Interleukin-1α induces corticotropin-releasing factor secretion and synthesis from NPLC-KC cells through various second messenger pathways

J. W. Kasckow, J. J. Mulcahey, J. H. Han, M. J. Owens, M. D. Stipetic, D. Breitman, Charles Nemeroff

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

Interleukin-1 (IL1) is a key messenger implicated in endocrine and immune systems that interact to mediate the stress response. Corticotropin-releasing factor (CRF) secretion and synthesis in the NPLC-KC human hepatoma cell line has been shown to respond to IL1 stimulation. We have studied how various inhibitors of second messenger pathways alter this IL1 effect. NPLC-KC cells were grown in six-well Costar plates and treated for 12 or 24 h with or without 500 pM IL1 (α form) in the presence of various inhibitors of second messenger pathways. Inhibitors included the protein kinase C (PKC) inhibitor, H-7; the protein kinase A inhibitor, IP20; or the cyclooxygenase inhibitor indomethacin (IND). Both cell extracts and secretion media were assayed for CRF-like immunoreactivity by radioimmunoassay. IP20, H-7, and IND all reduced basal CRF secretion at 24 h but not at 12 h. No effects were seen on basal CRF synthesis with these inhibitors. The three inhibitors also reduced IL1 effects on CRF secretion at 12 and 24 h. The reduction seen with all three inhibitors was statistically significant (P < 0.05) at 12 h. Although a reduction was seen with all three inhibitors at 24 h, a statistically significant reduction (P < 0.05) was demonstrable only for H-7. IL1 stimulated CRF synthesis in the NPLC-KC cells appears to only involve PKC pathways. Only the PKC inhibitor H-7 reduced the augmentation that IL1 produces on CRF synthesis. This effect was statistically significant at 12 and 24 h (P < 0.05).

Original languageEnglish
Pages (from-to)354-358
Number of pages5
JournalSynapse
Volume18
Issue number4
DOIs
StatePublished - Dec 7 1994
Externally publishedYes

Fingerprint

Corticotropin-Releasing Hormone
Second Messenger Systems
Interleukin-1
1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine
Protein Kinase Inhibitors
Protein Kinase C
Protein C Inhibitor
Indomethacin
Endocrine System
Cyclooxygenase Inhibitors
Cyclic AMP-Dependent Protein Kinases
Cell Extracts
Radioimmunoassay
Hepatocellular Carcinoma
Immune System
Cell Line

Keywords

  • Corticotropin-releasing factor
  • Cyclooxygenase
  • Interleukin 1
  • Protein kinase

ASJC Scopus subject areas

  • Neuroscience(all)
  • Physiology
  • Pharmacology

Cite this

Interleukin-1α induces corticotropin-releasing factor secretion and synthesis from NPLC-KC cells through various second messenger pathways. / Kasckow, J. W.; Mulcahey, J. J.; Han, J. H.; Owens, M. J.; Stipetic, M. D.; Breitman, D.; Nemeroff, Charles.

In: Synapse, Vol. 18, No. 4, 07.12.1994, p. 354-358.

Research output: Contribution to journalArticle

Kasckow, J. W. ; Mulcahey, J. J. ; Han, J. H. ; Owens, M. J. ; Stipetic, M. D. ; Breitman, D. ; Nemeroff, Charles. / Interleukin-1α induces corticotropin-releasing factor secretion and synthesis from NPLC-KC cells through various second messenger pathways. In: Synapse. 1994 ; Vol. 18, No. 4. pp. 354-358.
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