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PubMed2002

The initiation of follicle growth: the oocyte or the somatic cells?

The initiation of follicle growth is defined as the transition of primordial follicles from the quiescent to the growth phase. We have shown that follicle growth initiation consists of two distinct, consecutive phases. The first phase is characterized by the transformation of granulosa cells from flattened to cuboidal in shape and by their proliferation, this coincides with follistatin expression. During the second phase, an increase in the number of granulosa cells is accompanied by an increase in the size of the oocyte. Evidence from other species confirms this observation. It seems that a prerequisite for initiation of oocyte growth is the presence of cuboidal granulosa cells. The vast majority of bovine primordial follicles enter the first phase of growth when cultured in serum-free medium. Similar results have been obtained for human primordial follicles. Two proteins of oocyte origin, GDF9 and BMP15, play an essential role in granulosa cell proliferation beyond the primary stage. It can be speculated that the regulation of follicle growth initiation is a two-phase event: the first phase depends on locally produced inhibitory and stimulatory factor(s); in the second phase the follicle become an autonomous unit, whose further development depends on oocyte-produced GDF9/BMP15 and the kit ligand derived from granulosa cells.

Animals↗
PubMed2002

Connective tissue growth factor in the ovarian paracrine system.

The endocrine actions of follicle stimulating hormone and luteinising hormone on ovarian cells are transduced by locally produced paracrine factors that regulate the formation of extracellular matrix, proteolytic enzymes and protease inhibitors, which continuously remodel the parenchymal environment in which follicles develop. We recently identified connective tissue growth factor (CTGF) as a gene expressed during the predifferentiated stage of granulosa cell development in rat ovary. The CTGF gene encodes a protein that is implicated in the regulation of connective tissue synthesis, mototaxis, angiogenesis and cellular interaction with ECM at various sites in the body. Stimulation of granulosa cells by FSH in vitro and in vivo induces follicular maturation associated with down-regulation of granulosa cell CTGF mRNA expression. The gene remains expressed in cells of the innermost (antrally located) granulosa compartment up to and after the point of ovulation. Based on the inferred biological properties of CTGF protein and the spatiotemporal pattern of CTGF mRNA expression in the ovary, we postulate roles for ovarian CTGF during early stages of follicular development and after ovulation in the formation of the corpus luteum.

Animals↗
PubMed2002

Evidence that PACAP and GnRH down-regulate follicle-stimulating hormone-beta mRNA levels by stimulating follistatin gene expression: effects on folliculostellate cells, gonadotrophs and LbetaT2 gonadotroph cells.

Pituitary adenylate cyclase-activating polypeptide (PACAP) stimulates alpha-subunit transcription and lengthens LH-beta mRNA transcripts, but reduces FSH-beta mRNA levels in rat pituitary cell cultures. PACAP also stimulates follistatin transcription, an effect which may explain the decrease in FSH-beta mRNA. To begin to investigate the cells in which PACAP activates the follistatin gene, quantitative in situ hybridization for follistatin mRNA combined with immunostaining for LHbeta and S100 protein was performed. In control cultures, follistatin mRNA was expressed in 70% of gonadotrophs and in 47% of folliculostellate cells (S-100+). PACAP increased (P<0.001) both the number of follistatin-expressing cells as well as the number of grains per cell in both gonadotrophs and folliculostellate cells, while GnRH only affected (P=0.01) gonadotrophs. Follistatin and FSH-beta gene expression in rat pituitary cultures were also measured by competitive quantitative RT-PCR and northern analysis, respectively. Both PACAP and GnRH increased (P<0.05) follistatin gene expression and suppressed (P<0.05) FSH-beta mRNA, and the effect of PACAP together with GnRH on follistatin exceeded that of GnRH alone. PACAP regulation of follistatin and FSH-beta gene expression was studied further in LbetaT2 cells that were found to express receptors for the specific PACAP receptor, PAC(1). Follistatin mRNA was undetectable in cultures exposed to control media, or stimulated with PACAP, GnRH or rh-activin-A. In contrast to the results in primary pituitary cultures, PACAP increased FSH-beta mRNA in these follistatin-deficient cells. Moreover, using transient transfection, PACAP stimulated transcription of ovine-FSH-beta-luciferase. GnRH likewise increased FSH-beta mRNA and stimulated FSH-beta gene transcription in LbetaT2 cells. Activin-A increased FSH-beta gene expression dose-dependently, and activin induction of FSH-beta mRNA was blocked completely by 3-fold excess follistatin. These results indicate that PACAP stimulates follistatin gene expression in both gonadotrophs and folliculostellate cells, and provide further evidence that follistatin is required for PACAP or continuous GnRH to down-regulate FSH-beta mRNA. These experiments suggest a mechanism by which PACAP influences FSH production selectively by an autocrine effect on gonadotrophs and by a paracrine mechanism through folliculostellate cells that involves follistatin.

Activins↗
PubMed1997

Identification of neuropeptides in the midgut of parasitized insects: FLRFamides as candidate paracrines.

Parasitism of Manduca sexta (Lepidoptera: Sphingidae) larvae by the braconid wasp Cotesia congregata (Hymenoptera: Braconidae) leads to accumulation of peptides in host neurons and neurosecretory cells of the central nervous system (CNS) and neurons and endocrine/paracrine cells of the midgut. This accumulation has now facilitated the characterization of two new members of the FLRFamide family from midguts of parasitized larvae. The peptides, given the names F24 and F39, are 24 and 39 amino acids in length with the sequences VRDYPQLLDSGMKRQDVVHSFLRFamide and YAEAAGEQVPEYQALVRDYPQLLDSGMKRQDVVHSFLRFamide. The sequence of F24 is identical to the C-terminal 24 amino acids of F39. The C-terminal 10-mer of each is identical to a previously characterized decapeptide neurohormone (F10). This sequence is preceded by a potential processing site. In nonparasitized insects F39 was present at several-fold the amount of F24. In parasitized insects F24 and F39 accumulate in the middle and posterior regions of the midgut, which are enriched in endocrine/paracrine cells reacting with FLRFamide antisera. In the combined brain and subesophageal ganglion F39 was not detected and the amount of F24 never exceeded 2 fmol per Br/SEG. Of the three peptides, only F10 was found in the hemolymph. Thus, F24 and F39 may be intermediates in the biosynthesis of F10 and may themselves be released locally from endocrine/paracrine cells in the midgut epithelium.

Amino Acid Sequence↗
PubMed1999

Targeted ablation of gonadotrophs in transgenic mice affects embryonic development of lactotrophs.

Ablation of pituitary gonadotrophs was obtained in transgenic mice expressing diphtheria toxin A (DTA) under control of the -313/+48 bovine glycoprotein hormone alpha-subunit (alphaSU) promoter, previously shown to be active in mouse gonadotrophs but not in thyrotrophs. Development of hormone-producing cell types was assessed on the day of birth by computer-assisted image analysis on paraffin-embedded, immunostained pituitary sections. Six out of 50 transgenic F0 ('founder') mice (3 males and 3 females) showed a nearly complete disappearance of gonadotrophs but not of thyrotrophs. The number of lactotrophs and the relative area occupied by PRL-immunoreactivity were significantly reduced in the gonadotroph-depleted mice. The size of lactotroph clusters was smaller in the absence of gonadotrophs. The number and immunoreactive area of corticotrophs and somatotrophs, on the other hand, were not significantly affected by gonadotroph ablation. Based on the reported evidence that fetal ovaries do not produce steroid hormones as a result of lack of expression of at least three of the steroidogenic enzymes, P450scc, P450c17, and P450arom, the present observations can hardly be explained by a decline in estrogen levels due to gonadotroph ablation. Rather, the present data indicate that gonadotrophs directly stimulate the development of lactotrophs during fetal and early postnatal life, consistent with previous in vitro observations, and/or that gonadotrophs may share a cell-lineage relationship with a subpopulation of lactotrophs.

Animals↗
PubMed1999

Hormone regulation of chondrocyte differentiation and endochondral bone formation.

Endochondral bone formation, the formation of calcified bone on a cartilage scaffold, occurs during skeletal development, post natal growth and during bone remodelling and fracture repair. The epiphyseal growth plates represent classical tissues in which to study the ossification process, which requires two co-ordinated components; progressive chondrocyte differentiation and cartilage neovascularisation. Many gene knockout studies have produced new insights regarding how chondrocyte differentiation and angiogenesis are controlled at the molecular level. Additional genetic studies have produced new information regarding the role of hormones in the regulation of endochondral bone formation. The new challenge for the future is to determine how bone formation and turnover is physiologically regulated and co-ordinated to ensure that skeletal development and growth progresses correctly. This study reviews the emerging data in this quickly growing field which should ultimately provide fundamental insights into the normal control of endochondral ossification.

Animals↗
PubMed2000

Growth and paracrine factors regulating follicular formation and cellular function.

The purpose of this paper is to review, using fetal sheep as the animal model, aspects of ovarian development related to follicular formation and to report on the identity of growth and paracrine factors which might be involved in this process. Before follicular formation there is a massive and sustained colonisation of the fetal ovary by mesonephric cells, which become a precursor source of follicular cells. From within the ovarian medulla, somatic 'cell-streams' branch into the cortex around nests of oogonia and oocytes. These 'cell-streams', which contain elongated cells with either flattened or cuboidal shaped nuclei, express steroidogenic factor-1 (SF-1), steroid acute regulatory protein (StAR), 3beta-hydroxysteroid dehydrogenase (3beta-HSD), cytochrome P450(scc), and P450(aromatase) mRNA and/or protein. Follicles form from the association of an oocyte with the 'cell-stream' with either a single layer of flattened cells (i.e. type 1 follicle) or with a mixture of flattened and cuboidal cells (i.e. type 1a follicle). These newly-formed follicles have between 3 and 57 somatic cells (i.e. granulosa cells) and contain oocytes which vary in diameter between 23 and 52 microm. Newly formed and early growing follicles have been identified with growth factors or growth factor receptors in either the oocytes or granulosa cells. Many of the growth factors are from the TGFbeta superfamily and are expressed in a cell- and stage-specific manner.

Animals↗
PubMed1998

Paracrine production of nerve growth factor during rat dorsal root ganglion development.

Nerve growth factor is a target derived growth factor. In the peripheral nervous system, it is produced by tissues innervated by the sympathetic nervous system and small sensory neurons. In the present study, we tested the hypothesis that an alternate source of nerve growth factor must be available to support dorsal root ganglion neurons before they make connection with the target. Using reverse transcriptase polymerase chain reaction (RT-PCR), we detected nerve growth factor mRNA at embryonic day 12 to 17, but not in adult dorsal root ganglia. In situ hybridization studies revealed positive staining in satellite/supportive cells juxtaposed to dorsal root ganglion neurons. Our study suggests that nerve growth factor from supporting cells may have a paracrine function during development of primary sensory neurons.

Animals↗
PubMed2001

Interaction between paracrine tumor necrosis factor-alpha and paracrine angiotensin II during myocardial ischemia.

OBJECTIVES: The purpose of this study was to explore interactions between paracrine angiotensin II (Ang-II) and tumor necrosis factor-alpha (TNF-alpha) during myocardial ischemia. BACKGROUND: Ischemic myocardium releases significant amounts of TNF-alpha. This paracrine release correlated with postischemic myocardial injury. Other studies showed myocardial protection obtained by the use of angiotensin-converting enzyme inhibitors (i.e., captopril) and the Ang-II type 1 receptor antagonist losartan after ischemia. The possibility that these agents decrease TNF-alpha synthesis has not yet been investigated. METHODS: Using the modified Langendorff model, isolated rat hearts underwent either 90 min of nonischemic perfusion (control group) or 1 h of global cardioplegic ischemia. In both groups, either captopril (360 micromol/liter) or losartan (182.2 micromol/liter) was added before ischemia. The hearts were assayed for messenger ribonucleic acid (mRNA) expression and effluent TNF-alpha levels. In addition, cardiac myocytes were incubated in cell culture with Ang-II. RESULTS: After ischemia, TNF-alpha mRNA expression intensified from 0.63 +/- 0.06 (control group) to 0.92 +/- 0.12 (p < 0.03), and effluent TNF-alpha levels were 711 +/- 154 pg/ml. The TNF-alpha mRNA expression declined to 0.46 +/- 0.07 (p < 0.01) and 0.65 +/- 0.08 (p < 0.02) in captopril- and losartan-treated hearts, respectively. Effluent TNF-alpha was below detectable levels. Concentrations of TNF-alpha in supernatants of incubated cardiac myocytes treated with 10 and 50 nmol/liter of Ang-II were 206.0 +/- 47.0 pg/ml and 810 +/- 130 pg/ml, respectively (p < 0.004). When pretreated with 700 micromol/liter of losartan, TNF-alpha was below detectable levels. CONCLUSIONS: This study presents an original explanation for previously reported myocardial protection after ischemia, obtained by the use of captopril and losartan. These drugs reduce TNF-alpha synthesis, providing strong evidence of active interactions between paracrine TNF-alpha and Ang-II in the evolution of the ischemic cascade.

Angiotensin II↗
PubMed2000

Expression of insulin-like growth factor-I (IGF-I) and IGF-II in the avian brain: relationship of in situ hybridization patterns with IGF type 1 receptor expression.

Insulin-like growth factors (IGFs) are expressed in defined spatiotemporal patterns during the development of the mammalian central nervous system (CNS). Since IGF expression in avian species is less well documented, we studied here the expression of IGF-I and IGF-II during chicken CNS development, using in situ hybridization and reverse transcriptase-PCR, and compared the results with the expression of the IGF type 1 receptor (IGF-1R). IGF-II expression started early in embryonic life, shortly after the onset of IGF-1R expression. During organogenesis, IGF-II was strongly expressed in kidney, liver and gut primordia, in contrast with IGF-1R mRNA, which is highly enriched in proliferating neuroepithelia. During the second half of embryonic development, IGF-I and IGF-II had distinct expression patterns, suggesting specific roles for each ligand during brain maturation. IGF-II mRNA was found in numerous brainstem nuclei and in the optic tectum, whereas IGF-I mRNA was found predominantly in telencephalic regions. Both ligands were expressed in the cerebellum, but each by different cell layers. Some brain regions (olfactory bulb and olivo-cerebellar system) did not exhibit the postnatal downregulation typical of extrahepatic IGF-I expression, but continued to express IGF-I into adulthood. Purkinje cells expressed IGF-II in the embryo, but switched to IGF-I expression in the adult. The conservation of embryonic and postnatal IGF expression patterns in the CNS between avians and mammals suggests that the involvement of the IGF system in neurogenesis and differentiation, and possibly in neural plasticity and learning, may have arisen early during tetrapode/vertebrate evolution.

Age Factors↗
PubMed2003

Paracrine secretion of transforming growth factor-beta1 in aneurysm healing and stabilization with endovascular smooth muscle cell therapy.

BACKGROUND: Identification of molecular factors involved in artery wall stabilization after extracellular matrix injury elicited by inflammation and proteolysis has a major role in the development of new therapies for atherosclerosis. A study from our group demonstrated that endovascular seeding of vascular smooth muscle cells (VSMCs) promotes healing and stabilizes experimental aneurysms by downregulating matrix metalloproteinase and upregulating tissue inhibitor of metalloproteinase and collagen gene expression. We analyzed expression of transforming growth factor-beta (TGF-beta) and its receptors in experimental aneurysms treated with endovascular VSMC therapy. METHODS AND RESULTS: Aneurysms were generated in Fischer 344 rats by 14-day orthotopic implantation of a segment of guinea pig abdominal aorta (xenograft). During an endovascular repeat operation, syngeneic VSMCs were seeded in the aneurysm, always resulting in aneurysm diameter stabilization after 8 weeks, whereas diameter of control aneurysms infused with culture medium further increased. Seven days after repeat operation the intima or thrombus was separated from the aneurysmal wall in the two groups. Reverse transcriptase polymerase chain reaction with the domestic gene 18s as a standard demonstrated that aneurysm stabilization was associated with a statistically significant increase in TGF-beta(1), but not TGF-beta(2) or TGF-beta(3), messenger RNA levels in the intima. Enzyme-linked immunosorbent assay demonstrated increased TGF-beta(1) protein in the aneurysmal wall. mRNA levels of the two serine and threonine kinase TGF-beta receptors remained unchanged. CONCLUSIONS: Healing and stabilization of aneurysms with endovascular cell therapy is associated with a specific pattern of gene expression, resulting in paracrine secretion of TGF-beta(1). Our study provides insight into the molecular mechanisms of arterial aneurysm healing and stabilization.

Animals↗
PubMed1998

Growth hormone: a paracrine growth factor in embryonic development?

Although pituitary growth hormone is obligatory for normal postnatal growth and development, early embryonic and fetal growth is generally considered to be independent of pituitary GH. Indeed, in chickens, somatotrophs and serum GH are not detectable until late in embryogenesis, and neither partial decapitation nor pre-hatch GH administration greatly affects embryonic growth. However, since it is now known that GH can be produced and act in many extra-pituitary tissues, early embryonic growth may be independent of pituitary GH but dependent upon the paracrine actions of extra-pituitary GH. The possibility that growth hormone may be a paracrine growth factor during early development will therefore be considered in this brief review, which is based on the embryogenesis of the domestic fowl.

Animals↗
PubMed2001

Top-DER- and Dpp-dependent requirements for the Drosophila fos/kayak gene in follicular epithelium morphogenesis.

The Drosophila fos (Dfos)/kayak gene has been previously identified as a key regulator of epithelial cell morphogenesis during dorsal closure of the embryo and fusion of the adult thorax. We show here that it is also required for two morphogenetic movements of the follicular epithelium during oogenesis. Firstly, it is necessary for the proper posteriorward migration of main body follicle cells during stage 9. Secondly, it controls, from stage 11 onwards, the morphogenetic reorganization of the follicle cells that are committed to secrete the respiratory appendages. We demonstrate that DER pathway activation and a critical level of Dpp/TGFbeta signalling are required to pattern a high level of transcription of Dfos at the anterior and dorsal edges of the two groups of cells that will give rise to the respiratory appendages. In addition, we provide evidence that, within the dorsal-anterior territory, the level of paracrine Dpp/TGFbeta signalling controls the commitment of follicle cells towards either an operculum or an appendage secretion fate. Finally, we show that Dfos is required in follicle cells for the dumping of the nurse cell cytoplasm into the oocyte and the subsequent apoptosis of nurse cells. This suggests that in somatic follicle cells, Dfos controls the expression of one or several factors that are necessary for these processes in underlying germinal nurse cells.

Animals↗
PubMed1999

Repression by Notch is required before Wingless signalling during muscle progenitor cell development in Drosophila.

The larval muscles of Drosophila arise from the fusion of muscle founder cells, which give each individual muscle its identity, with myoblasts (reviewed in [1]). Muscle founder cells arise from the asymmetric division of muscle progenitor cells, each of which develops from a group of cells in the somatic mesoderm that express lethal of scute [2]. All the cells in a cluster can potentially form muscle progenitors, but owing to lateral inhibition, only one or two develop as such [2] [3] [4] [5]. Muscle progenitors, and the subsequent founder cells, then express transcription factors such as Krüppel, S59 and Even-skipped, which confer identity on the muscle [6] [7] [8]. Definition of some muscle progenitors, including three groups that express S59, depends on Wingless signalling [9]. Lateral inhibition requires Delta signalling through Notch and the transcription factor Suppressor of Hairless [3] [4] [5]. As the Wingless and lateral-inhibition signals are sequential [8], one might expect that muscle progenitors would fail to develop in the absence of Wingless signalling, regardless of the presence or absence of lateral-inhibition signalling. Here, we examine the development of the S59-expressing muscle progenitor cells in mutant backgrounds in which both Wingless signalling and lateral inhibition are disrupted. We show that progenitor cells failed to develop when both these processes were disrupted. Our analysis also reveals a repressive function of Notch, required before or concurrently with Wingless signalling, which is unrelated to its role in lateral inhibition.

Animals↗
PubMed2001

Paracrine regulation of keratinocyte proliferation and differentiation.

The histoarchitecture and function of the epidermis depend on a well-controlled balance between keratinocyte proliferation and differentiation. This balance is perturbed after skin injury, and imbalance is a characteristic feature of major human skin diseases such as psoriasis and epidermal cancers. Recent studies have highlighted the importance of fibroblast-derived soluble factors for the regulation of keratinocyte proliferation and differentiation. Therefore, identification of these paracrine-acting factors and the elucidation of their mechanisms of action are necessary for understanding epidermal homeostasis, repair and disease, and these approaches will offer new potential targets for drug therapy. Here, we review exciting recent findings on the identification, regulation and function of paracrine-acting cytokines in the skin. In particular, we describe the role of fibroblast-derived mitogens as regulators of keratinocyte proliferation and differentiation, and we summarize the regulation of these factors by keratinocyte-derived interleukin 1 that involves the transcription factors c-Jun and JunB.

Animals↗
PubMed2003

Histamine in the control of gastric acid secretion: a topic review.

In this paper, the current knowledge about the role of histamine in the control of gastric acid secretion is reviewed. In particular, we focus this topic into three sections considering the recent insights on: histamine receptor subtypes involved in gastric acid secretion, the interplay between neuronal-hormonal-paracrine pathways and the cerebral histaminergic control of gastric secretion. From the careful perusal of scientific literature, the fundamental role of histamine as local stimulator of gastric acid secretion via H(2) receptors is fairly confirmed while for the H(3) receptor only a minor modulating role is hypothesized. An undisputed function of ECL cells as controllable source of histamine within the so-called gastrin-ECL cell-parietal cell axis is generally proposed and the intriguing possibility of a remote control of gastric secretion via H(3) receptors is also suggested.

Acetylcholine↗
PubMed2001

Plasma and pericardial fluid natriuretic peptide levels in postinfarction ventricular dysfunction.

AIMS: In the present study we examined plasma and pericardial fluid ANP and BNP concentrations in postinfarction ventricular dysfunction. The association of peptide levels to left ventricular (LV) dysfunction and to the localization of the myocardial infarction (MI) was studied. METHODS AND RESULTS: Plasma and pericardial fluid samples were obtained from 37 patients undergoing coronary bypass surgery. According to the ECG and preceding coronary angiography, the patients were divided into three groups: previous anterior myocardial infarction (MI) (n=12), previous inferior/posterior MI (n=15) and no history of MI (n=10). When compared to the control group with no MI, the patients with anterior MI had elevated plasma ANP and BNP (134+/-13 vs. 81+/-15 pg/ml, P<0.01 and 95+/-10 pg/ml vs. 26+/-8 pg/ml, P<0.01, respectively) and pericardial fluid BNP (473+/-60 pg/ml vs. 57+/-8 pg/ml, P<0.001) levels. The plasma natriuretic peptide concentrations were not increased in the patients with inferior/posterior MI, but the pericardial fluid BNP concentrations were greater than in the patients with no history of MI (129+/-35 pg/ml vs. 57+/-8 pg/ml, P<0.05). Six of the 12 patients with previous anterior MI had LVEF> or =45%. Despite their normal LV systolic function, these patients had increased plasma and pericardial fluid BNP levels when compared to the group with no history of MI (68+/-18 pg/ml vs. 26+/-8 pg/ml, P<0.05 and 534+/-258 pg/ml vs. 57+/-8 pg/ml, P<0.01, respectively). CONCLUSIONS: Previous anterior myocardial infarction was associated with increased cardiac BNP production even if the LV systolic function was normal (LVEF> or =45%). The high pericardial fluid BNP concentrations in postinfarction patients suggest that the BNP synthesis and release are augmented in the ventricular myocardium independent from the LVEF.

Adult↗
PubMed2003

Paracrine relationships between adipose and lymphoid tissues: implications for the mechanism of HIV-associated adipose redistribution syndrome.

The adipocytes anatomically associated with lymph nodes and omental milky spots have site-specific properties that equip them to interact locally with lymphoid cells. Paracine provisioning of peripheral immune responses improves their efficiency and emancipates activated lymphocytes from competition with other tissues for blood-borne nutrients. Prolonged disruption to such paracine interactions might contribute to the HIV-associated adipose redistribution syndrome, causing selective hypertrophy of the mesentery, omentum and other lymphoid tissue-containing adipose depots, while nodeless depots atrophy.

Adipose Tissue↗