Investigation of the effect of anti-osteopontin antibody on renal crystal formation

2015 Fiscal Year Final Research Report

• Project/Area Number: 25462518
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Urology
• Research Institution: Nagoya City University
• Principal Investigator: Homma hideki 名古屋市立大学, 医学(系)研究科(研究院), 研究員 (20260789)
• Co-Investigator(Kenkyū-buntansha): Kohri Kenjiro 名古屋市立大学, 学長 (30122047) ; Tozawa Keiichi 名古屋市立大学, 大学院医学研究科, 准教授 (40264733) ; Yasui takahiro 名古屋市立大学, 大学院医学研究科, 教授 (40326153) ; Okada Atsushi 名古屋市立大学, 大学院医学研究科, 講師 (70444966) ; HAMAMOTO Shuzo 名古屋市立大学, 大学院医学研究科, 助教 (80551267)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 腎結石 / オステオポンチン

Outline of Final Research Achievements

We have previously shown that the impaired RGD sequence of osteopontin inhibits renal crystal formation by using OPN-transgenic mice and OPN-knockout mice. Here, we investigated the effects of an anti-murine osteopontin antibody (35B6-Ab) that specifically reacts with the 162SLAYGLR168 sequence on renal crystal formation. Scanning electron microscopy showed that the crystals in 35B6-Ab-treated mice were aberrantly formed and their density was low. Microstructure analysis of renal tubular cells by transmission electron microscopy revealed that untreated mice showed collapsed mitochondria in the flattened cytoplasm of renal tubular cells. In vitro, 35B6-Ab was found to inhibit the attachment of 14C-labeled crystals to renal tubular culture cells and reduce morphological damage of these cells.
In conclusion, that 35B6-Ab contributes to the remarkable inhibition of early-stage renal crystal formation by preventing renal tubular cell injury and crystal-cell attachment.

Free Research Field

尿路結石