Evaluation of Cx43 proteins for PGE2 release from retinal pigment epithelial cells for understanding the pathological role in age-related macular degeneration.

2017 Fiscal Year Final Research Report

• Project/Area Number: 16K15157
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Medical pharmacy
• Research Institution: University of Toyama
• Principal Investigator: HOSOYA Ken-ichi 富山大学, 大学院医学薬学研究部(薬学), 教授 (70301033)
• Co-Investigator(Kenkyū-buntansha): 久保 義行 富山大学, 大学院医学薬学研究部(薬学), 准教授 (20377427) ; 酒井 秀紀 富山大学, 大学院医学薬学研究部(薬学), 教授 (60242509)
• Co-Investigator(Renkei-kenkyūsha): TACHIKAWA Masanori 東北大学, 大学院薬学研究科, 准教授 (00401810)
• Project Period (FY): 2016-04-01 – 2018-03-31
• Keywords: 薬学 / 網膜色素上皮細胞 / プロスタグランジン / 外側血液網膜関門 / ヘミチャネル / Cx43 / PGE2

Outline of Final Research Achievements

In this study, we aim to evaluate the role of connexin (Cx) 43 on the retinal pigment epithelial (RPE) cells in the alteration of prostaglandin (PG) E2 release under the pathological conditions including age-related macular degeneration. Under the normal conditions, several fluorescent substances, such as Lucifer Yellow, do not cross the plasma membrane of the cells. With the stimulus which open the hemichannels, these fluorescent substances were actively taken up into RPE cells. In addition, gene-knockdown for Cx43 in RPE cells caused the decrease of hemichannel mediated uptake of the substances. Moreover, PGE2 release from the RPE cells was significantly decreased in the presence of a hemichannel inhibitor. Taking these lines of evidence into consideration, it is suggested that Cx43 is involved in PGE2 release under the pathological conditions.

Free Research Field

医療系薬学