HOMEPRODUCTSCOMPANYCONTACTFAQResearchDictionaryPharmaSign Up FREE or Login

Prostaglandin E1, E2, and cholera toxin increase transcription of the brain creatine kinase gene in human U87 glioblastoma cells.

Abstract
The creatine kinase isoenzymes play an important role in maintaining ATP levels in some cell types during times of high energy demand. We have previously shown in primary cell cultures from rat brain that glial cells express much higher levels of brain creatine kinase (CKB) mRNA than neurons. In a separate earlier study we observed that transcription of CKB mRNA in glial cells can be stimulated by a forskolin-mediated increase in cAMP via a pathway involving protein kinase A (PKA). In this report, we show that the level of CKB mRNA in human U87 glioblastoma cells can be increased by either prostaglandin E1 (PGE1), prostaglandin E2 (PGE2), or cholera toxin (an activator of G alpha s proteins). The induction of CKB mRNA occurs rapidly (with maximal induction after 6 h), is at the level of transcription, and is mediated specifically through PKA. In addition, the results indicate that both PGE1 and PGE2 use the same or related signal transduction pathways to increase CKB transcription. These results suggest that in glial cells CKB mRNA can be regulated by extracellular signals acting through G-protein-coupled receptors. This study may contribute to an understanding of the mechanisms underlying the previously-reported, early postnatal increase in CKB enzyme activity in rat brain. The results are also discussed with regard to the potential involvement of the expression of prostaglandins and CKB during hypoxia and ischemia.
AuthorsE V Kuzhikandathil, G R Molloy
JournalGlia (Glia) Vol. 15 Issue 4 Pg. 471-9 (Dec 1995) ISSN: 0894-1491 [Print] United States
PMID8926040 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • RNA, Messenger
  • Cholera Toxin
  • Cyclic AMP-Dependent Protein Kinases
  • Protein Kinase C
  • Creatine Kinase
  • Alprostadil
  • Dinoprostone
Topics
  • Alprostadil (pharmacology)
  • Animals
  • Brain Chemistry (drug effects, genetics)
  • Brain Neoplasms (enzymology, genetics)
  • Cholera Toxin (pharmacology)
  • Creatine Kinase (biosynthesis, genetics)
  • Cyclic AMP-Dependent Protein Kinases (physiology)
  • Dinoprostone (pharmacology)
  • Glioblastoma (enzymology, genetics)
  • Humans
  • In Situ Hybridization
  • Protein Kinase C (physiology)
  • RNA, Messenger (biosynthesis)
  • Rats
  • Transcription, Genetic (drug effects)
  • Transfection (drug effects)
  • Tumor Cells, Cultured
  • Up-Regulation (drug effects)

Join CureHunter, for free Research Interface BASIC access!

Take advantage of free CureHunter research engine access to explore the best drug and treatment options for any disease. Find out why thousands of doctors, pharma researchers and patient activists around the world use CureHunter every day.
Realize the full power of the drug-disease research graph!


Choose Username:
Email:
Password:
Verify Password:
Enter Code Shown: