undefined growth factors may be involved in stimulating LNCaP growth. These observations illustrate the importance of stromal-epithelial interaction in prostate tumor growth and suggest that extracellular matrix and paracrine-mediated growth factors play a role in prostate cancer growth and metastasis.

Androgens↗
PubMed1986

Paracrine control of the testis.

The mammalian testis is under the overall control of pituitary gonadotropins but the utilization of these signals to achieve normal testicular function involves complex local interactions between the Sertoli and germ cells, the Sertoli and peritubular cells, and the Sertoli and Leydig cells as well as local control of the testicular vasculature. These interactions serve two purposes: (1) to coordinate the functions of the three testicular compartments (seminiferous tubules, interstitium and the vasculature); and (2) to control the complex but orderly sequence of events that constitutes the spermatogenic cycle. This process, which involves multiplication, differentiation and translocation of the germ cells is organized into a sequence of stages, each of which is composed of a constant association of germ cells at four or five different stages of development. At each stage of the spermatogenic cycle, different events occur and the function of the Sertoli cells alters, probably in accordance with the changing requirements of the associated germ cells. As yet, our understanding of these many local events is extremely limited, particularly with respect to the identity of the hormones/factors involved in controlling the various processes. Our knowledge of paracrine control mechanisms in the testis is derived mainly from studies of the rat, but as the process of spermatogenesis is essentially the same in most mammals and involves the same sequence of events, then findings in the rat can probably be applied in general, if not in detail, to the human testis; the limited direct information available on the human testis supports this view. As most cases of infertility in men occur despite normal or raised serum gonadotropin levels and are characterized by the production of reduced or normal numbers of sperm, then it seems likely that malfunction of one or more of the intricate paracrine processes within the testis may be involved in the aetiology of idiopathic oligospermia. It is therefore argued that advances in our knowledge of the paracrine control of the testis should have major repercussions on our ability to understand, and eventually treat, idiopathic infertility in men, and also to induce infertility for contraceptive purposes.

Animals↗
PubMed1989

Anchorage-independent growth of synoviocytes from arthritic and normal joints. Stimulation by exogenous platelet-derived growth factor and inhibition by transforming growth factor-beta and retinoids.

Exuberant tumor-like synovial cell proliferation with invasion of periarticular bone is a feature of rheumatoid arthritis in humans and of streptococcal cell wall (SCW)-induced arthritis in rats. These histologic observations prompted us to examine synoviocytes from arthritic joints for phenotypic characteristics of transformed cells. The capacity to grow in vitro under anchorage-independent conditions is a characteristic that correlates closely with potential in vivo tumorigenicity. In medium supplemented with 20% serum or in basal media supplemented with platelet-derived growth factor (PDGF), early passage synoviocytes from both SCW-induced and rheumatoid arthritic joints formed colonies in soft agarose. Epidermal growth factor (EGF), interleukin 1 (IL-1), tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), and transforming growth factor-beta (TGF-beta) did not support growth, although EGF enhanced PDGF-dependent growth. On the other hand, TGF-beta, as well as all-trans-retinoic acid, inhibited colony growth. Early passage normal rat and human synoviocytes also grew under the same conditions, but lung, skin, and late-gestation embryonic fibroblast-like cells did not. Considered in the context of other published data our findings provide cogent evidence that synoviocytes, but not other types of fibroblast-like cells, readily acquire phenotypic characteristics commonly associated with transformed cells. Expression of the transformed phenotype in the inflammatory site is likely regulated by paracrine growth factors, such as PDGF and TGF-beta.

Animals↗
PubMed1993

Regulation of the acute phase response by cytokines.

Cytokines appear to function as part of a complex regulatory network, a signaling language in which informational content resides in the combinations, and perhaps sequence, of cytokines and other extracellular messenger molecules received by a cell. The effects of combinations of cytokines are complex and often differ from their in vitro effects or when administered by themselves. (From this perspective, to use a somewhat crude simile, individual cytokines can be thought of as words which bear informational content. Although individual cytokines may, on occasion, communicate a complete message, more commonly the actual messages received by cells probably resemble sentences, in which it is the combination and sequence of words which convey information.) Currently available data suggest an in vivo scenario in the acute phase response in which the hepatocyte receives a complex mixture of humoral or paracrine signals which are integrated by multiple interacting post-receptor and gene regulatory mechanisms to cause finely regulated changes in plasma protein synthesis. Regulation often occurs by transcriptional control, but post-transcriptional mechanisms, including translational regulation, may participate. Both the extracellular and intracellular mechanisms that mediate the response of the hepatocyte to inflammatory stimuli appear to be highly complex and involve multiple overlapping, concurrent, and parallel pathways. Enough is known at present to conclude that IL-6 is a major participant in these changes in man. Regulation of non-hepatocyte acute phase phenomena has not been delineated as thoroughly, but clearly involves a number of cytokines.

Acute-Phase Reaction↗
PubMed1991

Morphological evidence for a close interaction of chromaffin cells with cortical cells within the adrenal gland.

The adrenal medulla appears to exert a regulatory influence on adrenocortical steroidogenesis. We have therefore studied the morphology of rat, porcine and bovine adrenals in order to characterize the contact zones of adrenomedullary and adrenocortical tissues. The distribution of chromaffin cells located within the adrenal cortex and of cortical cells located within the adrenal medulla was investigated. Chromaffin cells were characterized by immunostaining for synaptophysin and chromogranin A, both being considered specific for neuroendocrine cells. Cortical cells were characterized by immunostaining for 17 alpha-hydroxylase, an enzyme of the steroid pathway. Cellular contacts of chromaffin cells and cortical cells were examined at the electron microscopical level. In rat and porcine adrenals, rays of chromaffin cells, small cell clusters and single chromaffin cells or small invaginations from the medulla could be detected in all three zones of the cortex. Chromaffin cells often spread in the subcapsular space of the zona glomerulosa. In porcine and bovine adrenals, 17 alpha-hydroxylase immunoreactive cells were localized within the medulla. Single cortical cells and small accumulations of cells were spread throughout this region. At the ultrastructural level, the chromaffin cells located within the cortex in pig and rat adrenals formed close cellular contacts with cortical cells in all three zones. Our morphological data provide evidence for a possible paracrine role of chromaffin cells; this may be important for the neuroregulation of the adrenal cortex.

Adrenal Cortex↗
PubMed1994

Paracrine factor and cell-cell contact-mediated induction of protease and c-ets gene expression in malignant keratinocyte/dermal fibroblast cocultures.

The purpose of this study was to characterize stromal-epithelial interactions that result in induction of protease gene expression in squamous cell carcinoma of the skin. Coculture of the human squamous cell carcinoma cell line II4 with primary human foreskin fibroblasts was observed to induce mRNA expression of urokinase-type plasminogen activator (uPa), matrilysin, 92-kDa type IV collagenase, and c-ets, a transcriptional activator of several genes within the serine and matrix metalloprotease families. uPA and c-ets induction were localized to the fibroblast cell population. uPa induction was found to be dependent upon cell-cell contact with the tumor cell population, whereas c-ets induction was due to a combination of cell-cell contact and a tumor cell-derived soluble factor. In contrast, matrilysin induction localized to the tumor cells and was shown by Northern and Western analyses to occur in response to a fibroblast-derived soluble factor. These data demonstrate that both paracrine factors and cell-cell contact between stromal fibroblasts and epithelial tumor cells can influence protease gene expression.

Blotting, Western↗
PubMed1984

Influence of rat seminiferous tubules on Leydig cell testosterone production in vitro.

The interaction of seminiferous tubules and Leydig cells was investigated in the rat in vitro. Crude collagenase-dispersed, or Percoll-purified, Leydig cells were incubated together with seminiferous tubules at different stages of the cycle, isolated by transillumination-assisted microdissection. The testosterone production was measured. Seminiferous tubules inhibited testosterone production of crude Leydig cell preparations, but induced a clear stimulation (30-100%) in Percoll-purified cells. The stimulation was maximal at stages VII and VIII of the cycle, significantly higher than at stages II-VI (P less than 0.05). The stimulation by seminiferous tubules was observed both in basal and hCG-stimulated testosterone production. The effect was independent of FSH or GnRH action. These results demonstrate the presence of paracrine regulatory interaction between seminiferous tubules and Leydig cells, and are in agreement with the concept of a preferential androgen requirement of stages VII and VIII of the cycle.

Animals↗
PubMed1994

Simulation of the diffusion and reaction of endogenously produced nitric oxide.

In spite of intense recent investigation of the physiological and pathophysiological roles of endogenously produced nitric oxide (.NO) in mammalian systems, little quantitative information exists concerning the diffusion of this small nonelectrolyte from its source (NO synthase) to its targets of action. I present here a conceptual framework for analyzing the intracellular and intercellular diffusion and reaction of free .NO, using kinetic modeling and calculations of the diffusibility of .NO and its reactions in aqueous solution based on published data. If the half-life of .NO is greater than approximately 25 msec and the rates of reaction of .NO with its targets are slower than its diffusion or reaction with O2 (for which there is experimental evidence in at least some systems), then (i) .NO acts in vivo in a mostly paracrine fashion for a collection of .NO-producing cells, (ii) .NO diffuses to significant concentrations at distances relatively far removed from a single .NO-producing cell, and (iii) localized sites of vascularization will scavenge .NO (and thus decrease its actions) at distances many cell diameters away from that site. These conclusions have important implications with regard to the mechanism of endothelium-dependent relaxation, the autocrine vs. paracrine actions of .NO, and the role of the spatial relationship between specific sites of .NO formation and neighboring blood vessels in .NO-effected and -affected neuronal signal transmission.

Animals↗
PubMed1989

Role of colony-stimulating factors in the biology of acute myelogenous leukemia.

A high proportion of acute myeloid leukemias (AML) recently investigated for their capacity to synthesize biologically active bioregulatory molecules was found to accumulate messenger (m) RNA and to produce membrane-bound or -secreted forms of stimulating factors for granulocyte, macrophage and mixed granulocyte-macrophage colony growth. Blast cells have also been found to secrete interleukin 1, tumor necrosis factor-alpha, interleukin 6, and to express receptors for various growth factors as well. However, growth factors like interleukin 2 and interleukin 3 have not been identified as AML products, and several other factors including interleukin 4, interleukin 5, etc. need further evaluation. Responsiveness of clonogenic leukemic cells to exogenous growth-promoting factors in vitro suggests a possible role of these biomolecules in the course of these disorders. Important evidence for the crucial role of growth factors, at least in some subtypes of AML, has been provided by demonstrating constitutive growth factor production by leukemic cells and their autonomous in vitro growth which is dependent on autocrine secretion of a specific growth factor. The concert of mechanisms providing stimulatory and inhibitory signals for hematopoiesis, which is adapted to the various physiological requirements of the organism, may have multiple defects in AML. This leads to successive steps of malfunctioning of cells, which finally express a fully malignant phenotype. In addition, these derangements also lead to defects in accessory cells on the level of mediator communication. However, there is evidence for autonomous growth promotion of AML blast by constitutive production of growth factors active in an autocrine fashion (GM-CSF, G-CSF, interleukin 6) and by recruitment of accessory cells to increase CSF supply (GM-CSF, G-CSF) via molecules such as interleukin 1 and TNF-alpha in a paracrine fashion. Molecular analysis of transformed hematopoietic cells has revealed changes of the genome, e.g., insertion of viral genetic information or cytogenetic fractures at DNA sites controlling growth factor gene activation. These events appear to be crucial in the induction of uncontrolled growth factor expression promoting oncogenic transformation of hematopoietic progenitor cells.

Colony-Stimulating Factors↗