Effect of prostaglandin I2 analogs on macrophage inflammatory protein 1α in human monocytes via I prostanoid receptor and cyclic adenosine monophosphate.
Autor: | Tsai MK; From the *Division of Nephrology, Department of Internal Medicine, Kaohsiung Armed Forces General Hospital, Kaohsiung; †Department of Nursing, MeiHo University, Pingtung; ‡Division of Cardiac Surgery, Department of Surgery, §Division of Cardiology, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung Medical University; ∥Department of Pediatrics, E-DA Hospital, I-Shou University; ¶Department of Marine Biotechnology and Resources, National Sun Yat-sen University; **Graduate Institute of Medicine, College of Medicine, ††Department of Pediatrics, Kaohsiung Medical University Hospital, and Department of Pediatrics, Faculty of Pediatrics, College of Medicine, Kaohsiung Medical University; ‡‡Department of Pediatrics, Kaohsiung Municipal Ta-Tung Hospital, Kaohsiung; §§Department of Radiation Oncology, ∥∥Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Kaohsiung Medical University, and ¶¶Department of Pediatrics, Kaohsiung Municipal Hsiao-Kang Hospital, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan, Republic of China., Hsieh CC, Kuo HF, Yang SN, Kuo CH, Huang MY, Tsai YM, Lee MS, Hung CH |
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Jazyk: | angličtina |
Zdroj: | Journal of investigative medicine : the official publication of the American Federation for Clinical Research [J Investig Med] 2014 Feb; Vol. 62 (2), pp. 332-9. |
DOI: | 10.2310/JIM.0000000000000042 |
Abstrakt: | Aims: Inflammation plays critical roles in atherosclerosis. Chemokines are responsible for leukocyte trafficking and involve in inflammatory diseases. Macrophage inflammatory protein 1α (MIP-1α) has been implicated in atherosclerotic lesion formation. Prostaglandin I2 (PGI2) analog, used in pulmonary hypertension, has been reported to have anti-inflammatory functions. However, little is known about its role in the MIP-1α production in human monocytes. Methods: We investigated the effects of 3 conventional (iloprost, beraprost, and treprostinil) and 1 new (ONO-1301) PGI2 analogs, on the expression of MIP-1α expression in human monocytes. Human primary monocytes from control subjects and THP-1 cell line were treated with PGI2 analogs, with or without lipopolysaccharide (LPS) stimulation. Supernatants were harvested to measure MIP-1α levels by enzyme-linked immunosorbent assay. To explore which receptors involved the effects of PGI2 analogs on the expression of MIP-1α expression, I prostanoid (IP) and E prostanoid, peroxisome proliferator-activated receptor (PPAR)-α, and PPAR-r receptor antagonists were used to pretreat THP-1 cells. Forskolin, a cyclic adenosine monophosphate (cAMP) activator, was also used to further confirm the cAMP involvement on the effect of PGI2 analogs in MIP-1α production. Results: Three PGI2 analogs could suppress LPS-induced MIP-1α production in THP-1 cells and human primary monocytes. ONO-1301 had a similar effect. CAY 10449, an IP receptor antagonist, could reverse the suppressive effects on MIP-1α production of iloprost. Forskolin, a cAMP activator, also suppressed MIP-1α production in THP-1 cells. Conclusions: Prostaglandin I2 analogs suppressed LPS-induced MIP-1α production in human monocytes via the IP receptor and cAMP pathway. The PGI2 analog may be potential in the treatment for atherosclerosis. |
Databáze: | MEDLINE |
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