Database : MEDLINE
Search on : adrenal and medulla [Words]
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[PMID]: 29077837
[Au] Autor:Li AJ; Wang Q; Ritter S
[Ad] Address:Programs in Neuroscience, Washington State University, Pullman, Washington 99164-7620, USA.
[Ti] Title:Selective pharmacogenetic activation of catecholamine subgroups in the ventrolateral medulla elicits key glucoregulatory responses.
[So] Source:Endocrinology;, 2017 Oct 24.
[Is] ISSN:1945-7170
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Catecholamine (CA) neurons in the ventrolateral medulla (VLM) contribute importantly to glucoregulation during glucose deficit. However, it is not known which CA neurons elicit different glucoregulatory responses or whether selective activation of CA neurons is sufficient to elicit these responses. Therefore, to selectively activate CA subpopulations, we injected male or female Th-Cre+ transgenic rats with the Cre-dependent DREADD construct, AAV2-DIO-hSyn-hM3D(Gq)-mCherry, at one of 4 rostrocaudal levels of the VLM: rostral C1 (C1r), middle C1 (C1m), the area of A1 and C1 overlap (A1/C1) or A1. Transfection was highly selective for CA neurons at each site. Systemic injection of the DREADD receptor agonist, clozapine-N-oxide (CNO), stimulated feeding in rats transfected at C1r, C1m or A1/C1, but not A1. CNO increased corticosterone secretion in rats transfected at C1m or A1/C1, but not A1. In contrast, CNO did not increase blood glucose or induce c-Fos expression in the spinal cord or adrenal medulla after transfection of any single VLM site, but required dual transfection of both C1m and C1r, possibly indicating that CA neurons mediating blood glucose responses are more sparsely distributed in C1r and C1m than those mediating feeding and corticosterone secretion. Results show that selective activation of C1 CA neurons is sufficient to increase feeding, blood glucose and corticosterone secretion and suggest that each of these responses is mediated by CA neurons concentrated at different levels of the C1 cell group.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1710
[Cu] Class update date: 171027
[Lr] Last revision date:171027
[St] Status:Publisher
[do] DOI:10.1210/en.2017-00630

  2 / 12039 MEDLINE  
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[PMID]: 28993160
[Au] Autor:Zhang Y; Wang K; Lin M; Li Q; Hong Y
[Ad] Address:Provincial Key Laboratory of Developmental Biology and Neuroscience, Fujian Normal University, Fuzhou, Fujian 350117, China.
[Ti] Title:Inhibition of morphine tolerance by MrgC receptor via modulation of interleukin-1ß and matrix metalloproteinase 9 in dorsal root ganglia in rats.
[So] Source:Eur J Pharmacol;815:10-17, 2017 Nov 15.
[Is] ISSN:1879-0712
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Opiate tolerance is a critical issue in pain management. Previous studies show that activation of Mas-related gene (Mrg) C receptor can modulate the development of morphine tolerance. This study was designed to investigate the underlying mechanism(s). Intrathecal (i.t.) administration of morphine (20µg) increased the expression of interleukin-1ß (IL-1ß) and matrix metalloproteinase-9 (MMP-9) in small- and medium-sized neurons in dorsal root ganglia (DRG). Co-administration of bovine adrenal medulla 8-22 (BAM8-22), a selective MrgC receptor agonist, via i.t. route inhibited the increase of IL-1ß and MMP-9 in the DRG. Exposure of DRG cultures to morphine (3.3µM) for 3 or 5 days, but not for 1 day, induced an increase in MMP-9 mRNA expression. The treatment with BAM8-22 (10nM) for 20, 40 or 60min abolished chronic (5 days) morphine-induced increase of MMP-9 mRNA in the cultured DRG. The treatment with BAM8-22 for 1h inhibited chronic morphine-induced increase of MMP-9 and IL-1ß mRNA in DRG but these effects were abolished by MrgC receptor antibody. The treatment with BAM8-22 for 24 and 72h respectively inhibited and enhanced morphine-induced expression of MMP-9 and IL-1ß mRNA in the cultured DRG. The BAM8-22-induced inhibition and enhancement were abolished by MrgC receptor antibody. The results suggest that the inhibition of IL-1ß and MMP-9 expressions in DRG underlain the modulation of morphine tolerance by the acute activation of MrgC receptors. The chronic activation of MrgC receptors can facilitate morphine-induced increase of MMP-9 and IL-1ß expressions in DRG.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1710
[Cu] Class update date: 171028
[Lr] Last revision date:171028
[St] Status:In-Process

  3 / 12039 MEDLINE  
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[PMID]: 28916336
[Au] Autor:De Jonghe S; Johnson MD; Mamidi RNVS; Vinken P; Feyen B; Lammens G; Proctor J
[Ad] Address:Janssen Research & Development, A Division of Janssen Pharmaceutica NV, Turnhoutseweg 30, B-2340 Beerse, Belgium. Electronic address: sdjonghe@its.jnj.com.
[Ti] Title:Renal tubular and adrenal medullary tumors in the 2-year rat study with canagliflozin confirmed to be secondary to carbohydrate (glucose) malabsorption in the 15-month mechanistic rat study.
[So] Source:Chem Biol Interact;277:85-90, 2017 Nov 01.
[Is] ISSN:1872-7786
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:During preclinical development of canagliflozin, an SGLT2 inhibitor, treatment-related pheochromocytomas, renal tubular tumors (RTT), and testicular Leydig cell tumors were reported in the 2-year rat toxicology study. In a previous 6-month rat mechanistic study, feeding a glucose free diet prevented canagliflozin effects on carbohydrate malabsorption as well as the increase in cell proliferation in adrenal medulla and kidneys, implicating carbohydrate malabsorption as the mechanism for tumor formation. In this chronic study male Sprague-Dawley rats were dosed orally with canagliflozin at high dose-levels (65 or 100 mg/kg/day) for 15 months and received either a standard diet or a glucose-free diet. Canagliflozin-dosed rats on standard diet showed presence of basophilic renal tubular tumors (6/90) and an increased incidence of adrenal medullary hyperplasia (35/90), which was fully prevented by feeding a glucose-free diet (no RTT's; adrenal medullary hyperplasia in ≤5/90). These data further confirm that kidney and adrenal medullary tumors in the 2-year rat study were secondary to carbohydrate (glucose) malabsorption and were not due to a direct effect of canagliflozin on these target tissues.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1709
[Cu] Class update date: 171026
[Lr] Last revision date:171026
[St] Status:In-Process

  4 / 12039 MEDLINE  
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[PMID]: 28731378
[Au] Autor:Okada H; Masujin K; Miyazawa K; Iwamaru Y; Imamura M; Matsuura Y; Arai S; Fukuda S; Murayama Y; Yokoyama T
[Ad] Address:1 National Institute of Animal Health, National Agriculture and Food Research Organization (NARO), Tsukuba, Ibaraki, Japan.
[Ti] Title:Experimental Infection of Cattle With a Novel Prion Derived From Atypical H-Type Bovine Spongiform Encephalopathy.
[So] Source:Vet Pathol;54(6):892-900, 2017 Nov.
[Is] ISSN:1544-2217
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:H-type bovine spongiform encephalopathy (H-BSE) is an atypical form of BSE in cattle. During passaging of H-BSE in transgenic bovinized (TgBoPrP) mice, a novel phenotype of BSE, termed BSE-SW emerged and was characterized by a short incubation time and host weight loss. To investigate the biological and biochemical properties of the BSE-SW prion, a transmission study was conducted in cattle, which were inoculated intracerebrally with brain homogenate from BSE-SW-infected TgBoPrP mice. The disease incubation period was approximately 15 months. The animals showed characteristic neurological signs of dullness, and severe spongiform changes and a widespread, uniform distribution of disease-associated prion protein (PrP ) were observed throughout the brain of infected cattle. Immunohistochemical PrP staining of the brain revealed the presence of intraglial accumulations and plaque-like deposits. No remarkable differences were identified in vacuolar lesion scores, topographical distribution patterns, and staining types of PrP in the brains of BSE-SW- vs H-BSE-infected cattle. PrP deposition was detected in the ganglia, vagus nerve, spinal nerve, cauda equina, adrenal medulla, and ocular muscle. Western blot analysis revealed that the specific biochemical properties of the BSE-SW prion, with an additional 10- to 12-kDa fragment, were well maintained after transmission. These findings indicated that the BSE-SW prion has biochemical properties distinct from those of H-BSE in cattle, although clinical and pathologic features of BSW-SW in cattle are indistinguishable from those of H-BSE. The results suggest that the 2 infectious agents, BSE-SW and H-BSE, are closely related strains.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1707
[Cu] Class update date: 171025
[Lr] Last revision date:171025
[St] Status:In-Process
[do] DOI:10.1177/0300985817717769

  5 / 12039 MEDLINE  
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[PMID]: 28223516
[Au] Autor:Li Z; Tseng PY; Tiwari V; Xu Q; He SQ; Wang Y; Zheng Q; Han L; Wu Z; Blobaum AL; Cui Y; Tiwari V; Sun S; Cheng Y; Huang-Lionnet JH; Geng Y; Xiao B; Peng J; Hopkins C; Raja SN; Guan Y; Dong X
[Ad] Address:The Solomon H. Snyder Department of Neuroscience, Center for Sensory Biology, Johns Hopkins University School of Medicine, Baltimore, MD 21205.
[Ti] Title:Targeting human Mas-related G protein-coupled receptor X1 to inhibit persistent pain.
[So] Source:Proc Natl Acad Sci U S A;114(10):E1996-E2005, 2017 Mar 07.
[Is] ISSN:1091-6490
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Human Mas-related G protein-coupled receptor X1 (MRGPRX1) is a promising target for pain inhibition, mainly because of its restricted expression in nociceptors within the peripheral nervous system. However, constrained by species differences across , drug candidates that activate MRGPRX1 do not activate rodent receptors, leaving no responsive animal model to test the effect on pain in vivo. Here, we generated a transgenic mouse line in which we replaced mouse with human This humanized mouse allowed us to characterize an agonist [bovine adrenal medulla 8-22 (BAM8-22)] and a positive allosteric modulator (PAM), ML382, of MRGPRX1. Cellular studies suggested that ML382 enhances the ability of BAM8-22 to inhibit high-voltage-activated Ca channels and attenuate spinal nociceptive transmission. Importantly, both BAM8-22 and ML382 effectively attenuated evoked, persistent, and spontaneous pain without causing obvious side effects. Notably, ML382 by itself attenuated both evoked pain hypersensitivity and spontaneous pain in mice after nerve injury without acquiring coadministration of an exogenous agonist. Our findings suggest that humanized mice provide a promising preclinical model and that activating MRGPRX1 is an effective way to treat persistent pain.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1702
[Cu] Class update date: 171024
[Lr] Last revision date:171024
[St] Status:In-Data-Review
[do] DOI:10.1073/pnas.1615255114

  6 / 12039 MEDLINE  
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[PMID]: 29058015
[Au] Autor:Becker J; Wilting J
[Ad] Address:Institute of Anatomy and Cell Biology, University Medical School Göttingen, 37075, Göttingen, Germany. juergen.becker@med.uni-goettingen.de.
[Ti] Title:WNT signaling, the development of the sympathoadrenal-paraganglionic system and neuroblastoma.
[So] Source:Cell Mol Life Sci;, 2017 Oct 22.
[Is] ISSN:1420-9071
[Cp] Country of publication:Switzerland
[La] Language:eng
[Ab] Abstract:Neuroblastoma (NB) is a tumor of the sympathoadrenal system arising in children under 15 years of age. In Germany, NB accounts for 7% of childhood cancer cases, but 11% of cancer deaths. It originates from highly migratory progenitor cells that leave the dorsal neural tube and contribute neurons and glial cells to sympathetic ganglia, and chromaffin and supportive cells to the adrenal medulla and paraganglia. Clinically, histologically and molecularly, NBs present as extremely heterogeneous, ranging from very good to very poor prognosis. The etiology of NB still remains unclear and needs to be elucidated, however, aberrant auto- and paracrine embryonic cell communications seem to be likely candidates to initiate or facilitate the emergence, progression and regression of NB. The wingless-type MMTV integration site (WNT) family of proteins represents an evolutionary highly conserved signaling system that orchestrates embryogenesis. At least 19 ligands in the human, numerous receptors and co-receptors are known, which control not only proliferation, but also cell polarity, migration and differentiation. Here we seek to interconnect aspects of WNT signaling with sympathoadrenal and paraganglionic development to define new WNT signaling cues in the etiology and progression of NB.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1710
[Cu] Class update date: 171023
[Lr] Last revision date:171023
[St] Status:Publisher
[do] DOI:10.1007/s00018-017-2685-8

  7 / 12039 MEDLINE  
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[PMID]: 29052004
[Au] Autor:Nurse CA; Salman S; Scott AL
[Ad] Address:Department of Biology and Molecular Medicine, McMaster University, 1280 Main St. West, Hamilton, ON, L8S 4K1, Canada. nursec@mcmaster.ca.
[Ti] Title:Hypoxia-regulated catecholamine secretion in chromaffin cells.
[So] Source:Cell Tissue Res;, 2017 Oct 19.
[Is] ISSN:1432-0878
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:Adrenal catecholamine (CAT) secretion is a general physiological response of animals to environmental stressors such as hypoxia. This represents an important adaptive mechanism to maintain homeostasis and protect vital organs such as the brain. In adult mammals, CAT secretory responses are triggered by activation of the sympathetic nervous system that supplies cholinergic innervation of adrenomedullary chromaffin cells (AMC) via the splanchnic nerve. In the neonate, the splanchnic innervation of AMC is immature or absent, yet hypoxia stimulates a non-neurogenic CAT secretion that is critical for adaptation to extra-uterine life. This non-neurogenic, hypoxia-sensing mechanism in AMC is gradually lost or suppressed postnatally along a time course that parallels the development of splanchnic innervation. Moreover, denervation of adult AMC results in a gradual return of the direct hypoxia-sensing mechanism. The signaling pathways by which neonatal AMC sense acute hypoxia leading to non-neurogenic CAT secretion and the mechanisms that underlie the re-acquisition of hypoxia-sensing properties by denervated adult AMC, are beginning to be understood. This review will focus on current views concerning the mechanisms responsible for direct acute hypoxia sensing and CAT secretion in perinatal AMC and how they are regulated by innervation during postnatal development. It will also briefly discuss plasticity mechanisms likely to contribute to CAT secretion during exposures to chronic and intermittent hypoxia.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1710
[Cu] Class update date: 171020
[Lr] Last revision date:171020
[St] Status:Publisher
[do] DOI:10.1007/s00441-017-2703-z

  8 / 12039 MEDLINE  
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[PMID]: 29030614
[Au] Autor:Aravindan S; Somasundaram DB; Kam KL; Subramanian K; Yu Z; Herman TS; Fung KM; Aravindan N
[Ad] Address:Stephenson Cancer Center, Oklahoma City, OK, USA.
[Ti] Title:Retinal Degeneration Protein 3 (RD3) in normal human tissues: Novel insights.
[So] Source:Sci Rep;7(1):13154, 2017 Oct 13.
[Is] ISSN:2045-2322
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:The 195-amino-acid-long human Retinal Degeneration Protein 3 (RD3) is critical in the regulation of guanylate cyclase (GC) signaling and photoreceptor cell survival. Recently, we identified significant loss of RD3 in high-risk neuroblastoma and the influential role of RD3 in tumor progression. However, the functional characterization of RD3 in tumor systems has been hampered by the dearth of information on its localization in normal tissue and by the lack of antibodies suitable for staining FFPE tissue, primarily due to the inaccessibility of the epitopes. In this study, we validated a custom-synthesized RD3 antibody and investigated the expression/localization of RD3 in assorted human tissues. We observed stratified expression of RD3 in different cell types and subcellular location of retina. We demonstrated extensive positive RD3 immunoreactivity in various normal tissues and particularly strong dot-like perinuclear staining in the lining epithelial cells, suggesting that RD3 may play an important role in the normal functioning of epithelial cells. RD3 expression is limited in the CNS. While neuroblastoma is often RD3-positive, the adrenal medulla, where many neuroblastomas originate, is RD3-negative. Meta-analysis of RD3 transcriptional expression across normal tissues confirmed tissue-specific RD3 mRNA levels. Our results revealed the tissue-specific expression/localization profile of RD3 for the first time.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1710
[Cu] Class update date: 171020
[Lr] Last revision date:171020
[St] Status:In-Data-Review
[do] DOI:10.1038/s41598-017-13337-9

  9 / 12039 MEDLINE  
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[PMID]: 28684471
[Au] Autor:Furlan A; Dyachuk V; Kastriti ME; Calvo-Enrique L; Abdo H; Hadjab S; Chontorotzea T; Akkuratova N; Usoskin D; Kamenev D; Petersen J; Sunadome K; Memic F; Marklund U; Fried K; Topilko P; Lallemend F; Kharchenko PV; Ernfors P; Adameyko I
[Ad] Address:Unit of Molecular Neurobiology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, 17177 Stockholm, Sweden.
[Ti] Title:Multipotent peripheral glial cells generate neuroendocrine cells of the adrenal medulla.
[So] Source:Science;357(6346), 2017 07 07.
[Is] ISSN:1095-9203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract: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.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Em] Entry month:1707
[Cu] Class update date: 171018
[Lr] Last revision date:171018
[St] Status:In-Process

  10 / 12039 MEDLINE  
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[PMID]: 29030008
[Au] Autor:Roman A; Kusmierczyk J; Kreiner G; Nalepa I
[Ad] Address:Institute of Pharmacology, Polish Academy of Sciences, Department of Brain Biochemistry, 31-343 Kraków, Smetna Street 12, Poland. Electronic address: roman@if-pan.krakow.pl.
[Ti] Title:Assessment of leukocyte activity in mice devoid of the glucocorticoid receptor in the noradrenergic system (GR ).
[So] Source:Immunobiology;, 2017 Oct 08.
[Is] ISSN:1878-3279
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Disturbances in brain monoamines, overactivity of the hypothalamo-pituitary adrenal (HPA) axis and pro-inflammatory tendency in the immune system are the key features of depressive disorders. Recently, several murine lines with mutations in glucocorticoid receptors (GRs) have been generated and these animals may be utilized for study depressive-like disorders. In the present study, we have investigated whether selective ablation of GRs in noradrenergic neurons affects functional properties of leukocytes and redirects them towards pro-inflammatory activity. Transgenic mice selectively devoid of GRs on noradrenergic cells were constructed using the Cre/loxP approach. Peritoneal leukocytes were collected from mutant and wild type (WT) animals of both sexes and were cultured in vitro for 24h both in basal conditions and after application of selected pro- or anti-inflammatory stimuli. Metabolic activity and adherence were measured in basal conditions. Nitric oxide (NO) synthesis and arginase (ARG) activity were assessed as the markers of functional status of the cells. Because adult mutant mice lack adrenal medulla and thereby peripheral adrenaline, we modulated pro- and anti-inflammatory culture conditions by addition of noradrenaline (10-6M). Finally, effects of in vivo pro-inflammatory challenge (with intraperitoneal administration of lipopolysaccharide) on properties of leukocytes were assessed 24h (in both sexes) and 48h later (in males only). The experiments indicated that selective ablation of GR in noradrenergic neurons did not affect fundamental properties of peritoneal leukocytes and exerted effects only under conditions of selected pro- or anti-inflammatory stimuli in vitro. Stronger response to pro-inflammatory stimulation in terms of NO synthesis and ARG activity may suggest pro-inflammatory tendency in mutant mice. In vivo inflammatory challenge failed to show any effect of GR ablation on selected parameters of leukocyte activity. Both in vitro studies and in vivo challenge revealed mainly sex-related differences in leukocyte activity.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1710
[Cu] Class update date: 171014
[Lr] Last revision date:171014
[St] Status:Publisher


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