Interleukin-1β induces the expression of lipocortin 1 mRNA in cultured rat cortical astrocytes

Taishi Miyachi, Kiyofumi Asai, Hideki Tsuiki, Haruo Mizuno, Naoki Yamamoto, Takashi Yokoi, Mineyoshi Aoyama, Hajime Togari, Yoshiro Wada, Yutaka Miura, Taiji Kato

Research output: Contribution to journalArticlepeer-review

31 Citations (Scopus)


Lipocortin 1 (LC1) has been shown to increase in neuronal damage and act as a neuroprotectant and a neurotrophic factor. IL-1β acts as a mediator of inflammation and has been reported as a potent inducer of various neurotrophic factors including nerve growth factor and fibroblast growth factor. In this study, we investigated the relationship between LC1 and IL-1β in cultured rat astrocytes. Time-and dose-dependent experiments of IL-1β on rat cortical astrocytes in culture revealed that the expression of LC1 mRNA was significantly augmented by IL-1β at 8 h, 10 ng/ml. In addition, IL-1β evoked an extracellular secretion of LC1 without its cytotoxic effects. The effect of IL-1β was completely abolished when we treated cells with inhibitor of mitogen-activated protein kinases (MAPKs) (PD98059) (25 μM), phospholipase A2 inhibitor mepacrine (30 μM) and protein synthesis inhibitor cycloheximide (CHX) (10 μg/ml). This suggests that induction of LC1 by IL-1β is through a MAPKs and phospholipaseA2 pathway and requires protein synthesis. These results indicate that IL-1β released in the central nervous system (CNS) injury can stimulate the transcription of the LC1 gene. Subsequent synthesis and release of LC1 may provide trophic support to neurons and modulate the action of IL-1β in brain damage.

Original languageEnglish
Pages (from-to)53-60
Number of pages8
JournalNeuroscience Research
Issue number1
Publication statusPublished - 2001
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)


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