TY - JOUR
T1 - Involvement of Ca2+ in globular adiponectin-induced reactive oxygen species
AU - Akifusa, Sumio
AU - Kamio, Noriaki
AU - Shimazaki, Yoshihiro
AU - Yamaguchi, Noboru
AU - Yamashita, Yoshihisa
N1 - Funding Information:
Support for this research was provided by a Grant-in-Aid for Scientific Research (C) 18592285 from the Ministry of Education, Culture, Sports, Science, and Technology of Japan.
PY - 2009/4/17
Y1 - 2009/4/17
N2 - Globular adiponectin (gAd) induces the generation of reactive oxygen species (ROS) and nitric oxide (NO) in the murine macrophage cell line RAW 264. We investigated the role of Ca2+ in gAd-induced ROS and NO generation. Pretreatment with BAPTA-AM, a selective chelator of intracellular Ca2+ ([Ca2+]i), partially reduced gAd-induced generation of ROS and NO in gAd-treated RAW 264 cells. The lowest [Ca2+]i occurred 30 min after gAd treatment, after which [Ca2+]i increased continually and exceeded the initial level. The mitochondrial Ca2+ ([Ca2+]m) detected by Rhod-2 fluorescence started to increase at 6 h after gAd treatment. Pretreatment with a NAD(P)H oxidase inhibitor, diphenyleneiodonium, prevented the reduction of [Ca2+]i in the early phase after gAd treatment. Calcium depletion by BAPTA-AM had no effect on the gAd-induced [Ca2+]m oscillation. The administration of a specific calmodulin inhibitor, calmidazolium, significantly suppressed gAd-induced ROS and NO generation and NOS activity.
AB - Globular adiponectin (gAd) induces the generation of reactive oxygen species (ROS) and nitric oxide (NO) in the murine macrophage cell line RAW 264. We investigated the role of Ca2+ in gAd-induced ROS and NO generation. Pretreatment with BAPTA-AM, a selective chelator of intracellular Ca2+ ([Ca2+]i), partially reduced gAd-induced generation of ROS and NO in gAd-treated RAW 264 cells. The lowest [Ca2+]i occurred 30 min after gAd treatment, after which [Ca2+]i increased continually and exceeded the initial level. The mitochondrial Ca2+ ([Ca2+]m) detected by Rhod-2 fluorescence started to increase at 6 h after gAd treatment. Pretreatment with a NAD(P)H oxidase inhibitor, diphenyleneiodonium, prevented the reduction of [Ca2+]i in the early phase after gAd treatment. Calcium depletion by BAPTA-AM had no effect on the gAd-induced [Ca2+]m oscillation. The administration of a specific calmodulin inhibitor, calmidazolium, significantly suppressed gAd-induced ROS and NO generation and NOS activity.
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U2 - 10.1016/j.bbrc.2009.02.115
DO - 10.1016/j.bbrc.2009.02.115
M3 - Article
C2 - 19249286
AN - SCOPUS:62649096153
VL - 381
SP - 649
EP - 653
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
SN - 0006-291X
IS - 4
ER -