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At least 865 records · Page 48Linked to original sources
PubMed1999

Prolactin is an autocrine or paracrine growth factor for human myometrial and leiomyoma cells.

OBJECTIVE: To test the hypothesis that prolactin (PRL) acts as a mitogenic growth factor for human leiomyoma and myometrial cells. METHODS: To test this hypothesis, we performed three different types of experiments. First, we assessed whether exogenous PRL acted as a mitogen for cultured uterine smooth muscle cells. Second, we examined the role of endogenous PRL by assessing the cell number after exposure of the cultures to a neutralizing antibody to PRL. Finally, we examined both fresh tissues and cultured cells for expression of the PRL receptor messenger ribonucleic acid using the techniques of reverse-transcriptase polymerase chain reaction and Southern blotting. RESULTS: A significant suppression in cell number was seen after 5 days of culture for leiomyoma cells but not for myometrial cells after treatment with exogenous PRL. Both cell types showed a significant decrease in cell number after treatment with anti-PRL antibody. A 893-bp segment consistent with the cytoplasmic domain of the long form of the PRL receptor was amplified from both fresh and cultured tissues and confirmed by Southern blotting and sequencing. CONCLUSIONS: PRL appears to be an autocrine or paracrine growth factor for both leiomyoma and myometrial cells. However, there are some differences between tissues in their sensitivity to this growth factor.

Antibodies↗
PubMedDate not supplied

Mechanisms and pharmacologic control of basophil-derived IL-4 and IL-13.

Human basophils represent a major source of interleukin (IL) 4 and 13 protein, cytokines which share several biological activities central to the pathogenesis of allergic inflammation. Studies show that the production of these cytokines differs with respect to mode of activation and the time course of their secretion. Pharmacologic evidence indicates that IL-4 generation, which is most prominent with IgE-dependent activation, is mediated through a calcineurin-dependent pathway. In contrast, multiple pathways seem evident in the regulation of IL-13 in basophils.

Autocrine Communication↗
PubMedDate not supplied

Novel autocrine and paracrine loops of the stem cell factor/chymase network.

BACKGROUND: The aim of this study was to investigate whether the secretory granules of human mast cells store stem cell factor (SCF). We also addressed the question whether mast cell chymase, a chymotrypsin-like protease, also present in the secretory granules of human mast cells cleaves SCF at the peptide bound between Phe 158 and Met159. METHODS: The skin samples were obtained from patients with mastocytosis, undergoing skin biopsy for diagnostic purposes. Mast cells were isolated and purified from human lung parenchyma (human lung mast cells, HLMC) by countercurrent elutriation followed by discontinuous Percoll density gradient. SCF contents of human mast cells were assessed for immunoreactive SCF by ELISA. Western blot analysis of SCF and its cleavage products were performed with the MoAb anti-SCF 7H6. SCF and its proteolytic fragment were characterized by electrospray mass spectrometry (ES/MS). RESULTS: SCF is present in the secretory granules of human skin and lung mast cells. Immunoreactive SCF (iSCF) was detected in the cell lysates of HLMC, but not in basophils. iSCF was rapidly (3 min) released after challenge with anti-IgE, and iSCF in supernatants rapidly declined after 30 min. ES/MS analysis of rhSCF1-166 treated with recombinant human chymase showed a polypeptide of 17,977.1+/-0.6 Da and a minor component of 697.4+/-0.1 Da generated by specific cleavage at Phe159. SCF1-166 and SCF1-159 similarly activated HLMC and potentiated anti-IgE-induced activation of these cells. The cleavage product SCF160-166 had no effect on mast cells. Western blot analysis of supernatants of anti-IgE activated HLMC incubated for various intervals with rhSCF1-166 showed that rhSCF1-166 was converted to a faster-migrating form with a molecular weight compatible with SCF1-159 and to several SCF species. CONCLUSION: SCF is stored in human mast cell secretory granules and is immunologically released by mast cells. SCF1-166 is rapidly cleaved by chymase and other proteases to several SCF species.

Autocrine Communication↗
PubMed2000

Characterization of the promoter-directing expression of growth hormone in a monocyte cell line.

Previous work from our laboratory has shown that cells of the immune system produce a growth hormone (GH) molecule similar to that produced by the pituitary. In the present study, using Southern analysis of RT-PCR products and sequencing of cloned cDNA molecules, we demonstrate that lymphoid cell lines utilize the same promoter and first exon as the pituitary somatotrope. To identify the cis-elements involved in transcriptional regulation of immune cell-derived GH, we have coupled rat GH promoter fragments to a luciferase reporter gene and transfected a monocyte cell line (P-388) by electroporation. The results suggest the presence of both positive (-299/-193 bp) and negative (-193/-107 bp) regulatory elements. The same constructs transfected in the pituitary cell line, GH3, in contrast to the monocyte cell line, showed a gradual decrease in luciferase expression. The overexpression of GHF-1 or GHF-2 resulted in a modest but significant reduction in rat GH promoter activity in the P-388 cell line. Taken together, the data suggest that immune cells utilize the same first exon and promoter sequence for the expression of monocyte GH as that reported for the expression of pituitary GH. Further, it appears that sequences between -299 and -107 bp are important in the regulation of the promoter where different transcription factors may be recruited to promote GH expression in a monocyte cell line.

Animals↗
PubMed2002

Autocrine production and synergistic growth-promoting activity of interleukin-6 and oncostatin M in a new human myeloma cell line TU-1.

Human myeloma cell lines are difficult to establish, and they usually originate from patients with extramedullary disease. We describe a new human myeloma cell line, TU-1, which was established from the bone marrow of a patient without extramedullary myeloma. The myeloma cells were initially maintained in a conditioned medium derived from another well-known myeloma cell line U-266. This conditioned medium contained interleukin-6 (IL-6) and oncostatin M (OSM), and possibly other unknown growth factors as well. In 3 months the TU-1 cell line proliferated autonomously and secreted IL-6 and OSM with a synergistic growth response. As we have previously shown the cell line acquired a p53 mutation in vitro, which may be an important factor causing autonomous proliferation. In patients with multiple myeloma OSM is frequently found in the serum and OSM has been associated with serum IL-6 and progressive disease. Our study demonstrates the close relationship of OSM and IL-6 also in vitro.

Autocrine Communication↗
PubMed2002

Direct visualization of internalization and intracellular trafficking of dopamine-releasing protein-36aa.

Dopamine-releasing protein (DARP) is a potent regulator of dopamine (DA) release known to be involved in the development of rat catecholaminergic systems. In the present study, we examined the internalization and transport of DARP-36aa, a synthetic peptide derived from the N-terminal sequence of DARP, in rat C6 glioma cells. A colloidal gold DARP-36aa conjugate (DARP-36aa: AU) and biotinylated DARP-36aa were employed to visualize internalization and intracellular transport of DARP-36aa. Electron microscopy demonstrated that DARP-36aa: AU was rapidly incorporated into C6 glioma cells. Internalization via clathrin-coated pits and vesicles was clearly observed followed by transport and sorting of DARP-36aa: AU into multivesicular bodies, tubulo-vesicular endosomes, and lysosomes. Internalization of DARP-36aa: AU was also examined in primary mesencephalic cell cultures where a similar pattern of internalization and transport via clathrin-coated pits and vesicles was observed. Fluorescence microscopy using a biotinylated DARP-36aa/avidin-rhodamine conjugate revealed that DARP-36aa is diffusely distributed on the plasmalemma prior to internalization at 4 degrees C. Following a 30-min incubation at 37 degrees C DARP-36aa was concentrated in the cytosol, particularly in areas surrounding cellular projections and the perikaryon. Immunocytochemical studies employing biotinylated DARP-36aa and an anti-clathrin heavy chain antibody demonstrated that DARP-36aa and clathrin colocalize during DARP-36aa internalization. We also observed a marked increase in tyrosine phosphorylation of a 45-kD protein in response to DARP-33a stimulation in C6 glioma cells. Genistein, a specific tyrosine kinase inhibitor, significantly inhibited DARP-36aa: AU internalization and transport in C6 glioma cells. These findings suggest that tyrosine kinase activity may result in DARP-36aa receptor-mediated endocytosis.

Amino Acid Sequence↗
PubMed1998

Dopamine produced by the stomach may act as a paracrine/autocrine hormone in the rat.

Dopamine (DA) has been suggested to be a protective factor in the gastrointestinal tract but neither a source of DA nor its exact targets of action have been identified. In this study, we demonstrate high levels of DA (and DOPA) which persist after chemical sympathectomy in the gastric juice of rats. Immunostaining and in situ hybridization histochemistry reveal the presence of tyrosine hydroxylase (TH), DA transporter and vesicular monamine transporters in the acid-producing parietal cells. Like DA, TH enzyme activity remains after chemical sympathectomy. We also demonstrate active reuptake and storage of DA that indicates a regulated release of this neurohormone from parietal cells. DA D1b receptor mRNA is the most abundant DA receptor subtype in gastric and duodenal epithelium. Therefore, we suggest that selective DA D1b receptor agonists may be useful adjuncts in the treatment of duodenal and gastric ulcers. Gastric epithelia possess the hallmarks of functional DA neuroendocrine cells, suggesting that DA has an important role in self-protective mechanisms of the gastrointestinal tract. These findings should allow elucidation of DA role in normal and disease states in the stomach and duodenum.

Animals↗
PubMed1998

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

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

Adrenocorticotropic Hormone↗
PubMed2001

Stimulation of porcine pituitary luteinizing hormone release by galanin: putative auto/paracrine regulation.

It has repeatedly been suggested that galanin acts within the anterior pituitary (AP) in an auto/paracrine manner to modulate luteinizing hormone (LH) release. Except for one recent report in the rat, evidence for this notion is absent. The purpose of this study was to investigate in the pig the effects of galanin on LH and growth hormone (GH) release and to evaluate putative local effects using various AP culture systems (monolayer, perifusion, reaggregates). Independent of age galanin dose dependently (0.05, 0.2, 1 microM) stimulated basal but not gonadotropin-releasing hormone (GnRH; > or =0.01 nM)-induced LH release. Neither basal nor GH-releasing hormone (GHRH)-stimulated GH release was affected at any age. Of 4 galanin receptor antagonists (0.2, 1 microM) tested C7 proved to have agonistic effects, whereas M40 and M15 (galantide) were ineffective in blocking galanin (0.2 microM)-induced LH secretion or affecting basal or GnRH-induced LH release. M32 [galanin (1-13) NPY (25-36) amide] inhibited (p < or = 0.05) GnRH-induced LH release at doses of > or =2 microM, an effect which could be totally compensated by 1 microM galanin. However, the neuropeptide (NPY) antagonist BIBP 3226 (1 microM) partially overcame the effect of M32 (M32 is known to also bind to NPY receptors and NPY is inhibitory in the pig). In further studies using APs from preovulatory gilts a specific well-characterized galanin antiserum diluted 1:20 or 1:50 attenuated GnRH-induced LH release (p < or = 0.05). However, an NPY antiserum (also affinity purified and at the same dilution) used as control unexpectedly inhibited GnRH (and galanin)-induced LH release as well, thus suggesting that attenuation of GnRH-induced LH release by galanin antiserum might be at least partly nonspecific. Furthermore 96-hour exposure of AP reaggregates to two types of porcine preprogalanin antisense oligodeoxynucleotides neither affected basal nor GnRH-induced LH release. In line with the failure to unequivocally prove paracrine effects of galanin, concentrations of galanin in AP cultures and AP culture medium were very low (< or =2 pg galanin/10(5) AP cells). In conclusion the present study provides some evidence to ascribe a hypophysiotropic role to galanin in regulating LH but not GH secretion in the pig. The study also points to the critical role of appropriate controls when trying to prove auto/paracrine control mechanisms within the anterior pituitary. Our findings do not provide convincing evidence to support the notion that intrapituitary galanin is involved in the fine tuning of LH secretion, at least in the preovulatory pig.

Animals↗
PubMed1999

Can an autocrine loop explain sex-hormone-dependent tumor growth? A brief overview.

Sex hormones and their related compounds have been known to regulate the target cell growth positively or negatively in the receptor-dependent manner. The molecular mechanism of these complicated events, especially sex hormone-dependent growth enhancement, has been studied extensively. In MCF-7 cells, estrogen-induced autocrine loop has been demonstrated to play the important role for estrogen-dependent growth. Androgen has been also found to promote the growth of SC-3 cell through the induction of an autocrine growth factor (FGF 8). The blockade of FGF 8 activity resulted in a complete inhibition of androgen-dependent growth of SC-3 cells, suggesting that FGF 8 acts as an essential component of androgen-dependent growth. However, the constitutional expression of FGF 8 failed to convert SC-3 cells from an androgen-dependent to an androgen-independent phenotype. These observations would suggest that sex hormone-induced autocrine loop is an obligatory but not sufficient component for the growth of sex hormone-dependent tumor.

Androgens↗
PubMed1999

Aromatase and intracrinology of estrogen in hormone-dependent tumors.

Aromatase (estrogen synthetase) has been shown to occur in various extragonadal tissues as well as gonadal tissues, to be tissue-specifically regulated by various factors, and to play important roles in physiological functions in various tissues. The human gene is revealed to contain multiple variants of exon 1 which are tissue-specifically selected. Each exon 1 is flanked with a unique promoter region, which may explain tissue-specific transcription. All results strongly support an idea of intracrinology of estrogen. The validity of this concept is verified in connection with plasma levels of various steroid hormones and association constants of aromatase and estrogen receptor. 17beta-Estradiol is locally produced through several metabolic pathways. In this context, aromatase, steroid sulfatase, estrogen sulfotransferase, and 17beta-hydroxysteroid dehydrogenases I and II are considered to be important factors in the development of hormone-dependent tumors.

17-Hydroxysteroid Dehydrogenases↗
PubMed2002

An autocrine role for pituitary GABA: activation of GABA-B receptors and regulation of growth hormone levels.

There is increasing evidence suggesting that the neurotransmitter gamma-aminobutyric acid (GABA) is a local factor involved in the regulation of endocrine organs. Examples of such functions are documented in the pancreas, but recent results suggest that GABA may act in a similar way in the pituitary, in which GABA receptors are expressed and pituitary growth hormone (GH) cells provide a source of GABA. We hypothesised that GABA secreted in somatotropes may act as an autoregulatory signaling molecule. To test this hypothesis we first examined the nature of GABA receptors expressed by GH cells. RT-PCR analysis demonstrated that GABA-B receptor subunits R1 and R2 are present in the whole rat pituitary. Laser microdissection of immunostained GH cells, followed by RT-PCR as well as immunoelectron microscopy, showed that GABA-B receptors are expressed on somatotropes. To investigate GABA-B receptor function in somatotropes, we used rat GH3 adenoma cells, which, like pituitary GH cells, express GABA-B R1 and R2 (as assessed by RT-PCR and immunoelectron microscopy) and produce GABA (checked by high performance liquid chromatography). After inhibition of endogenous GABA synthesis, GH production was stimulated by baclofen, a chromatography). After inhibition of endogenous GABA synthesis, GH production was stimulated by baclofen, a GABA-B receptor agonist. By contrast, blocking GABA-B receptors by an antagonist, phaclofen, decreased GH levels. We conclude that in GH-producing cells, GABA acts as an autocrine factor via GABA-B receptors to control GH levels.

Animals↗
PubMedDate not supplied

Autocrine stimulation by insulin-like growth factor I is involved in the growth, tumorigenicity and chemoresistance of human esophageal carcinoma cells.

Insulin-like growth factor I (IGF-I) receptor (IGF-IR)-mediated signals are known to be involved in cell growth and transformation and prevention of apoptosis. In this study, we demonstrated the coexpression of IGF-I and IGF-IR in human esophageal carcinoma tissues. We also demonstrated the IGF-I autocrine system in esophageal carcinoma cell lines. Both the CE48T/VGH and CE81T/VGH cell lines showed proliferative responses to IGF-I stimulation. Autokinase activity of IGF-IR in these cells can be triggered by the exogenous addition of IGF-I. In addition, an IGF-I peptide antagonist, JB1, specifically inhibited ligand-induced receptor autophosphorylation in a dose-dependent manner. Under serum-free conditions, JB1 also reduced the degree of IGF-IR phosphorylation and cell numbers. Furthermore, the addition of JB1 decreased the number of CE81T/VGH colonies formed in methyl cellulose agar and the size and the incidence of tumors which grew in mice with severe combined immunodeficiency. These results imply that an IGF-I autocrine system in human esophageal carcinoma cells could stimulate tumor growth. Finally, we found that IGF-I prevented the apoptosis of CE81T/VGH cells induced by chemotherapeutic drugs, such as cisplatin, 5-fluorouracil and camptothecin. Thus, interruption of IGF-IR function may provide a way to retard tumor growth and increase the sensitivity of esophageal carcinoma to chemotherapy.

Animals↗
PubMed2002

Mechanisms sensing and modulating signals arising from cell swelling.

Cell volume alterations are involved in numerous cellular events like epithelial transport, metabolic processes, hormone secretion, cell migration, proliferation and apoptosis. Above all it is a need for every cell to counteract osmotic cell swelling in order to avoid cell damage. The defence against excess cell swelling is accomplished by a reduction of the intracellular osmolarity by release of organic- or inorganic osmolytes from the cell or by synthesis of osmotically less active macromolecules from their specific subunits. De-spite the large amount of experimental data that has accumulated, the intracellular mechanisms underlying the sensing of cell volume perturbations and the activation of volume compensatory processes, commonly summarized as regulatory volume decrease (RVD), are still only partly revealed. Moving into this field opens a complex scenario of molecular rearrangements and interactions involving intracellular messengers such as calcium, phosphoinositides and inositolphosphates as well as phosphoryla-tion/dephosphorylation processes and cytoskeletal reorganization with marked cell type- and tissue specific variations. Even in one and the same cell type significant differences regarding the activated pathways during RVD may be evident. This makes it virtually im-possible to unambigously define common sensing- and sinaling pathways used by differ-ent cells to readjust their celll volume, even if all these pathways converge to the activa-tion of comparatively few sets of effectors serving for osmolyte extrusion, including ion channels and transporters. This review is aimed at providing an insight into the manifold cellular mechanisms and alterations occuring during cell swelling and RVD.

Animals↗
PubMed2004

Stimulation of NHE3 in OKP cells by an autocrine mechanism.

BACKGROUND/AIMS: Chronic hypokalemia increases NHE3 activity in OKP cells. The aim of the present study was to determine whether an autocrine mechanism is involved in this activation. METHODS: After incubation of OKP cells in normal-K(+) and low-K(+) media for 24 h, the potassium concentration in the low-K(+) media was adjusted to a normal level. These conditioned media were then used as the normal-K(+) and low-K(+) supernatants. Other OKP cells were incubated in these normal-K(+) and low-K(+) supernatants and the mechanism of Na(+)/H(+) antiporter activation was examined. RESULTS: The EIPA-resistant Na(+)/H(+) antiporter activity of OKP cells increased after 4 h incubation in the low-K(+) supernatant, and the amount of NHE3 protein increased at 24 h. Since both BQ788 and saralasin blocked this antiporter activation, the supernatant concentration of endothelin I (ET-I) and angiotensin II (Ang-II) were measured. The ET-I concentration was reduced, but the Ang-II concentration remained unchanged. There was a significant association between a reduction in the ET-I concentration and an increase in Na(+)/H(+) antiporter activity, but only when Ang-II was present in the supernatant. CONCLUSION: An autocrine mechanism is involved in the activation of NHE3 in OKP cells. Both ET-I and Ang-II play a role in this activation.

Acidosis↗
PubMed2004

Neonatal capsaicin treatment affects rat thymocyte proliferation and cell death by modulating substance P and neurokinin-1 receptor expression.

Herein we provide evidence that substance P (SP) and its neurokinin-1 receptor (NK-1R) expressed on thymocytes counteract thymus depletion induced by neonatal capsaicin (CPS) treatment by affecting thymocyte proliferation and apoptotic death. SP administration reversed the CPS-mediated inhibitory effects on the total thymocyte number and subset distribution, namely CD4+ and CD4- CD8- cells, through its interaction with NK-1R as shown by concomitant NK-1R (SR140333) antagonist administration. SP-induced enhancement of thymus cellularity parallels its ability of inhibiting the thymocyte apoptotic program. Indeed, exogenously administered SP completely nullified CPS-induced apoptosis, and SR140333 abrogated the SP-mediated protective effect. SP administration also stimulated concanavalin A (Con A)-induced thymocyte proliferation of CPS-treated rats, completely reversing the CPS-induced inhibition. The SP-mediated stimulation of Con A-induced thymocyte proliferation was NK-1R dependent as shown by concomitant administration of SP and SR140333 to CPS-treated rats. Our results also demonstrate that CPS treatment induces a marked decrease of thymocyte PPT-A mRNA level and endogenous SP content as evaluated by quantitative RT-PCR, in situ hybridization and cytofluorimetric analysis. By contrast, NK-1R mRNA levels were increased in thymocytes from CPS-treated rats. Exogenous SP administration augmented PPT-A, SP and NK-1R thymocyte expression in CPS-treated rats, and this enhancement was antagonized by SR140333 administration. Overall, our results strongly suggest that the immunomodulatory effects of neonatal CPS treatment on rat thymocyte functions are dependent on vanilloid-mediated regulation of SP and NK-1R functional expression by neuronal and immune cells.

Adjuvants, Immunologic↗
PubMed2005

The Viscum album extract Iscador P does not cause an autocrine interleukin-6 loop in B-Non-Hodgkin's Lymphoma cell lines.

BACKGROUND: Single cases of clinical observations suggest the efficacy of the Viscum album (VA) extract Iscador P in the treatment of follicular B-Non-Hodgkin's Lymphoma (B-NHL). A previously published study aroused a controversial dispute as it indicated that IL-6 serum levels are elevated following i.v. VA treatment. Increased IL-6 levels have been shown to promote the progression of B-cell neoplasia such as B-NHL. Objective of this study was to investigate whether the VA extract influences the expression of IL-6 and its receptor components in follicular B-NHL cell lines. METHODS: Follicular B-NHL cell lines (WSU-NHL, DoHH-2) were incubated with clinically relevant doses of VA extract for up to 3 days. At specified time points (6, 24, 48, 72 h) samples were taken and the expression of IL-6 and its receptor components were analysed by real-time-RT-PCR, flow cytometry and ELISA. RESULTS: Treatment of follicular B-NHL cell lines with VA extract did not alter the expression level of IL-6 and its' receptor components at any time and with any of the applied VA extract concentrations. CONCLUSIONS: Clinically relevant doses of the VA extract do not trigger an autocrine or paracrine IL-6 loop nor do they initiate IL-6 trans-signalling in follicular B-NHL cell lines.

Antineoplastic Agents, Phytogenic↗
PubMed2006

The role of growth hormone in neural development.

Growth hormone (GH) is integrally involved in the development of the central nervous system (CNS), as well as during its recovery from injury, two processes that share many similarities and may influence CNS functionality. This review discusses some of the most recent findings in the field and, in particular, the ontogeny, distribution, regulation and putative functions of GH and its receptor within the CNS, particularly during development. The relative roles of peripheral GH, acting in part through insulin-like growth factor-I, and of the autocrine/paracrine GH system within the brain are considered. The potential role of GH as a therapeutic agent to influence brain development and function is discussed.

Animals↗