TY - JOUR
T1 - Interleukin-1β induces the expression of lipocortin 1 mRNA in cultured rat cortical astrocytes
AU - Miyachi, Taishi
AU - Asai, Kiyofumi
AU - Tsuiki, Hideki
AU - Mizuno, Haruo
AU - Yamamoto, Naoki
AU - Yokoi, Takashi
AU - Aoyama, Mineyoshi
AU - Togari, Hajime
AU - Wada, Yoshiro
AU - Miura, Yutaka
AU - Kato, Taiji
N1 - Funding Information:
This work was supported by a Grant-in-Aid for Scientific Research on Priority Area (B), a Grant-in-Aid for Scientific Research (B) and (C), the Ministry of Education, Science, Sports and Culture of Japan; and a Grant for Nervous and Mental Disorders from the Ministry of Health and Welfare of Japan.
PY - 2001
Y1 - 2001
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=0034744676&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0034744676&partnerID=8YFLogxK
U2 - 10.1016/S0168-0102(01)00208-5
DO - 10.1016/S0168-0102(01)00208-5
M3 - Article
C2 - 11311405
AN - SCOPUS:0034744676
SN - 0168-0102
VL - 40
SP - 53
EP - 60
JO - Neuroscience Research
JF - Neuroscience Research
IS - 1
ER -