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Neuroprotective role of bradykinin because of the attenuation of pro-inflammatory cytokine release from activated microglia.
J Neurochem. 2007 Apr; 101(2):397-410.JN

Abstract

Bradykinin (BK) has been reported to be a mediator of brain damage in acute insults. Receptors for BK have been identified on microglia, the pathologic sensors of the brain. Here, we report that BK attenuated lipopolysaccharide (LPS)-induced release of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta from microglial cells, thus acting as an anti-inflammatory mediator in the brain. This effect was mimicked by raising intracellular cAMP or stimulating the prostanoid receptors EP2 and EP4, while it was abolished by a cAMP antagonist, a prostanoid receptor antagonist, or by an inhibitor of the inducible cyclooxygenase (cyclooxygenase-2). BK also enhanced formation of prostaglandin E(2) and expression of microsomal prostaglandin E synthase. Expression of BK receptors and EP2/EP4 receptors were also enhanced. Using physiological techniques, we identified functional BK receptors not only in culture, but also in microglia from acute brain slices. BK reduced LPS-induced neuronal death in neuron-microglia co-cultures. This was probably mediated via microglia as it did not affect TNF-alpha-induced neuronal death in pure neuronal cultures. Our data imply that BK has anti-inflammatory and neuroprotective effects in the central nervous system by modulating microglial function.

Authors+Show Affiliations

Laboratory of Pathophysiology, Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17402969

Citation

Noda, Mami, et al. "Neuroprotective Role of Bradykinin Because of the Attenuation of Pro-inflammatory Cytokine Release From Activated Microglia." Journal of Neurochemistry, vol. 101, no. 2, 2007, pp. 397-410.
Noda M, Kariura Y, Pannasch U, et al. Neuroprotective role of bradykinin because of the attenuation of pro-inflammatory cytokine release from activated microglia. J Neurochem. 2007;101(2):397-410.
Noda, M., Kariura, Y., Pannasch, U., Nishikawa, K., Wang, L., Seike, T., Ifuku, M., Kosai, Y., Wang, B., Nolte, C., Aoki, S., Kettenmann, H., & Wada, K. (2007). Neuroprotective role of bradykinin because of the attenuation of pro-inflammatory cytokine release from activated microglia. Journal of Neurochemistry, 101(2), 397-410.
Noda M, et al. Neuroprotective Role of Bradykinin Because of the Attenuation of Pro-inflammatory Cytokine Release From Activated Microglia. J Neurochem. 2007;101(2):397-410. PubMed PMID: 17402969.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Neuroprotective role of bradykinin because of the attenuation of pro-inflammatory cytokine release from activated microglia. AU - Noda,Mami, AU - Kariura,Yukihiro, AU - Pannasch,Ulrike, AU - Nishikawa,Kaori, AU - Wang,Liping, AU - Seike,Toshihiro, AU - Ifuku,Masataka, AU - Kosai,Yuki, AU - Wang,Bing, AU - Nolte,Christiane, AU - Aoki,Shunsuke, AU - Kettenmann,Helmut, AU - Wada,Keiji, PY - 2007/4/4/pubmed PY - 2007/6/2/medline PY - 2007/4/4/entrez SP - 397 EP - 410 JF - Journal of neurochemistry JO - J Neurochem VL - 101 IS - 2 N2 - Bradykinin (BK) has been reported to be a mediator of brain damage in acute insults. Receptors for BK have been identified on microglia, the pathologic sensors of the brain. Here, we report that BK attenuated lipopolysaccharide (LPS)-induced release of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta from microglial cells, thus acting as an anti-inflammatory mediator in the brain. This effect was mimicked by raising intracellular cAMP or stimulating the prostanoid receptors EP2 and EP4, while it was abolished by a cAMP antagonist, a prostanoid receptor antagonist, or by an inhibitor of the inducible cyclooxygenase (cyclooxygenase-2). BK also enhanced formation of prostaglandin E(2) and expression of microsomal prostaglandin E synthase. Expression of BK receptors and EP2/EP4 receptors were also enhanced. Using physiological techniques, we identified functional BK receptors not only in culture, but also in microglia from acute brain slices. BK reduced LPS-induced neuronal death in neuron-microglia co-cultures. This was probably mediated via microglia as it did not affect TNF-alpha-induced neuronal death in pure neuronal cultures. Our data imply that BK has anti-inflammatory and neuroprotective effects in the central nervous system by modulating microglial function. SN - 0022-3042 UR - https://www.unboundmedicine.com/medline/citation/17402969/Neuroprotective_role_of_bradykinin_because_of_the_attenuation_of_pro_inflammatory_cytokine_release_from_activated_microglia_ L2 - https://doi.org/10.1111/j.1471-4159.2006.04339.x DB - PRIME DP - Unbound Medicine ER -