C-type natriuretic peptide stimulates function of the murine Sertoli cells via activation of the NPR-B/cGMP/PKG signaling pathway.

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  • Additional Information
    • Source:
      Publisher: Panstwowe Wydawnictwo Naukowe Country of Publication: Poland NLM ID: 14520300R Publication Model: Print Cited Medium: Internet ISSN: 1734-154X (Electronic) Linking ISSN: 0001527X NLM ISO Abbreviation: Acta Biochim Pol Subsets: MEDLINE
    • Publication Information:
      Publication: Warszawa : Panstwowe Wydawnictwo Naukowe
      Original Publication: Warszawa.
    • Subject Terms:
      Cyclic GMP/*metabolism ; Cyclic GMP-Dependent Protein Kinases/*metabolism ; Natriuretic Peptide, C-Type/*metabolism ; Receptors, Atrial Natriuretic Factor/*metabolism ; Sertoli Cells/*drug effects ; Signal Transduction/*drug effects; Androgen-Binding Protein/genetics ; Animals ; Male ; Mice ; RNA, Messenger/genetics ; Rats ; Rats, Sprague-Dawley ; Sertoli Cells/metabolism ; Testis/metabolism ; Transferrin/genetics
    • Abstract:
      C-type natriuretic peptide (CNP) is an important regulator of the male reproductive process. Our previous investigations showed that CNP can significantly stimulate the mRNA expression of androgen-binding protein (Abp) and transferrin (Trf) in the rat Sertoli cells, but the pathways responsible for this process remain to be elucidated. We predict that CNP binds the natriuretic peptide receptor B (NPR-B) to regulate expression of ABP and TRF through the intracellular cyclic guanosine monophosphate (cGMP) pathway. To address this question, in this study, we first confirmed the expression and localization of CNP and NPR-B in rat testes by immunohistochemistry and western blotting. Then, ELISA and real-time PCR were performed to investigate the signaling pathway of CNP in Sertoli cells in rat testes. Our results showed that CNP was mainly localized in the germ cells and Leydig cells, and its receptor, NPR-B, was mostly expressed in the Sertoli cells and vascular endothelial cells. CNP supplementation in the Sertoli cell medium was accompanied by an increase in the amount of intracellular cGMP and in the production of Abp and Trf mRNA, whereas inhibition of PKG with KT5823 led to a decrease in the expression of Abp and Trf mRNA. Moreover, Abp and Trf mRNA were no longer elevated when we used liposome-mediated RNA interference technology to silence the NPR-B gene in a mouse Sertoli cell line (TM4). These results suggest that CNP contributes to the regulation of ABP and TRF in the Sertoli cells through the NPR-B/cGMP/PKG signaling pathways.
    • Accession Number:
      0 (Androgen-Binding Protein)
      0 (RNA, Messenger)
      0 (Transferrin)
      127869-51-6 (Natriuretic Peptide, C-Type)
      EC 2.7.11.12 (Cyclic GMP-Dependent Protein Kinases)
      EC 4.6.1.2 (Receptors, Atrial Natriuretic Factor)
      EC 4.6.1.2 (atrial natriuretic factor receptor B)
      H2D2X058MU (Cyclic GMP)
    • Publication Date:
      Date Created: 20210708 Date Completed: 20220318 Latest Revision: 20220318
    • Publication Date:
      20240829
    • Accession Number:
      10.18388/abp.2020_5442
    • Accession Number:
      34237204