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Auswahl der wissenschaftlichen Literatur zum Thema „Chromaffin cells“
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Zeitschriftenartikel zum Thema "Chromaffin cells"
1
Coupland, R. E. „MAST CELLS AND CHROMAFFIN CELLS“. Annals of the New York Academy of Sciences 103, Nr. 1 (15.12.2006): 139–50. http://dx.doi.org/10.1111/j.1749-6632.1963.tb53694.x.
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2
Shepherd, S. P., und M. A. Holzwarth. „Chromaffin-adrenocortical cell interactions: effects of chromaffin cell activation in adrenal cell cocultures“. American Journal of Physiology-Cell Physiology 280, Nr. 1 (01.01.2001): C61—C71. http://dx.doi.org/10.1152/ajpcell.2001.280.1.c61.
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Although the adrenal cortex and medulla are both involved in the maintenance of homeostasis and stress response, the functional importance of intra-adrenal interactions remains unclear. When primary cocultures of frog ( Rana pipiens) adrenocortical and chromaffin cells were used, selective chromaffin cell activation dramatically affected both chromaffin and adrenocortical cells. Depolarization with 50 μm veratridine enhanced chromaffin cell neuronal phenotype, contacts with adrenocortical cells, and secretion of norepinephrine, epinephrine, and serotonin. Time-lapse video microscopy recorded the rapid establishment of growth cones on the activated chromaffin cell neurites, neurite branching, and outgrowth toward adrenocortical cells. Simultaneously, adrenocortical cells migrated toward chromaffin cells. Following chromaffin cell activation, adrenocortical cell Fos protein expression and corticosteroid secretion were increased, indicating that chromaffin cell modulation of adrenocortical cells is at the transcriptional level. These results provide evidence that intra-adrenal interactions affect cellular differentiation and modulate steroidogenesis. Furthermore, this suggests that the activity-related plasticity of chromaffin and adrenocortical cells is developmentally and physiologically important.
3
Furlan, Alessandro, Vyacheslav Dyachuk, Maria Eleni Kastriti, Laura Calvo-Enrique, Hind Abdo, Saida Hadjab, Tatiana Chontorotzea et al. „Multipotent peripheral glial cells generate neuroendocrine cells of the adrenal medulla“. Science 357, Nr. 6346 (06.07.2017): eaal3753. http://dx.doi.org/10.1126/science.aal3753.
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Adrenaline is a fundamental circulating hormone for bodily responses to internal and external stressors. Chromaffin cells of the adrenal medulla (AM) represent the main neuroendocrine adrenergic component and are believed to differentiate from neural crest cells. We demonstrate that large numbers of chromaffin cells arise from peripheral glial stem cells, termed Schwann cell precursors (SCPs). SCPs migrate along the visceral motor nerve to the vicinity of the forming adrenal gland, where they detach from the nerve and form postsynaptic neuroendocrine chromaffin cells. An intricate molecular logic drives two sequential phases of gene expression, one unique for a distinct transient cellular state and another for cell type specification. Subsequently, these programs down-regulate SCP-gene and up-regulate chromaffin cell–gene networks. The AM forms through limited cell expansion and requires the recruitment of numerous SCPs. Thus, peripheral nerves serve as a stem cell niche for neuroendocrine system development.
4
Kim, Yu Mi, Young Hoon Jeon, Gwang Chun Jin, Jeong Ok Lim und Woon Yi Baek. „In Vivo Biocompatibility of Alginate-PLL Microcapsules with Chromaffin Cells for the Alleviation of Chronic Pain“. Key Engineering Materials 277-279 (Januar 2005): 62–66. http://dx.doi.org/10.4028/www.scientific.net/kem.277-279.62.
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Intrathecal implants of adrenal medullary chromaffin cells relieve chronic pain by secreting catecholamines, opioids and other neuroactive substances. Recently, macrocapsules with hollow fibers were employed to isolate immunologically xenogeneic chromaffin cells, but the poor viability in vivo of the encapsulated chromaffin cells limited the usefulness of this method. In this study, we used microencapsulation technology to increase the viability of chromaffin cells. Bovine adrenal chromaffin cells were microencapsulated with alginate and poly-L-lysine and implanted intrathecally in a rat using the neuropathic pain model. Intrathecal implants of microencapsulated cells relieved cold allodynia, which is the most prominent symptom of the neuropathic pain model in a rat. Furthermore, the microencapsulated chromaffin cells were morphologically normal and retained their functionality. These findings suggest that the intrathecal implant of microencapsulated chromaffin cells might be a useful method for treating chronic pain.
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Finotto, S., K. Krieglstein, A. Schober, F. Deimling, K. Lindner, B. Bruhl, K. Beier et al. „Analysis of mice carrying targeted mutations of the glucocorticoid receptor gene argues against an essential role of glucocorticoid signalling for generating adrenal chromaffin cells“. Development 126, Nr. 13 (01.07.1999): 2935–44. http://dx.doi.org/10.1242/dev.126.13.2935.
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Molecular mechanisms underlying the generation of distinct cell phenotypes is a key issue in developmental biology. A major paradigm of determination of neural cell fate concerns the development of sympathetic neurones and neuroendocrine chromaffin cells from a common sympathoadrenal (SA) progenitor cell. Two decades of in vitro experiments have suggested an essential role of glucocorticoid receptor (GR)-mediated signalling in generating chromaffin cells. Targeted mutation of the GR should consequently abolish chromaffin cells. The present analysis of mice lacking GR gene product demonstrates that animals have normal numbers of adrenal chromaffin cells. Moreover, there are no differences in terms of apoptosis and proliferation or in expression of several markers (e.g. GAP43, acetylcholinesterase, adhesion molecule L1) of chromaffin cells in GR-deficient and wild-type mice. However, GR mutant mice lack the adrenaline-synthesizing enzyme PNMT and secretogranin II. Chromaffin cells of GR-deficient mice exhibit the typical ultrastructural features of this cell phenotype, including the large chromaffin granules that distinguish them from sympathetic neurones. Peripherin, an intermediate filament of sympathetic neurones, is undetectable in chromaffin cells of GR mutants. Finally, when stimulated with nerve growth factor in vitro, identical proportions of chromaffin cells from GR-deficient and wild-type mice extend neuritic processes. We conclude that important phenotypic features of chromaffin cells that distinguish them from sympathetic neurones develop normally in the absence of GR-mediated signalling. Most importantly, chromaffin cells in GR-deficient mice do not convert to a neuronal phenotype. These data strongly suggest that the dogma of an essential role of glucocorticoid signalling for the development of chromaffin cells must be abandoned.
6
Hong, Hai Yan, Jeong Ok Lim und Woon Yi Baek. „Effect of Morphine and Bupivacaine on Nicotine-Induced Catecholamine Secretion from Encapsulated Chromaffin Cells“. Key Engineering Materials 277-279 (Januar 2005): 56–61. http://dx.doi.org/10.4028/www.scientific.net/kem.277-279.56.
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The control of intractable pain through transplanted of chromaffin cells has been recently reported where the analgesic effects are principally due to the production of opioid peptides and catecholamines (CAs) by the chromaffin cells. Currently many cancer patients receive general opioids or local anesthetics, such as bupivacaine. Therefore, the present study investigated the effect of morphine or bupivacaine on the secretion of nicotine-induced CAs from encapsulated chromaffin cells over a period of 180 min. As such, bovine chromaffin cells were isolated and encapsulated with alginate–poly–L–lysine–alginate (APA) biomaterials to prevent immunorejection. The capsules were then pre-incubated with nicotine for 5 min prior to morphine or bupivacaine stimulation, and the quantity of CAs analyzed using a high performance liquid chromatography (HPLC) analysis system. The resulting data showed that the encapsulated chromaffin cells retained the ability of their parent chromaffin cells when responding to opioids by suppressing the release of CAs. In contrast, bupivacaine did not have any statistically significant affect on the basal and nicotine-induced CA release from the encapsulated chromaffin cells.
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Sol, J. C., R. Y. Li, B. Sallerin, S. Jozan, H. Zhou, V. Lauwers-Cances, F. Tortosa et al. „Intrathecal Grafting of Porcine Chromaffin Cells Reduces Formalin-Evoked c-Fos Expression in the Rat Spinal Cord“. Cell Transplantation 14, Nr. 6 (Juli 2005): 353–65. http://dx.doi.org/10.3727/000000005783982963.
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Chromaffin cells from the adrenal gland secrete a combination of neuroactive compounds including catecholamines, opioid peptides, and growth factors that have strong analgesic effects, especially when administered intrathecally. Preclinical studies of intrathecal implantation with xenogeneic bovine chromaffin cells in rats have provided conflicting data with regard to analgesic effects, and recent concern over risk of prion transmission has precluded their use in human clinical trials. We previously developed a new, safer source of adult adrenal chromaffin cells of porcine origin and demonstrated an in vivo antinociceptive effect in the formalin test, a rodent model of tonic pain. The goal of the present study was to confirm porcine chromaffin cell analgesic effects at the molecular level by evaluating neural activity as reflected by spinal cord c-Fos protein expression. To this end, the expression of c-Fos in response to intraplantar formalin injection was evaluated in animals following intrathecal grafting of 106 porcine or bovine chromaffin cells. For the two species, adrenal chromaffin cells significantly reduced the tonic phases of the formalin response. Similarly, c-Fos-like immunoreactive neurons were markedly reduced in the dorsal horns of animals that had received injections of xenogeneic chromaffin cells. This reduction was observed in both the superficial (I—II) and deep (V—VI) lamina of the dorsal horn. The present study demonstrates that both xenogeneic porcine and bovine chromaffin cells transplanted into the spinal subarachnoid space of the rat can suppress formalin-evoked c-Fos expression equally, in parallel with suppression of nociceptive behaviors in the tonic phase of the test. These findings confirm previous reports that adrenal chromaffin cells may produce antinociception by inhibiting activation of nociceptive neurons in the spinal dorsal horn. Taken together these results support the concept that porcine chromaffin cells may offer an alternative xenogeneic cell source for transplants delivering pain-reducing neuroactive substances.
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Eaton, M. J., M. Martinez, S. Karmally, T. Lopez und J. Sagen. „Initial Characterization of the Transplant of Immortalized Chromaffin Cells for the Attenuation of Chronic Neuropathic Pain“. Cell Transplantation 9, Nr. 5 (September 2000): 637–56. http://dx.doi.org/10.1177/096368970000900509.
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Cultures of embryonic day 17 (E17) rat adrenal and neonatal bovine adrenal cells were conditionally immortalized with the temperature-sensitive allele of SV40 large T antigen (tsTag) and chromaffin cell lines established. Indicative of the adrenal chromaffin phenotype, these cells expressed immunoreactivity (ir) for tyrosine hydroxylase (TH), the first enzyme in the synthetic pathway for catecholamines. At permissive temperature in vitro (33°C), these chromaffin cells are proliferative, have a typical rounded chromaffin-like morphology, and contain detectable TH-ir. At nonpermissive temperature in vitro (39°C), these cells stop proliferating and express increased TH-ir. When these immortalized chromaffin cells were transplanted in the lumbar subarachnoid space of the spinal cord 1 week after a unilateral chronic constriction injury (CCI) of the rat sciatic nerve, they survived longer than 7 weeks on the pia mater around the spinal cord and continued to express TH-ir. Conversely, grafted chromaffin cells lost Tag-ir after transplant and Tag-ir was undetectible in the grafts after 7 weeks in the subarachnoid space. At no time did the grafts form tumors after transplant into the host animals. These grafted chromaffin cells also expressed immunoreactivities for the other catecholamine-synthesizing enzymes 7 weeks after grafting, including: dopamine-β-hydroxylase (DβH) and phenylethanolamine-N-methyltransferase (PNMT). The grafted cells also expressed detectable immunoreactivities for the opioid met-enkephalin (ENK), the peptide galanin (GAL), and the neurotransmitters γ-aminobutyric acid (GABA) and serotonin (5-HT). Furthermore, after transplantation, tactile and cold allodynia and tactile and thermal hyperalgesia induced by CCI were significantly reduced during a 2–8-week period, related to the chromaffin cell transplants. The maximal antinociceptive effect occurred 1–3 weeks after grafting. Control adrenal fibroblasts, similarly immortalized and similarly transplanted after CCI, did not express any of the chromaffin antigenic markers, and fibroblast grafts had no effect on the allodynia and hyperalgesia induced by CCI. These data suggest that embryonic and neonatal chromaffin cells can be conditionally immortalized and will continue to express the phenotype of primary chromaffin cells in vitro and in vivo; grafted cells will ameliorate neuropathic pain after nerve injury and can be used as a homogeneous source to examine the mechanisms by which chromaffin transplants reverse chronic pain. The use of such chromaffin cell lines that are able to deliver antinociceptive molecules in models of chronic pain after nerve and spinal cord injury (SCI) offers a novel approach to pain management.
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DUNCAN, Rory R., Andrew C. DON-WAUCHOPE, Sompol TAPECHUM, Michael J. SHIPSTON, Robert H. CHOW und Peter ESTIBEIRO. „High-efficiency Semliki Forest virus-mediated transduction in bovine adrenal chromaffin cells“. Biochemical Journal 342, Nr. 3 (05.09.1999): 497–501. http://dx.doi.org/10.1042/bj3420497.
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Adrenal chromaffin cells are commonly used in studies of exocytosis. Progress in characterizing the molecular mechanisms has been slow, because no simple, high-efficiency technique is available for introducing and expressing heterologous cDNA in chromaffin cells. Here we demonstrate that Semliki Forest virus (SFV) vectors allow high-efficiency expression of heterologous protein in chromaffin cells.
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Vukicevic, Vladimir, Janine Schmid, Andreas Hermann, Sven Lange, Nan Qin, Linda Gebauer, Kuei-Fang Chung et al. „Differentiation of Chromaffin Progenitor Cells to Dopaminergic Neurons“. Cell Transplantation 21, Nr. 11 (November 2012): 2471–86. http://dx.doi.org/10.3727/096368912x638874.
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The differentiation of dopamine-producing neurons from chromaffin progenitors might represent a new valuable source for replacement therapies in Parkinson's disease. However, characterization of their differentiation potential is an important prerequisite for efficient engraftment. Based on our previous studies on isolation and characterization of chromaffin progenitors from adult adrenals, this study investigates their potential to produce dopaminergic neurons and means to enhance their dopaminergic differentiation. Chromaffin progenitors grown in sphere culture showed an increased expression of nestin and Mash1, indicating an increase of the progenitor subset. Proneurogenic culture conditions induced the differentiation into neurons positive for neural markers β-III-tubulin, MAP2, and TH accompanied by a decrease of Mash1 and nestin. Furthermore, Notch2 expression decreased concomitantly with a downregulation of downstream effectors Hes1 and Hes5 responsible for self-renewal and proliferation maintenance of progenitor cells. Chromaffin progenitor-derived neurons secreted dopamine upon stimulation by potassium. Strikingly, treatment of differentiating cells with retinoic and ascorbic acid resulted in a twofold increase of dopamine secretion while norepinephrine and epinephrine were decreased. Initiation of dopamine synthesis and neural maturation is controlled by Pitx3 and Nurr1. Both Pitx3 and Nurr1 were identified in differentiating chromaffin progenitors. Along with the gained dopaminergic function, electrophysiology revealed features of mature neurons, such as sodium channels and the capability to fire multiple action potentials. In summary, this study elucidates the capacity of chromaffin progenitor cells to generate functional dopaminergic neurons, indicating their potential use in cell replacement therapies.
Dissertationen zum Thema "Chromaffin cells"
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Owen, Penelope Jane. „Bradykinin stimulation of bovine adrenal chromaffin cells“. Thesis, University of Leicester, 1991. http://hdl.handle.net/2381/33600.
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Cultured bovine adrenal chromaffin cells provide a useful model of stimulus secretion coupling and respond to cholinergic agonists by secreting catecholamines. Work in this thesis concentrates on the responses to a non-cholinergic agonist, bradykinin. Bradykinin as shown to stimulate a two phase, dose dependent increase in catecholamine release which is mediated by a receptor of the B2 subtype. Calcium entry is shown to be required for release to occur but studies with various calcium channel blockers suggest that, in contrast to the response to potassium, a non-voltage sensitive calcium channel is involved. Other possible alternatives are discussed. As bradykinin stimulated an increase in inositol phosphate production, I attempted to measure the production of the other product of phospholipase C action on inositol phospholipids, diacylglycerol, in order to evaluate its possible role in the release response. This was attempted using both mass measurement, by the diacylglycerol kinase assay, and lipid labelling techniques. No increases in diacylglycerol in response to bradykinin were observed, even in the presence of inhibitors of diacylglycerol breakdown, which were able to increase basal diacylglycerol levels when added alone. These inhibitors, along with TPA, were used to evaluate the possible mechanism of action of protein kinase C in chromaffin cells, eg. feedback regulation or stimulation of release mechanisms. Failure to detect rises in diacylglycerol in response to bradykinin led to the final section of this work which looks at the production of one of the metabolic products of diacylglycerol breakdown, phosphatidic acid. Bradykinin is shown to stimulate a rapid, dose dependent increase in phosphatidic acid in chromaffin cells, which is, partially independent of extracellular calcium, independent of protein kinase C activation, and may be G-protein mediated. Studies of the route of formation of the phosphatidic acid show that phospholipase D is not involved and that inositol phospholipids or phosphatidylcholine are unlikely to be the main substrates for a phospholipase C mediated route, leaving the possibility of phospholipase C action on an alternative phospholipid. Finally the possible role of this production of phosphatidic acid in the chromaffin cell is discussed.
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Pappas, Vassilios Konstantinos. „Ca2+ signalling in bovine adrenal chromaffin cells“. Thesis, University of Leicester, 1995. http://hdl.handle.net/2381/33634.
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Cells possess two mechanisms, the inositol 1,4,5-trisphosphate (Ins(l,4,5)P3) and ryanodine receptors, by which Ca2+ in intracellular stores can be mobilised. There are also a number of pathways which can mediate Ca2+ entry across the cell plasma membrane. In this study bovine adrenal chromaffin cells were used to investigate the role of intracellular Ca2+ stores in Ca2+ signalling and the relationship between Ca2+ entry and store release. The major part of the exocytotic process in chromaffin cells is due to Ca2+ entry across the plasma membrane. Bradykinin (an Ins(l,4,5)P3 generating agonist) and nicotine (a depolarising stimulus) were found to evoke catecholamine secretion in the presence of extracellular Ca2+. Nicotinic responses were abolished in the absence of extracellular Ca2+, whereas bradykinin resulted in reduced catecholamine secretion, indicating that Ca2+ release from intracellular stores may activate secretion. Studies in permeabilised chromaffin cells showed that both Ins(l,4,5)P3 and caffeine induced Ca2+ mobilisation from intracellular Ca2+ stores. Challenge of the chromaffin cells with inositol 4,5-bisphosphorothioate resulted in depletion of the Ins(l,4,5)P3-sensitive Ca2+ stores. However, subsequent addition of caffeine stimulated Ca2+ mobilisation, indicating that the caffeine releasable stores had not been emptied. Ins(l,4,5)P3 and caffeine, when added simultaneously, resulted in a larger response than each of these agonists alone. Ryanodine pretreatment inhibited subsequent caffeine responses. Ins(l,4,5)P3 was able to stimulate Ca2+ release after prior depletion of the ryanodine-sensitive Ca2+ stores, providing a pharmacological differentiation of these stores, suggesting that the Ins(l,4,5)P3 receptor-expressing stores may be physically different from the ryanodine receptor-expressing Ca2+ stores in chromaffin cells. Experiments using epifluorescence microscopy were carried out to investigate the relationship between Ins(l,4,5)P3- and caffeine-sensitive Ca2+ stores in fura-2 loaded intact chromaffin cells. Bradykinin evoked Ca2+ responses appeared to involve activation of ryanodine receptors, probably occuring secondary to Ca2+ release via Ins(l,4,5)P3 receptors. Depletion of the Ins(l,4,5)P3- and caffeine-sensitive Ca2+ stores resulted in activation of Ca2+ entry indicating that the Ins(l,4,5)P3- and ryanodine-sensitive Ca2+ stores are both linked to the promotion of Ca2+ entry. Several aspects of Ca2+ signalling have been elucidated in this study, notably the possible expression of at least two different Ca2+ stores and the degree of physical or functional overlap between the Ins(l,4,5)P3 receptor-expressing and ryanodine-receptor expressing Ca2+ stores. Ca2+ release from the ryanodine-sensitive Ca2+ stores was found to activate Ca2+ entry across the chromaffin cells plasma membrane. These findings may have important implications for our understanding of how Ca2+ signalling occurs in adrenal chromaffin and other excitable cells in vivo.
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Hagan, Todd. „Finite-difference time-domain modeling of a waveguide-based radiofrequency exposure system for studying non-thermal effects on catecholamine release from chromaffin cells : characterization and optimization /“. abstract and full text PDF (free order & download UNR users only), 2005. http://0-wwwlib.umi.com.innopac.library.unr.edu/dissertations/fullcit/1433103.
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Thesis (M.S.)--University of Nevada, Reno, 2005."May, 2005." Includes bibliographical references. Library also has microfilm. Ann Arbor, Mich. : ProQuest Information and Learning Company, [2005]. 1 microfilm reel ; 35 mm. Online version available on the World Wide Web.
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gov, Clearys@ninds nih, und Susannah Cleary. „From chromaffin cells to Phaeochromocytoma : insight into the sympathoadrenal cell lineage“. Murdoch University, 2007. http://wwwlib.murdoch.edu.au/adt/browse/view/adt-MU20080526.105525.
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Chromaffin cells are a modified post-ganglionic sympathetic neuron, which synthesise and secrete catecholamines. The neoplastic transformation of chromaffin cells is demonstrated by the tumour phaeochromocytoma, a functional tumour that recapitulates the normal role of chromaffin cells by synthesising, storing and releasing excess catecholamines. Within this thesis we have explored several aspects of chromaffin cell and phaeochromocytoma tumour biology, including the specific expression of key sympathoadrenal markers such as the noradrenaline transporter (NAT), neuropeptide Y (NPY) and chromogranin A (CGA) in normal human and mouse chromaffin cells versus phaeochromocytomas of human and mouse origin.
Catecholamine-mediated signalling in chromaffin cells is terminated by the sequestration of extracellular catecholamines back into the cell via the noradrenaline transporter (NAT). Following observations that within the rat adrenal medulla, NAT is expressed in PNMT-positive chromaffin cells we explored whether this pattern of expression is also present in the human adrenal medulla. While we successfully established that NAT and PNMT are co localised, we also found that all human adrenal chromaffin cells are PNMT-positive. In the rat, NAT is also observed within the cytoplasm and has been suggested to be associated with secretory vesicles, thus using the secretory vesicle marker, CGA, we demonstrate that NAT is associated with secretory vesicles. However, in contrast to our findings within the normal chromaffin cells, in situ NAT expression in human phaeochromocytoma tumour samples was distorted, with observed changes including the level and type of staining observed, and disruptions to the strict NAT-CGA association observed in the normal adrenal.
Continuing our theme of NAT, we investigated if pre treating the phaeochromocytoma PC12 cell line with the chemotherapy drug cisplatin had an effect on the expression of NAT, to give an indication of the efficacy of this compound in the treatment of metastatic phaeochromocytoma with radiolabelled 131Iodometabenzylguanidine (131I-MIBG), a noradrenaline analogue which can be incorporated into phaeochromocytoma tumour cells though uptake through NAT. The premise of this study is derived from previous work in which neuroblastoma cells pre-treated with cisplatin were more responsive to (131I-MIBG) accumulation due to increased activity and expression of the transporter. Thus we treated PC12 cells for 24-hours in a range of cisplatin concentrations and measured the effect on NAT expression. However, unlike the findings in neuroblastoma cells, in our study, we did not observe an effect of cisplatin pretreatment on NAT activity or expression in PC12 cells.
Upto 30% of phaeochromocytoma arise as apart of a hereditary syndrome. The von Hippel-Lindau (VHL) syndrome, due to germline mutations to the VHL gene, and Multiple Endocrine Neoplasia type 2 (MEN 2), due to germline mutations to the RET gene represent two examples of hereditable endocrine disorders where phaeochromocytoma is a presenting feature. Notable differences in clinical presentation and tumour biology have been identified in phaeochromocytomas from patients with VHL and MEN 2. These differences prompted us to explore whether these observations extend to the chromaffin granule constituents, NPY and CGA.
Patients with MEN 2 disease have a greater incidence of hypertension than patients with VHL disease, MEN 2 are characterised by an adrenergic phenotype (produce predominantly-adrenaline), whereas VHL phaeochromocytomas are noradrenergic (produce predominantly-noradrenaline). Neuropeptide Y, which has powerful vasoactive properties capable of significantly elevating blood pressure, is stored and released with catecholamines and is thought to be associated with PNMT-positive chromaffin cells. Thus, we questioned whether the differences in the symptomatology between VHL and MEN 2 patients may be related to differences in NPY expression between the two groups, and whether any differences in NPY relate to adrenaline and/or PNMT content, or are linked to hereditary factors. Thus we compared tumour samples from four cohorts of patients: (i) adrenergic versus noradrenergic phenotype, (ii) hereditary versus no hereditary syndrome. Results demonstrated that although tumour NPY levels (mRNA and peptide) correlate with PNMT expression and/or adrenaline content, when NPY expression was compared between groups of patients (adrenergic vs noradrenergic; hereditary versus nonhereditary) difference in NPY levels were only significant between VHL and MEN 2 tumour and not between sporadic adrenergic and noradrenergic Immunohistochemistry also supported the above observations. Hence, we concluded that NPY expression in all groups of phaeochromocytoma examined in this study, this effect is not related to tumour biochemical phenotype but rather appears to be a specific unique trait of VHL phaeochromocytomas.
Continuing our theme of the possible differential expression of chromaffin granule constituents between VHL and MEN 2 patients, we also investigated CGA levels in plasma and tumour samples. Given, VHL tumours possess less chromaffin granules than MEN 2 tumours, and CGA has been implicated as a key director of secretory vesicle biogenesis we investigated whether CGA was differentially expressed between VHL and MEN 2 tumours. We found CGA expression was significantly greater in MEN 2 tumours (mRNA; 3-fold, and protein; 20-fold), with western blot confirming this trend. We also found that plasma CGA was greater in MEN 2 patients but not significantly, consequently, we explored the co-variables tumour size and tumour secretory activity (measured by plasma catecholamine concentrations), which influence plasma CGA and found that tumour size and plasma CGA are related but there was no influence of genotype on this relationship. In contrast, plasma CGA was significantly related to tumour secretory activity and the effect of genotype on this relationship narrowly missed significance, but when we expressed plasma CGA as a ratio of plasma catecholamines, plasma CGA was 2-fold greater in MEN 2 patients than VHL patients. Thus despite the tendency of phaeochromocytomas from VHL disease to readily and continuously release their catecholamine stores, plasma CGA levels still appeared to be higher in MEN 2 patients.
Finally, we examined whether the expression of NPY, Leu- enkephalin (Leu-Enk), NAT and the vesicular monoamine transporters type 1 and 2 (VMAT1 and VMAT2,), in normal mouse adrenal glands, and in histologically-confirmed adrenal phaeochromocytomas generated by injected nude mice with a phaeochromocytoma (MPC) cells line. The results of this study established that similar to the rat and human NAT expression is preferentially localised with PNMT within mouse chromaffin cells, while VMAT1 and NPY are found in both PNMT-negative and PNMT-positive cell populations, although expression of NPY was reduced in PNMT-negative cells. In contrast, both VMAT2 and Leu-Enk were found in PNMT-negative noradrenergic cells, and VMAT2 was present in all noradrenergic chromaffin cells while Leu-Enk was observed in a subpopulation of noradrenergic chromaffin cells. In contrast to the normal adrenal but similar to our findings in human phaeochromocytoma, the pattern of marker expression within adrenal phaeochromocytoma lesions of MPC-injected mice are severely disrupted related to both the level of expression of the respective markers, and association with PNMT within the tissue. Thus, the experimentally generated phaeochromocytoma mouse model provides a valuable tool in studying human phaeochromocytoma.
The data presented in this thesis further validate the heterogeneity observed in many aspects of phaeochromocytoma tumour biology, including the expression several chromaffin cell markers such as NAT, NPY and CGA. The altered expression of these markers may contribute to the clinical picture of these tumours, particularly relating to hereditary phaeochromocytoma from VHL and MEN 2 disease.
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Cleary, Susannah. „From chromaffin cells to Phaeochromocytoma: insight into the sympathoadrenal cell lineage“. Thesis, Cleary, Susannah (2007) From chromaffin cells to Phaeochromocytoma: insight into the sympathoadrenal cell lineage. PhD thesis, Murdoch University, 2007. https://researchrepository.murdoch.edu.au/id/eprint/659/.
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Chromaffin cells are a modified post-ganglionic sympathetic neuron, which synthesise and secrete catecholamines. The neoplastic transformation of chromaffin cells is demonstrated by the tumour phaeochromocytoma, a functional tumour that recapitulates the normal role of chromaffin cells by synthesising, storing and releasing excess catecholamines. Within this thesis we have explored several aspects of chromaffin cell and phaeochromocytoma tumour biology, including the specific expression of key sympathoadrenal markers such as the noradrenaline transporter (NAT), neuropeptide Y (NPY) and chromogranin A (CGA) in normal human and mouse chromaffin cells versus phaeochromocytomas of human and mouse origin.
Catecholamine-mediated signalling in chromaffin cells is terminated by the sequestration of extracellular catecholamines back into the cell via the noradrenaline transporter (NAT). Following observations that within the rat adrenal medulla, NAT is expressed in PNMT-positive chromaffin cells we explored whether this pattern of expression is also present in the human adrenal medulla. While we successfully established that NAT and PNMT are co localised, we also found that all human adrenal chromaffin cells are PNMT-positive. In the rat, NAT is also observed within the cytoplasm and has been suggested to be associated with secretory vesicles, thus using the secretory vesicle marker, CGA, we demonstrate that NAT is associated with secretory vesicles. However, in contrast to our findings within the normal chromaffin cells, in situ NAT expression in human phaeochromocytoma tumour samples was distorted, with observed changes including the level and type of staining observed, and disruptions to the strict NAT-CGA association observed in the normal adrenal.
Continuing our theme of NAT, we investigated if pre treating the phaeochromocytoma PC12 cell line with the chemotherapy drug cisplatin had an effect on the expression of NAT, to give an indication of the efficacy of this compound in the treatment of metastatic phaeochromocytoma with radiolabelled 131Iodometabenzylguanidine (131I-MIBG), a noradrenaline analogue which can be incorporated into phaeochromocytoma tumour cells though uptake through NAT. The premise of this study is derived from previous work in which neuroblastoma cells pre-treated with cisplatin were more responsive to (131I-MIBG) accumulation due to increased activity and expression of the transporter. Thus we treated PC12 cells for 24-hours in a range of cisplatin concentrations and measured the effect on NAT expression. However, unlike the findings in neuroblastoma cells, in our study, we did not observe an effect of cisplatin pretreatment on NAT activity or expression in PC12 cells.
Upto 30% of phaeochromocytoma arise as apart of a hereditary syndrome. The von Hippel-Lindau (VHL) syndrome, due to germline mutations to the VHL gene, and Multiple Endocrine Neoplasia type 2 (MEN 2), due to germline mutations to the RET gene represent two examples of hereditable endocrine disorders where phaeochromocytoma is a presenting feature. Notable differences in clinical presentation and tumour biology have been identified in phaeochromocytomas from patients with VHL and MEN 2. These differences prompted us to explore whether these observations extend to the chromaffin granule constituents, NPY and CGA.
Patients with MEN 2 disease have a greater incidence of hypertension than patients with VHL disease, MEN 2 are characterised by an adrenergic phenotype (produce predominantly-adrenaline), whereas VHL phaeochromocytomas are noradrenergic (produce predominantly-noradrenaline). Neuropeptide Y, which has powerful vasoactive properties capable of significantly elevating blood pressure, is stored and released with catecholamines and is thought to be associated with PNMT-positive chromaffin cells. Thus, we questioned whether the differences in the symptomatology between VHL and MEN 2 patients may be related to differences in NPY expression between the two groups, and whether any differences in NPY relate to adrenaline and/or PNMT content, or are linked to hereditary factors. Thus we compared tumour samples from four cohorts of patients: (i) adrenergic versus noradrenergic phenotype, (ii) hereditary versus no hereditary syndrome. Results demonstrated that although tumour NPY levels (mRNA and peptide) correlate with PNMT expression and/or adrenaline content, when NPY expression was compared between groups of patients (adrenergic vs noradrenergic; hereditary versus nonhereditary) difference in NPY levels were only significant between VHL and MEN 2 tumour and not between sporadic adrenergic and noradrenergic Immunohistochemistry also supported the above observations. Hence, we concluded that NPY expression in all groups of phaeochromocytoma examined in this study, this effect is not related to tumour biochemical phenotype but rather appears to be a specific unique trait of VHL phaeochromocytomas.
Continuing our theme of the possible differential expression of chromaffin granule constituents between VHL and MEN 2 patients, we also investigated CGA levels in plasma and tumour samples. Given, VHL tumours possess less chromaffin granules than MEN 2 tumours, and CGA has been implicated as a key director of secretory vesicle biogenesis we investigated whether CGA was differentially expressed between VHL and MEN 2 tumours. We found CGA expression was significantly greater in MEN 2 tumours (mRNA; 3-fold, and protein; 20-fold), with western blot confirming this trend. We also found that plasma CGA was greater in MEN 2 patients but not significantly, consequently, we explored the co-variables tumour size and tumour secretory activity (measured by plasma catecholamine concentrations), which influence plasma CGA and found that tumour size and plasma CGA are related but there was no influence of genotype on this relationship. In contrast, plasma CGA was significantly related to tumour secretory activity and the effect of genotype on this relationship narrowly missed significance, but when we expressed plasma CGA as a ratio of plasma catecholamines, plasma CGA was 2-fold greater in MEN 2 patients than VHL patients. Thus despite the tendency of phaeochromocytomas from VHL disease to readily and continuously release their catecholamine stores, plasma CGA levels still appeared to be higher in MEN 2 patients.
Finally, we examined whether the expression of NPY, Leu- enkephalin (Leu-Enk), NAT and the vesicular monoamine transporters type 1 and 2 (VMAT1 and VMAT2,), in normal mouse adrenal glands, and in histologically-confirmed adrenal phaeochromocytomas generated by injected nude mice with a phaeochromocytoma (MPC) cells line. The results of this study established that similar to the rat and human NAT expression is preferentially localised with PNMT within mouse chromaffin cells, while VMAT1 and NPY are found in both PNMT-negative and PNMT-positive cell populations, although expression of NPY was reduced in PNMT-negative cells. In contrast, both VMAT2 and Leu-Enk were found in PNMT-negative noradrenergic cells, and VMAT2 was present in all noradrenergic chromaffin cells while Leu-Enk was observed in a subpopulation of noradrenergic chromaffin cells. In contrast to the normal adrenal but similar to our findings in human phaeochromocytoma, the pattern of marker expression within adrenal phaeochromocytoma lesions of MPC-injected mice are severely disrupted related to both the level of expression of the respective markers, and association with PNMT within the tissue. Thus, the experimentally generated phaeochromocytoma mouse model provides a valuable tool in studying human phaeochromocytoma.
The data presented in this thesis further validate the heterogeneity observed in many aspects of phaeochromocytoma tumour biology, including the expression several chromaffin cell markers such as NAT, NPY and CGA. The altered expression of these markers may contribute to the clinical picture of these tumours, particularly relating to hereditary phaeochromocytoma from VHL and MEN 2 disease.
6
Cleary, Susannah. „From chromaffin cells to Phaeochromocytoma: insight into the sympathoadrenal cell lineage“. Cleary, Susannah (2007) From chromaffin cells to Phaeochromocytoma: insight into the sympathoadrenal cell lineage. PhD thesis, Murdoch University, 2007. http://researchrepository.murdoch.edu.au/659/.
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Chromaffin cells are a modified post-ganglionic sympathetic neuron, which synthesise and secrete catecholamines. The neoplastic transformation of chromaffin cells is demonstrated by the tumour phaeochromocytoma, a functional tumour that recapitulates the normal role of chromaffin cells by synthesising, storing and releasing excess catecholamines. Within this thesis we have explored several aspects of chromaffin cell and phaeochromocytoma tumour biology, including the specific expression of key sympathoadrenal markers such as the noradrenaline transporter (NAT), neuropeptide Y (NPY) and chromogranin A (CGA) in normal human and mouse chromaffin cells versus phaeochromocytomas of human and mouse origin.
Catecholamine-mediated signalling in chromaffin cells is terminated by the sequestration of extracellular catecholamines back into the cell via the noradrenaline transporter (NAT). Following observations that within the rat adrenal medulla, NAT is expressed in PNMT-positive chromaffin cells we explored whether this pattern of expression is also present in the human adrenal medulla. While we successfully established that NAT and PNMT are co localised, we also found that all human adrenal chromaffin cells are PNMT-positive. In the rat, NAT is also observed within the cytoplasm and has been suggested to be associated with secretory vesicles, thus using the secretory vesicle marker, CGA, we demonstrate that NAT is associated with secretory vesicles. However, in contrast to our findings within the normal chromaffin cells, in situ NAT expression in human phaeochromocytoma tumour samples was distorted, with observed changes including the level and type of staining observed, and disruptions to the strict NAT-CGA association observed in the normal adrenal.
Continuing our theme of NAT, we investigated if pre treating the phaeochromocytoma PC12 cell line with the chemotherapy drug cisplatin had an effect on the expression of NAT, to give an indication of the efficacy of this compound in the treatment of metastatic phaeochromocytoma with radiolabelled 131Iodometabenzylguanidine (131I-MIBG), a noradrenaline analogue which can be incorporated into phaeochromocytoma tumour cells though uptake through NAT. The premise of this study is derived from previous work in which neuroblastoma cells pre-treated with cisplatin were more responsive to (131I-MIBG) accumulation due to increased activity and expression of the transporter. Thus we treated PC12 cells for 24-hours in a range of cisplatin concentrations and measured the effect on NAT expression. However, unlike the findings in neuroblastoma cells, in our study, we did not observe an effect of cisplatin pretreatment on NAT activity or expression in PC12 cells.
Upto 30% of phaeochromocytoma arise as apart of a hereditary syndrome. The von Hippel-Lindau (VHL) syndrome, due to germline mutations to the VHL gene, and Multiple Endocrine Neoplasia type 2 (MEN 2), due to germline mutations to the RET gene represent two examples of hereditable endocrine disorders where phaeochromocytoma is a presenting feature. Notable differences in clinical presentation and tumour biology have been identified in phaeochromocytomas from patients with VHL and MEN 2. These differences prompted us to explore whether these observations extend to the chromaffin granule constituents, NPY and CGA.
Patients with MEN 2 disease have a greater incidence of hypertension than patients with VHL disease, MEN 2 are characterised by an adrenergic phenotype (produce predominantly-adrenaline), whereas VHL phaeochromocytomas are noradrenergic (produce predominantly-noradrenaline). Neuropeptide Y, which has powerful vasoactive properties capable of significantly elevating blood pressure, is stored and released with catecholamines and is thought to be associated with PNMT-positive chromaffin cells. Thus, we questioned whether the differences in the symptomatology between VHL and MEN 2 patients may be related to differences in NPY expression between the two groups, and whether any differences in NPY relate to adrenaline and/or PNMT content, or are linked to hereditary factors. Thus we compared tumour samples from four cohorts of patients: (i) adrenergic versus noradrenergic phenotype, (ii) hereditary versus no hereditary syndrome. Results demonstrated that although tumour NPY levels (mRNA and peptide) correlate with PNMT expression and/or adrenaline content, when NPY expression was compared between groups of patients (adrenergic vs noradrenergic; hereditary versus nonhereditary) difference in NPY levels were only significant between VHL and MEN 2 tumour and not between sporadic adrenergic and noradrenergic Immunohistochemistry also supported the above observations. Hence, we concluded that NPY expression in all groups of phaeochromocytoma examined in this study, this effect is not related to tumour biochemical phenotype but rather appears to be a specific unique trait of VHL phaeochromocytomas.
Continuing our theme of the possible differential expression of chromaffin granule constituents between VHL and MEN 2 patients, we also investigated CGA levels in plasma and tumour samples. Given, VHL tumours possess less chromaffin granules than MEN 2 tumours, and CGA has been implicated as a key director of secretory vesicle biogenesis we investigated whether CGA was differentially expressed between VHL and MEN 2 tumours. We found CGA expression was significantly greater in MEN 2 tumours (mRNA; 3-fold, and protein; 20-fold), with western blot confirming this trend. We also found that plasma CGA was greater in MEN 2 patients but not significantly, consequently, we explored the co-variables tumour size and tumour secretory activity (measured by plasma catecholamine concentrations), which influence plasma CGA and found that tumour size and plasma CGA are related but there was no influence of genotype on this relationship. In contrast, plasma CGA was significantly related to tumour secretory activity and the effect of genotype on this relationship narrowly missed significance, but when we expressed plasma CGA as a ratio of plasma catecholamines, plasma CGA was 2-fold greater in MEN 2 patients than VHL patients. Thus despite the tendency of phaeochromocytomas from VHL disease to readily and continuously release their catecholamine stores, plasma CGA levels still appeared to be higher in MEN 2 patients.
Finally, we examined whether the expression of NPY, Leu- enkephalin (Leu-Enk), NAT and the vesicular monoamine transporters type 1 and 2 (VMAT1 and VMAT2,), in normal mouse adrenal glands, and in histologically-confirmed adrenal phaeochromocytomas generated by injected nude mice with a phaeochromocytoma (MPC) cells line. The results of this study established that similar to the rat and human NAT expression is preferentially localised with PNMT within mouse chromaffin cells, while VMAT1 and NPY are found in both PNMT-negative and PNMT-positive cell populations, although expression of NPY was reduced in PNMT-negative cells. In contrast, both VMAT2 and Leu-Enk were found in PNMT-negative noradrenergic cells, and VMAT2 was present in all noradrenergic chromaffin cells while Leu-Enk was observed in a subpopulation of noradrenergic chromaffin cells. In contrast to the normal adrenal but similar to our findings in human phaeochromocytoma, the pattern of marker expression within adrenal phaeochromocytoma lesions of MPC-injected mice are severely disrupted related to both the level of expression of the respective markers, and association with PNMT within the tissue. Thus, the experimentally generated phaeochromocytoma mouse model provides a valuable tool in studying human phaeochromocytoma.
The data presented in this thesis further validate the heterogeneity observed in many aspects of phaeochromocytoma tumour biology, including the expression several chromaffin cell markers such as NAT, NPY and CGA. The altered expression of these markers may contribute to the clinical picture of these tumours, particularly relating to hereditary phaeochromocytoma from VHL and MEN 2 disease.
7
Zhu, Jinghua. „The transformation of chromaffin cells into sympathetic neurons“. Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.386926.
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8
Robinson, Iain Martin. „Ca'2'+ signalling in bovine adrenal chromaffin cells“. Thesis, University of Liverpool, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.317281.
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9
Fisher, Richard James. „Amperometric analysis of exocytosis in adrenal chromaffin cells“. Thesis, University of Liverpool, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.367144.
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10
Powell, Andrew Dennis. „Modulation of neurotransmitter release from adrenal chromaffin cells“. Thesis, University of Bristol, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.310685.
Der volle Inhalt der QuelleBücher zum Thema "Chromaffin cells"
1
Borges, Ricardo, Hrsg. Chromaffin Cells. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-2671-9.
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2
Kurt, Rosenheck, und Lelkes Peter I, Hrsg. Stimulus-secretion coupling in chromaffin cells. Boca Raton, Fla: CRC Press, 1987.
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3
Christine, Heym, und Deutsche Forschungsgemeinschaft, Hrsg. Histochemistry and cell biology of autonomic neurons and paraganglia. Berlin: Springer-Verlag, 1987.
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4
(Editor), Daniel T. O'Connor, Hrsg. The Chromaffin Cell: Transmitter Biosynthesis, Storage, Release, Actions, and Informatics (Annals of the New York Academy of Sciences). New York Academy of Sciences, 2002.
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5
Borges, Ricardo. Chromaffin Cells: Methods and Protocols. Springer, 2022.
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6
Rosenheck, Kurt. Stimulus-Secretion Coupling in Chromaffin Cells, Vol. 1. CRC Press, 1987.
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7
Rosenheck, Kurt Ed. Stimulus-Secretion Coupling in Chromaffin Cells Volume 2. CRC Press, 1987.
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8
Jane, Knoth-Anderson, und United States. Environmental Protection Agency., Hrsg. Triphenyl phosphite-induced ultrastructural changes in bovine adrenomedullary chromaffin cells. [Washington, D.C: U.S. Environmental Protection Agency, 1992.
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9
Triphenyl phosphite-induced ultrastructural changes in bovine adrenomedullary chromaffin cells. [Washington, D.C: U.S. Environmental Protection Agency, 1992.
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10
Triphenyl phosphite-induced ultrastructural changes in bovine adrenomedullary chromaffin cells. [Washington, D.C: U.S. Environmental Protection Agency, 1992.
Den vollen Inhalt der Quelle findenBuchteile zum Thema "Chromaffin cells"
1
Fujita, Tsuneo, Tomio Kanno und Shigeru Kobayashi. „Adrenal Chromaffin Cells“. In The Paraneuron, 135–44. Tokyo: Springer Japan, 1988. http://dx.doi.org/10.1007/978-4-431-68066-6_12.
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2
Partoens, Peter, Dirk Slembrouck, Hilde De Busser, Peter F. T. Vaughan, Guido A. F. Van Dessel, Werner P. De Potter und Albert R. Lagrou. „Neurons, Chromaffin Cells and Membrane Fusion“. In Subcellular Biochemistry, 323–78. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/0-306-46824-7_9.
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3
Domínguez, Natalia, Miriam Rodríguez, J. David Machado und Ricardo Borges. „Preparation and Culture of Adrenal Chromaffin Cells“. In Neurotrophic Factors, 223–34. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-536-7_20.
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4
Morgan, Alan, Isabelle Cenci de Bello, Ulrich Weller, J. Oliver Dolly und Robert D. Burgoyne. „Intracellular Control of Exocytosis in Chromaffin Cells“. In Botulinum and Tetanus Neurotoxins, 95–104. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4757-9542-4_12.
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5
Thahouly, Tamou, Emeline Tanguy, Juliette Raherindratsara, Marie-France Bader, Sylvette Chasserot-Golaz, Stéphane Gasman und Nicolas Vitale. „Bovine Chromaffin Cells: and Fluorescence Assay for“. In Methods in Molecular Biology, 169–79. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-1044-2_11.
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6
Luján, Rafael, Rocío Alfaro-Ruiz und Carolina Aguado. „Immunogold for Protein Location in Chromaffin Cells“. In Methods in Molecular Biology, 57–75. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2671-9_5.
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7
de Pascual, Ricardo, Alicia Muñoz-Montero und Luis Gandía. „Real Time Recording of Perifused Chromaffin Cells“. In Methods in Molecular Biology, 105–12. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2671-9_8.
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8
O’sullivan, Antony J., und Robert D. Burgoyne. „Control of Exocytosis in Secretory Cells: the Adrenal Chromaffin Cell“. In Current Aspects of the Neurosciences, 191–218. London: Macmillan Education UK, 1990. http://dx.doi.org/10.1007/978-1-349-11922-6_7.
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9
Unsicker, K., R. Lietzke, D. Gehrke und F. Stögbauer. „Chromaffin Cells: A Novel Source for Neuronotrophic Factors“. In Histochemistry and Cell Biology of Autonomic Neurons and Paraganglia, 120–24. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-72749-8_21.
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10
Thompson, Roger J., und Colin A. Nurse. „O2-Chemosensitivity in Developing Rat Adrenal Chromaffin Cells“. In Oxygen Sensing, 601–9. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/0-306-46825-5_58.
Der volle Inhalt der QuelleKonferenzberichte zum Thema "Chromaffin cells"
1
Yaglov, Valentin Vasilyevich, Nataliya Valentinovna Yaglova, Dibakhan Aslanbekovna Tsomartova und Ekaterina Petrovna Timokhina. „CHANGES IN FINE STRUCTURE OF ADRENAL CHROMAFFIN CELLS AFTER DEVELOPMENTAL EXPOSURE TO ENDOCRINE DISRUPTER DDT“. In International conference New technologies in medicine, biology, pharmacology and ecology (NT +M&Ec ' 2020). Institute of information technology, 2020. http://dx.doi.org/10.47501/978-5-6044060-0-7.12.
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2
Souvannakitti, Dangjai, Guoxiang Yuan, Jayasri Nanduri, Ganesh K. Kumar, Aaron Fox und Nanduri R. Prabhakar. „Intermittent Hypoxia Activates Ryanodine Receptors (RyRs) Via S-glutathionylation In Neonatal Rat Adrenal Chromaffin Cells And Contributes To Augmented Catecholamines secretion“. In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2479.
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3
Wu, Hongxiu, Shunhui Wei, Anlian Qu und Zhuan Zhou. „Chromaffin cell calcium signal and morphology study based on multispectral images“. In International Symposium on Multispectral Image Processing, herausgegeben von Ji Zhou, Anil K. Jain, Tianxu Zhang, Yaoting Zhu, Mingyue Ding und Jianguo Liu. SPIE, 1998. http://dx.doi.org/10.1117/12.323594.
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