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Arg-Phe-amide-related peptides influence gonadotropin-releasing hormone neurons(star.)

Kelestimur, Haluk; Kacar, Emine; Uzun, Aysegul; Ozcan, Mete; Kutlu, Selim


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  <identifier identifierType="URL">https://aperta.ulakbim.gov.tr/record/12881</identifier>
  <creators>
    <creator>
      <creatorName>Kelestimur, Haluk</creatorName>
      <givenName>Haluk</givenName>
      <familyName>Kelestimur</familyName>
      <affiliation>Firat Univ, Sch Med, Dept Physiol, TR-23119 Elazig, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Kacar, Emine</creatorName>
      <givenName>Emine</givenName>
      <familyName>Kacar</familyName>
      <affiliation>Firat Univ, Sch Med, Dept Physiol, TR-23119 Elazig, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Uzun, Aysegul</creatorName>
      <givenName>Aysegul</givenName>
      <familyName>Uzun</familyName>
      <affiliation>Karadeniz Tech Univ, Sch Med, Dept Biochem, Elazig, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Ozcan, Mete</creatorName>
      <givenName>Mete</givenName>
      <familyName>Ozcan</familyName>
      <affiliation>Firat Univ, Sch Med, Dept Biophys, TR-23119 Elazig, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Kutlu, Selim</creatorName>
      <givenName>Selim</givenName>
      <familyName>Kutlu</familyName>
      <affiliation>Firat Univ, Sch Med, Dept Physiol, TR-23119 Elazig, Turkey</affiliation>
    </creator>
  </creators>
  <titles>
    <title>Arg-Phe-Amide-Related Peptides Influence Gonadotropin-Releasing Hormone Neurons(Star.)</title>
  </titles>
  <publisher>Aperta</publisher>
  <publicationYear>2013</publicationYear>
  <dates>
    <date dateType="Issued">2013-01-01</date>
  </dates>
  <resourceType resourceTypeGeneral="Text">Journal article</resourceType>
  <alternateIdentifiers>
    <alternateIdentifier alternateIdentifierType="url">https://aperta.ulakbim.gov.tr/record/12881</alternateIdentifier>
  </alternateIdentifiers>
  <relatedIdentifiers>
    <relatedIdentifier relatedIdentifierType="DOI" relationType="IsIdenticalTo">10.3969/j.issn.1673-5374.2013.18.009</relatedIdentifier>
  </relatedIdentifiers>
  <rightsList>
    <rights rightsURI="http://www.opendefinition.org/licenses/cc-by">Creative Commons Attribution</rights>
    <rights rightsURI="info:eu-repo/semantics/openAccess">Open Access</rights>
  </rightsList>
  <descriptions>
    <description descriptionType="Abstract">The hypothalamic Arg-Phe-amide-related peptides, gonadotropin-inhibitory hormone and orthologous mammalian peptides of Arg-Phe-amide, may be important regulators of the hypothalamus-pituitary-gonadal reproductive axis. These peptides may modulate the effects of kisspeptins because they are presently recognized as the most potent activators of the hypothalamus-pituitary-gonadal axis. However, their effects on gonadotropin-releasing hormone neurons have not been investigated. In the current study, the GT1-7 cell line-expressing gonadotropin-releasing hormone was used as a model to explore the effects of Arg-Phe-amide-related peptides on kisspeptin activation. Intracellular calcium concentration was quantified using the calcium-sensitive dye, fura-2 acetoxymethyl ester. Gonadotropin-releasing hormone released into the medium was detected via enzyme-linked immunosorbent assay. Results showed that 100 nmol/L kisspeptin-10 significantly increased gonadotropin-releasing hormone levels (at 120 minutes of exposure) and intracellular calcium concentrations. Co-treatment of kisspeptin with 1 mu mol/L gonadotropin-inhibitory hormone or 1 mu mol/L Arg-Phe-amide-related peptide-1 significantly attenuated levels of kisspeptin-induced gonadotropin-releasing hormone but did not affect kisspeptin-induced elevations of intracellular calcium concentration. Overall, the results suggest that gonadotropin-inhibitory hormone and Arg-Phe-amide-related peptide-1 may have inhibitory effects on kisspeptin-activated gonadotropin-releasing hormone neurons independent of the calcium signaling pathway.</description>
  </descriptions>
</resource>
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