TY - JOUR
T1 - Prostaglandin D2 induces heme oxygenase-1 in human retinal pigment epithelial cells
AU - Kuesap, Jiraporn
AU - Li, Bin
AU - Satarug, Soisungwan
AU - Takeda, Kazuhisa
AU - Numata, Ikuko
AU - Na-Bangchang, Kesara
AU - Shibahara, Shigeki
N1 - Funding Information:
This work was supported in part by Grant-in-Aid for Scientific Research (B) and the 21st Century COE Program Special Research Grant “the Center for Innovative Therapeutic Development for Common Diseases” from the Ministry of Education, Science, Sports, and Culture of Japan, and by the grant provided by the Cosmetology Foundation. J.K. was supported by the Scholarship for Higher Education from the Ministry of Education, Thailand, and S. Satarug (ID NO. L 07568) was supported by the Scholarship (long-term) from Japan Society for the Promotion of Science (JSPS).
PY - 2008/3/7
Y1 - 2008/3/7
N2 - The retinal pigment epithelium (RPE) constitutes the blood-retinal barrier, whose function is impaired in various pathological conditions, including cerebral malaria, a lethal complication of Plasmodium falciparum infection. Prostaglandin (PG) D2 is abundantly produced in the brain to regulate sleep responses. Moreover, PGD2 is a potential factor derived from intra-erythrocyte falciparum parasites. Heme oxygenase-1 (HO-1) is important for iron homeostasis via catalysis of heme degradation to release iron, carbon monoxide and biliverdin/bilirubin, and may influence iron supply to the intra-erythrocyte falciparum parasites. Here, we showed that treatment of human RPE cell lines, ARPE-19 and D407, with PGD2 significantly increased the expression levels of HO-1 mRNA, in a dose- and time-dependent manner. Transient expression assays showed that PGD2 treatment increased the HO-1-gene promoter activity through the enhancer sequence, containing a Maf-recognition element. Thus, PGD2 may contribute to the maintenance of heme homeostasis in the brain by inducing HO-1 expression.
AB - The retinal pigment epithelium (RPE) constitutes the blood-retinal barrier, whose function is impaired in various pathological conditions, including cerebral malaria, a lethal complication of Plasmodium falciparum infection. Prostaglandin (PG) D2 is abundantly produced in the brain to regulate sleep responses. Moreover, PGD2 is a potential factor derived from intra-erythrocyte falciparum parasites. Heme oxygenase-1 (HO-1) is important for iron homeostasis via catalysis of heme degradation to release iron, carbon monoxide and biliverdin/bilirubin, and may influence iron supply to the intra-erythrocyte falciparum parasites. Here, we showed that treatment of human RPE cell lines, ARPE-19 and D407, with PGD2 significantly increased the expression levels of HO-1 mRNA, in a dose- and time-dependent manner. Transient expression assays showed that PGD2 treatment increased the HO-1-gene promoter activity through the enhancer sequence, containing a Maf-recognition element. Thus, PGD2 may contribute to the maintenance of heme homeostasis in the brain by inducing HO-1 expression.
KW - Brain
KW - Erythrocyte
KW - Heme
KW - Heme oxygenase
KW - Iron
KW - Malaria
KW - Plasmodium falciparum
KW - Prostaglandin D
KW - Retina
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U2 - 10.1016/j.bbrc.2007.12.148
DO - 10.1016/j.bbrc.2007.12.148
M3 - Article
C2 - 18174022
AN - SCOPUS:38349022149
SN - 0006-291X
VL - 367
SP - 413
EP - 419
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 2
ER -
