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PubMed1992

Induction of human microvascular endothelial tubular morphogenesis by human keratinocytes: involvement of transforming growth factor-alpha.

Transforming growth factor-alpha(TGF-alpha), homologous to epidermal growth factor(EGF), is closely involved in hyperproliferation of human keratinocytes. Psoriasis is a common hyperproliferative skin disease characterized by hyperproliferation of keratinocytes and abnormal development of dermal capillary networks. In this study, we have examined whether keratinocytes could enhance angiogenesis. TGF-alpha or EGF efficiently stimulated formation of tubular-like structures of human omental microvascular endothelial(HOME) cells in type I collagen gels. Human keratinocytes produced TGF-alpha. To examine whether co-cultured keratinocytes could induce tubulogenesis of HOME cells in collagen gel, we have developed a co-culture system with human keratinocytes. Surprisingly, there appeared new development of many tubular-like structures of HOME cells in collagen gels when co-cultured with keratinocytes. This keratinocytes-dependent tubulogenesis was almost completely blocked when anti-TGF-alpha-antibody was present. The TGF-alpha molecules derived from keratinocytes appeared to enhance tubulogenesis of human microvascular endothelial cells. We propose the hypothesis that secretory TGF-alpha from human keratinocytes may promote an autocrine loop to proliferate the skin keratinocytes and also a paracrine loop to induce the skin angiogenesis.

Blotting, Northern↗
PubMed1991

Factors regulating interaction between trophoblast and human endometrium.

Implantation is a crucial step in human reproduction. Disturbances of this process are responsible for pregnancy failure after both in vivo and in vitro fertilization. The endometrium provides the implanting embryo with a unique substratum where the embryo communicates with biochemical signals, attaches itself, penetrates and grows without blood circulation. The highly proliferative phase of the cytotrophoblast, during early human embryogenesis, may be due to endogenous production of growth factors that may establish autocrine/short range paracrine stimulator loops which explain the tumor-like properties of these tissues. Endometrial BM penetration and stroma invasion may be due to the proteolytic capability of the human embryo. It is suggested that collagenase and the urokinase-like plasminogen activator are responsible for this activity. To clarify the molecular mechanisms involved in human embryo implantation several models are suggested: culture of blastocysts, culture of endometrial cells, and endometrial explant co-culture. Human blastocysts cultured with whole perfused human uteri make it possible to recognize some aspects of the entire implantation process and give us the possibility of improving the benefits provided by new technologies in reproductive medicine and reducing embryonic loss at an early stage.

Endometrium↗
PubMed1994

[The metastatic process].

All the malignant tumors possess the same characteristic to form distant secondary tumors or metastasis. The acquisition of the metastatic potential takes place in random accumulation of different genetic and cellular changes. Their combination allows one or several tumor cells to achieve the whole metastatic process. The metastatic process involves numerous interactions between the tumor cells and the host cells of the tumor cells and the extracellular matrix. The attachment of the metastatic cells to the extracellular matrix specific glycoproteins involves cell surface receptors as integrins, sialyled residues or CD44. On the other hand, other adhesive molecules (Cadherins) display inhibitory action on the metastatic process. The enzymatic lysis is carried out by glycolytic enzymes and proteases: metalloproteases (inhibitors TIMP1 et TIMP2), serine proteases (tPA, uPA-inhibitors: PAI1 and PAI2). Cathepsin D or Heparanases. Several enzymes may be necessary for the degradation of the basal membrane. The crossing of both basal membrane and stroma can be made on account of the cell motility. Some factors can modify this property as AMF (Autocrin Motility Factor) or ATX (Autotoxin) but the molecular mechanisms involved in the migration are not yet completely understood. The last stage is relative to the cells proliferation in the site organ; it depends on autocrine (CSF1, IL2, Bombesine...) or some paracrine growth factors. However, the formation of metastasis is possible only in the site organ attaching the cells.

Animals↗
PubMed1994

The acute phase response: general aspects.

The acute phase response in a given individual represents the integrated sum of multiple, separately regulated changes. Although many of these changes commonly occur together in affected individuals, clinical experience indicates that not all of them occur in all individuals, indicating that they must be individually regulated. For example, febrile patients may have normal blood levels of CRP and vice versa, leukocytosis does not always accompany other acute phase phenomena, and many instances of discordance between levels of the various acute phase proteins are seen. Cytokines function as part of a complex regulatory network, a signalling language in which information is conveyed to cells by combinations, and perhaps sequence, of intercellular messenger molecules. The effects of combinations of cytokines are complex. To use a somewhat crude simile, individual cytokines can be thought of as words which bear informational content and which may, on occasion, communicate a complete message. More commonly, however, the actual messages received by cells probably resemble sentences, in which combinations and sequences of words convey information. Currently available data suggest that hepatocytes receive a complex mixture of humoral or paracrine signals during the acute phase response. These are integrated by multiple interacting signal transducing mechanisms to cause finely regulated changes in plasma protein synthesis. Regulation largely occurs by transcriptional control, but post-transcriptional mechanisms, including translational regulation, may also 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 plasma protein changes. Regulation of non-hepatocyte acute phase phenomena has not been delineated as thoroughly, but clearly involves a number of inflammation-associated cytokines.

Acute-Phase Proteins↗
PubMed1991

Regulation of growth by a nerve growth factor-like protein which modulates paracrine interactions between a neoplastic epithelial cell line and stromal cells of the human prostate.

Nerve growth factor-like substance(s) were identified in both conditioned media of a human prostatic tumor epithelial cell line (TSU-pr1) and a human prostatic stromal cell line (HPS) by Western blot analysis and bioassay of neurite outgrowth of PC12 cells. Nerve growth factor-beta (NGF) immunofluorescence was also localized to secretory vesicles in the cytoplasm of both the TSU-pr1 and HPS cells. Western blot of the TSU-pr1 and HPS cell-secreted protein identified an Mr 65,000 major protein which immunoreacted with murine NGF antibody. NGF Western blot of HPS cell-secreted protein also identified an Mr 42,000 minor band under reduced and nonreduced conditions and an Mr 61,000 minor band under reduced conditions. The secreted protein from the TSU-pr1 cells (50 micrograms/ml) and HPS (50 micrograms/ml), as well as murine NGF (50 ng/ml) or human recombinant NGF (50 ng/ml), stimulated neurite outgrowth from PC12 cells. This neurite outgrowth activity was partially inhibited by treatment with NGF antibody. Neither the serum containing growth medium nor bovine serum albumin (50 micrograms/ml) stimulated neurite outgrowth. The NGF-like secretory protein appeared to play a role in the paracrine regulation of prostatic growth between TSU-pr1 cells and HPS cells. The relative growth of TSU-pr1 cells, as indicated by [3H]thymidine incorporation, in response to HPS secretory protein was stimulated 2.8-fold in a dose-dependent manner. In the converse interaction, the relative growth of HPS cells in response to TSU-pr1 secretory protein was stimulated 1.8-fold in a dose-dependent manner. Immunoneutralization of TSU-pr1 and HPS secretory protein was performed with antibody against NGF, acidic fibroblast growth factor, and basic fibroblast growth factor. Removal of the NGF-like protein from the maximal stimulatory dose of TSU-pr1 secretory protein (100 micrograms/ml) with NGF antibody reduced HPS proliferation to 52% of maximal levels, and immunoneutralization of the NGF-like protein in the maximal stimulatory dose of HPS secretory protein (20 micrograms/ml) also reduced TSU-pr1 proliferation to 16% of maximal levels. Addition of normal rabbit serum or prior immunoprecipitation of either TSU-pr1 or HPS secretory protein with antibody against acidic fibroblast growth factor and basic fibroblast growth factor did not inhibit the proliferation of either cell type. These results suggest that TSU-pr1 tumor cells and HPS cells secrete NGF-like protein(s) which modulate their paracrine interactive growth in vitro.

Adrenal Gland Neoplasms↗
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↗
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↗
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↗
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↗