Continuous stress promotes expression of VGF in melanotroph via suppression of dopamine

•VGF mRNA is induced in the intermediate lobe of pituitary under continuous stress (CS).•C-terminal peptide of VGF is induced in melanotroph under CS.•The CS-induced VGF expression is negatively regulated by dopamine. Prolonged exposure to stress elicits profound effects on homeostasis that may lead...

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Veröffentlicht in:Molecular and cellular endocrinology 2013-06, Vol.372 (1-2), p.49-56
Hauptverfasser: Tokizane, Kyohei, Konishi, Hiroyuki, Yasui, Masaya, Ogawa, Tokiko, Sasaki, Kazuki, Minamino, Naoto, Kiyama, Hiroshi
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container_issue 1-2
container_start_page 49
container_title Molecular and cellular endocrinology
container_volume 372
creator Tokizane, Kyohei
Konishi, Hiroyuki
Yasui, Masaya
Ogawa, Tokiko
Sasaki, Kazuki
Minamino, Naoto
Kiyama, Hiroshi
description •VGF mRNA is induced in the intermediate lobe of pituitary under continuous stress (CS).•C-terminal peptide of VGF is induced in melanotroph under CS.•The CS-induced VGF expression is negatively regulated by dopamine. Prolonged exposure to stress elicits profound effects on homeostasis that may lead to cryptogenic disorders such as chronic fatigue syndrome. To investigate the pathophysiology associated with the syndrome, we used a rat continuous stress (CS) model where the pituitary represents one of the most affected organs. Here we found that mRNA for VGF (non-acronymic), a member of the granin family, was induced specifically in the intermediate lobe (IL). This was matched by a concomitant increase at the peptide/protein level assessed by C-terminal antibody. Furthermore, the up-regulation of VGF was confirmed by immunohistochemistry in a subset of melanotrophs. VGF expression was altered in the IL of rats receivingthe dopamine D2 receptor agonist bromocriptine or the antagonist sulpiride. In vitro, dopamine dose-dependently decreased the mRNA levels in cultured melanotrophs. These findings suggest that VGF expression under CS is negatively regulated by dopaminergic neurons projecting from the hypothalamus.
doi_str_mv 10.1016/j.mce.2013.03.012
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Prolonged exposure to stress elicits profound effects on homeostasis that may lead to cryptogenic disorders such as chronic fatigue syndrome. To investigate the pathophysiology associated with the syndrome, we used a rat continuous stress (CS) model where the pituitary represents one of the most affected organs. Here we found that mRNA for VGF (non-acronymic), a member of the granin family, was induced specifically in the intermediate lobe (IL). This was matched by a concomitant increase at the peptide/protein level assessed by C-terminal antibody. Furthermore, the up-regulation of VGF was confirmed by immunohistochemistry in a subset of melanotrophs. VGF expression was altered in the IL of rats receivingthe dopamine D2 receptor agonist bromocriptine or the antagonist sulpiride. In vitro, dopamine dose-dependently decreased the mRNA levels in cultured melanotrophs. 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Prolonged exposure to stress elicits profound effects on homeostasis that may lead to cryptogenic disorders such as chronic fatigue syndrome. To investigate the pathophysiology associated with the syndrome, we used a rat continuous stress (CS) model where the pituitary represents one of the most affected organs. Here we found that mRNA for VGF (non-acronymic), a member of the granin family, was induced specifically in the intermediate lobe (IL). This was matched by a concomitant increase at the peptide/protein level assessed by C-terminal antibody. Furthermore, the up-regulation of VGF was confirmed by immunohistochemistry in a subset of melanotrophs. VGF expression was altered in the IL of rats receivingthe dopamine D2 receptor agonist bromocriptine or the antagonist sulpiride. In vitro, dopamine dose-dependently decreased the mRNA levels in cultured melanotrophs. 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Konishi, Hiroyuki ; Yasui, Masaya ; Ogawa, Tokiko ; Sasaki, Kazuki ; Minamino, Naoto ; Kiyama, Hiroshi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c410t-bac3ddf941fec3e3ac429c728b43cc53ef24c37cd815f6f8540dee1a53f950b13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>agonists</topic><topic>Animals</topic><topic>antagonists</topic><topic>antibodies</topic><topic>bromocriptine</topic><topic>Bromocriptine - pharmacology</topic><topic>Cells, Cultured</topic><topic>Cellular</topic><topic>Chronic fatigue syndrome</topic><topic>Chronic stress</topic><topic>Disorders</topic><topic>Dopamine</topic><topic>Dopamine - physiology</topic><topic>Dopamine Agonists - pharmacology</topic><topic>Dopamine Antagonists - pharmacology</topic><topic>Dopaminergic Neurons - metabolism</topic><topic>Fatigue (materials)</topic><topic>Gene Expression</topic><topic>homeostasis</topic><topic>Hypothalamus</topic><topic>Hypothalamus - cytology</topic><topic>Hypothalamus - metabolism</topic><topic>immunohistochemistry</topic><topic>Male</topic><topic>Melanotrophs - metabolism</topic><topic>messenger RNA</topic><topic>neurons</topic><topic>Neuropeptides - genetics</topic><topic>Neuropeptides - metabolism</topic><topic>pathophysiology</topic><topic>Peptides</topic><topic>Pituitary</topic><topic>Pituitary Gland, Intermediate - cytology</topic><topic>Pituitary Gland, Intermediate - drug effects</topic><topic>Pituitary Gland, Intermediate - metabolism</topic><topic>Primary Cell Culture</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receiving</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>Signal Transduction</topic><topic>Stress, Physiological</topic><topic>Stresses</topic><topic>Sulpiride - pharmacology</topic><topic>Transcriptional Activation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tokizane, Kyohei</creatorcontrib><creatorcontrib>Konishi, Hiroyuki</creatorcontrib><creatorcontrib>Yasui, Masaya</creatorcontrib><creatorcontrib>Ogawa, Tokiko</creatorcontrib><creatorcontrib>Sasaki, Kazuki</creatorcontrib><creatorcontrib>Minamino, Naoto</creatorcontrib><creatorcontrib>Kiyama, Hiroshi</creatorcontrib><collection>AGRIS</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Solid State and Superconductivity Abstracts</collection><collection>Technology Research Database</collection><collection>Advanced Technologies Database with Aerospace</collection><jtitle>Molecular and cellular endocrinology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tokizane, Kyohei</au><au>Konishi, Hiroyuki</au><au>Yasui, Masaya</au><au>Ogawa, Tokiko</au><au>Sasaki, Kazuki</au><au>Minamino, Naoto</au><au>Kiyama, Hiroshi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Continuous stress promotes expression of VGF in melanotroph via suppression of dopamine</atitle><jtitle>Molecular and cellular endocrinology</jtitle><addtitle>Mol Cell Endocrinol</addtitle><date>2013-06-15</date><risdate>2013</risdate><volume>372</volume><issue>1-2</issue><spage>49</spage><epage>56</epage><pages>49-56</pages><issn>0303-7207</issn><eissn>1872-8057</eissn><abstract>•VGF mRNA is induced in the intermediate lobe of pituitary under continuous stress (CS).•C-terminal peptide of VGF is induced in melanotroph under CS.•The CS-induced VGF expression is negatively regulated by dopamine. Prolonged exposure to stress elicits profound effects on homeostasis that may lead to cryptogenic disorders such as chronic fatigue syndrome. To investigate the pathophysiology associated with the syndrome, we used a rat continuous stress (CS) model where the pituitary represents one of the most affected organs. Here we found that mRNA for VGF (non-acronymic), a member of the granin family, was induced specifically in the intermediate lobe (IL). This was matched by a concomitant increase at the peptide/protein level assessed by C-terminal antibody. Furthermore, the up-regulation of VGF was confirmed by immunohistochemistry in a subset of melanotrophs. VGF expression was altered in the IL of rats receivingthe dopamine D2 receptor agonist bromocriptine or the antagonist sulpiride. In vitro, dopamine dose-dependently decreased the mRNA levels in cultured melanotrophs. These findings suggest that VGF expression under CS is negatively regulated by dopaminergic neurons projecting from the hypothalamus.</abstract><cop>Ireland</cop><pub>Elsevier Ireland Ltd</pub><pmid>23541636</pmid><doi>10.1016/j.mce.2013.03.012</doi><tpages>8</tpages></addata></record>
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subjects agonists
Animals
antagonists
antibodies
bromocriptine
Bromocriptine - pharmacology
Cells, Cultured
Cellular
Chronic fatigue syndrome
Chronic stress
Disorders
Dopamine
Dopamine - physiology
Dopamine Agonists - pharmacology
Dopamine Antagonists - pharmacology
Dopaminergic Neurons - metabolism
Fatigue (materials)
Gene Expression
homeostasis
Hypothalamus
Hypothalamus - cytology
Hypothalamus - metabolism
immunohistochemistry
Male
Melanotrophs - metabolism
messenger RNA
neurons
Neuropeptides - genetics
Neuropeptides - metabolism
pathophysiology
Peptides
Pituitary
Pituitary Gland, Intermediate - cytology
Pituitary Gland, Intermediate - drug effects
Pituitary Gland, Intermediate - metabolism
Primary Cell Culture
Rats
Rats, Sprague-Dawley
Receiving
RNA, Messenger - genetics
RNA, Messenger - metabolism
Signal Transduction
Stress, Physiological
Stresses
Sulpiride - pharmacology
Transcriptional Activation
title Continuous stress promotes expression of VGF in melanotroph via suppression of dopamine
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