Expression and function of bradykinin receptors in microglia

Mami Noda; Yukihiro Kariura; Taiju Amano; Yoshimasa Manago; Kaori Nishikawa; Shunsuke Aoki; Keiji Wada

doi:10.1016/S0024-3205(02)02449-9

Expression and function of bradykinin receptors in microglia

Mami Noda, Yukihiro Kariura, Taiju Amano, Yoshimasa Manago, Kaori Nishikawa, Shunsuke Aoki, Keiji Wada

Research output: Contribution to journal › Article › peer-review

55 Citations (Scopus)

Abstract

Expression of bradykinin (BK) receptors and their cellular function were investigated in microglia. Microglial cells were isolated from mixed cultures of cerebrocortical cells from postnatal day 3 Wistar rats. Reverse transcription-PCR (RT-PCR) showed that rat primary microglia express mRNAs for the type 2 bradykinin (B₂) receptor subtype but not the type 1 (B₁) receptor subtype under our experimental condition. However, the expression of B₁ receptor was greatly up-regulated after the treatment of microglia with BK for 24 hours. The expression of B₂ receptor in microglia was further confirmed by immunocytochemistry. Membrane currents were measured using whole-cell recording under voltage-clamp conditions. In 14% of patched cells (12/85 cells), BK (100-200 nM) induced an outward current at the holding potential of -20 mV, with oscillations in 2 cases. The BK-induced outward current was transient and desensitized rapidly. TEA inhibited the BK-induced outward current in a dose-dependent manner. These results suggest that microglia express B₂ receptors and presumably increase the intracellular Ca²⁺ concentration via inositol trisphosphate with the subsequent activation of Ca²⁺-dependent K⁺ channels. Our data provide the first evidence that microglia express functional BK receptors and support the idea that microglia play an important role in CNS inflammatory responses.

Original language	English
Pages (from-to)	1573-1581
Number of pages	9
Journal	Life Sciences
Volume	72
Issue number	14
DOIs	https://doi.org/10.1016/S0024-3205(02)02449-9
Publication status	Published - Feb 21 2003
Externally published	Yes

All Science Journal Classification (ASJC) codes

Biochemistry, Genetics and Molecular Biology(all)
Pharmacology, Toxicology and Pharmaceutics(all)

Access to Document

10.1016/S0024-3205(02)02449-9

Cite this

@article{f777a5447c864c20b3602d4d79b75bbc,

title = "Expression and function of bradykinin receptors in microglia",

abstract = "Expression of bradykinin (BK) receptors and their cellular function were investigated in microglia. Microglial cells were isolated from mixed cultures of cerebrocortical cells from postnatal day 3 Wistar rats. Reverse transcription-PCR (RT-PCR) showed that rat primary microglia express mRNAs for the type 2 bradykinin (B2) receptor subtype but not the type 1 (B1) receptor subtype under our experimental condition. However, the expression of B1 receptor was greatly up-regulated after the treatment of microglia with BK for 24 hours. The expression of B2 receptor in microglia was further confirmed by immunocytochemistry. Membrane currents were measured using whole-cell recording under voltage-clamp conditions. In 14% of patched cells (12/85 cells), BK (100-200 nM) induced an outward current at the holding potential of -20 mV, with oscillations in 2 cases. The BK-induced outward current was transient and desensitized rapidly. TEA inhibited the BK-induced outward current in a dose-dependent manner. These results suggest that microglia express B2 receptors and presumably increase the intracellular Ca2+ concentration via inositol trisphosphate with the subsequent activation of Ca2+-dependent K+ channels. Our data provide the first evidence that microglia express functional BK receptors and support the idea that microglia play an important role in CNS inflammatory responses.",

author = "Mami Noda and Yukihiro Kariura and Taiju Amano and Yoshimasa Manago and Kaori Nishikawa and Shunsuke Aoki and Keiji Wada",

note = "Funding Information: We thank Prof. H. Nakanishi (Kyushu University) for providing microglia and teaching us the culture method at the beginning of this work. We also thank Prof. N. Akaike (Kyushu University) for providing some of experimental equipments, and Prof. D. A. Brown (University College London) and Dr. M. Brodwick (University of Texas Medical Branch) for their helpful comments. This work was supported in part by Grants-in-Aid for Scientific Research (No. 13680845 to M. N) of Japan Society for the Promotion of Science, Research Grant in Priority Area Research of the Ministry of Education, Science and Culture, Japan (to K.W.), Kyushu University Foundation (to M. N.), and Grants-in-Aid for Brain Science of the Ministry of Health, Labour and Welfare (to K. W.).",

year = "2003",

month = feb,

day = "21",

doi = "10.1016/S0024-3205(02)02449-9",

language = "English",

volume = "72",

pages = "1573--1581",

journal = "Life Sciences",

issn = "0024-3205",

publisher = "Elsevier Inc.",

number = "14",

}

TY - JOUR

T1 - Expression and function of bradykinin receptors in microglia

AU - Noda, Mami

AU - Kariura, Yukihiro

AU - Amano, Taiju

AU - Manago, Yoshimasa

AU - Nishikawa, Kaori

AU - Aoki, Shunsuke

AU - Wada, Keiji

N1 - Funding Information: We thank Prof. H. Nakanishi (Kyushu University) for providing microglia and teaching us the culture method at the beginning of this work. We also thank Prof. N. Akaike (Kyushu University) for providing some of experimental equipments, and Prof. D. A. Brown (University College London) and Dr. M. Brodwick (University of Texas Medical Branch) for their helpful comments. This work was supported in part by Grants-in-Aid for Scientific Research (No. 13680845 to M. N) of Japan Society for the Promotion of Science, Research Grant in Priority Area Research of the Ministry of Education, Science and Culture, Japan (to K.W.), Kyushu University Foundation (to M. N.), and Grants-in-Aid for Brain Science of the Ministry of Health, Labour and Welfare (to K. W.).

PY - 2003/2/21

Y1 - 2003/2/21

N2 - Expression of bradykinin (BK) receptors and their cellular function were investigated in microglia. Microglial cells were isolated from mixed cultures of cerebrocortical cells from postnatal day 3 Wistar rats. Reverse transcription-PCR (RT-PCR) showed that rat primary microglia express mRNAs for the type 2 bradykinin (B2) receptor subtype but not the type 1 (B1) receptor subtype under our experimental condition. However, the expression of B1 receptor was greatly up-regulated after the treatment of microglia with BK for 24 hours. The expression of B2 receptor in microglia was further confirmed by immunocytochemistry. Membrane currents were measured using whole-cell recording under voltage-clamp conditions. In 14% of patched cells (12/85 cells), BK (100-200 nM) induced an outward current at the holding potential of -20 mV, with oscillations in 2 cases. The BK-induced outward current was transient and desensitized rapidly. TEA inhibited the BK-induced outward current in a dose-dependent manner. These results suggest that microglia express B2 receptors and presumably increase the intracellular Ca2+ concentration via inositol trisphosphate with the subsequent activation of Ca2+-dependent K+ channels. Our data provide the first evidence that microglia express functional BK receptors and support the idea that microglia play an important role in CNS inflammatory responses.

AB - Expression of bradykinin (BK) receptors and their cellular function were investigated in microglia. Microglial cells were isolated from mixed cultures of cerebrocortical cells from postnatal day 3 Wistar rats. Reverse transcription-PCR (RT-PCR) showed that rat primary microglia express mRNAs for the type 2 bradykinin (B2) receptor subtype but not the type 1 (B1) receptor subtype under our experimental condition. However, the expression of B1 receptor was greatly up-regulated after the treatment of microglia with BK for 24 hours. The expression of B2 receptor in microglia was further confirmed by immunocytochemistry. Membrane currents were measured using whole-cell recording under voltage-clamp conditions. In 14% of patched cells (12/85 cells), BK (100-200 nM) induced an outward current at the holding potential of -20 mV, with oscillations in 2 cases. The BK-induced outward current was transient and desensitized rapidly. TEA inhibited the BK-induced outward current in a dose-dependent manner. These results suggest that microglia express B2 receptors and presumably increase the intracellular Ca2+ concentration via inositol trisphosphate with the subsequent activation of Ca2+-dependent K+ channels. Our data provide the first evidence that microglia express functional BK receptors and support the idea that microglia play an important role in CNS inflammatory responses.

UR - http://www.scopus.com/inward/record.url?scp=0037458425&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0037458425&partnerID=8YFLogxK

U2 - 10.1016/S0024-3205(02)02449-9

DO - 10.1016/S0024-3205(02)02449-9

M3 - Article

C2 - 12551746

AN - SCOPUS:0037458425

VL - 72

SP - 1573

EP - 1581

JO - Life Sciences

JF - Life Sciences

SN - 0024-3205

IS - 14

ER -

Expression and function of bradykinin receptors in microglia

Abstract

All Science Journal Classification (ASJC) codes

Access to Document

Other files and links

Fingerprint

Cite this