TY - JOUR
T1 - Multifunctional effects of bradykinin on glial cells in relation to potential anti-inflammatory effects
AU - Noda, Mami
AU - Sasaki, Kenjiro
AU - Ifuku, Masataka
AU - Wada, Keiji
N1 - Funding Information:
We thank Prof. D.A. Brown (University College London, UK) for valuable suggestions. We also thank Prof. H. Kettenmann, Drs. K. Färber, and L. Wang (Max-Delbrück Center for Molecular Medicine, Berlin, Germany) for experimental help and useful comments. This work was supported by Grants-in Aid for Scientific Research of Japan Society for Promotion of Science, and Research Grant in Priority Area Research of the Ministry of Education, Culture, Sports, Science and Technology, Japan.
PY - 2007/7
Y1 - 2007/7
N2 - Kinins have been reported to be produced and act at the site of injury and inflammation. Despite many reports that they are likely to initiate a particular cascade of inflammatory events, bradykinin (BK) has anti-inflammatory effects in the brain mediated by glial cells. In the present review, we have attempted to describe the complex responses and immediate reaction of glial cells to BK. Glial cells express BK receptors and induce Ca2+-dependent signal cascades. Among them, production of prostaglandin E2 (PGE2), via B1 receptors in primary cultured microglia, has a negative feedback effect on lipopolysaccharide (LPS)-induced release of tumor necrosis factor-α (TNF-α) via increasing intracellular cyclic adenosine monophosphate (cAMP). In addition, BK up-regulates the production of neurotrophic factors such as nerve growth factor (NGF) via B2 receptors in astrocytes. These results suggest that BK may have anti-inflammatory and neuroprotective effects in the brain through multiple functions on glial cells. These observations may help to understand the paradox on the role of kinins in the central nervous system and may be useful for therapeutic strategy.
AB - Kinins have been reported to be produced and act at the site of injury and inflammation. Despite many reports that they are likely to initiate a particular cascade of inflammatory events, bradykinin (BK) has anti-inflammatory effects in the brain mediated by glial cells. In the present review, we have attempted to describe the complex responses and immediate reaction of glial cells to BK. Glial cells express BK receptors and induce Ca2+-dependent signal cascades. Among them, production of prostaglandin E2 (PGE2), via B1 receptors in primary cultured microglia, has a negative feedback effect on lipopolysaccharide (LPS)-induced release of tumor necrosis factor-α (TNF-α) via increasing intracellular cyclic adenosine monophosphate (cAMP). In addition, BK up-regulates the production of neurotrophic factors such as nerve growth factor (NGF) via B2 receptors in astrocytes. These results suggest that BK may have anti-inflammatory and neuroprotective effects in the brain through multiple functions on glial cells. These observations may help to understand the paradox on the role of kinins in the central nervous system and may be useful for therapeutic strategy.
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U2 - 10.1016/j.neuint.2007.06.017
DO - 10.1016/j.neuint.2007.06.017
M3 - Review article
C2 - 17669557
AN - SCOPUS:34547485957
SN - 0197-0186
VL - 51
SP - 185
EP - 191
JO - Neurochemistry International
JF - Neurochemistry International
IS - 2-4 SPEC. ISS.
ER -