Abstract: TH-PO896
Relationship Between Endothelial Damage and Expression of Tropomyosin on Peritubular Capillary During the Progression of Experimental Obstructive Nephropathy
Session Information
- Molecular Mechanisms of CKD - I
October 25, 2018 | Location: Exhibit Hall, San Diego Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: CKD (Non-Dialysis)
- 1903 CKD (Non-Dialysis): Mechanisms
Authors
- Kitamura, Ken, Kita-Harima Medical Center, Ono, Japan
- Nakai, Kentaro, Fukuoka Red Cross Hospital, Fukuoka, Japan
- Fujii, Hideki, Kobe University Graduate School of Medicine, Kobe, Japan
- Nishi, Shinichi, Kobe University Graduate School of Medicine, Kobe, Japan
Background
Tubulointerstitial injury(TI) is a major determinant factor in progressive renal diseases. Although the injuries to peritubular capillary (PTC) network is crucial for the progression of TI, it has been few reported about marker for detecting endothelial damage on PTC. We investigated expression of Tropomyosin (TM), one of the actin-associated proteins on PTC during the progression of experimental obstructive nephropathy.
Methods
Male Wister rats (7 week old) were subjected to UUO or sham-operation, and kidneys were harvested on days 3, 7 and 14 post-surgery after pimonidazole infusion for evaluation of low oxygen area. We evaluated the expression of TM on PTC by immunostaining and immunoelectron microscopy. And real-time polymerase chain reaction, and western blot were performed. To clarify the mechanism, we assessed the expression of TM in human umbilical vein endothelial cells (HUVEC) exposed to hypoxia condition .
Results
The expression of TM on PTC significantly increased on day 3, reached a peak at day 7, and decreased on day14 by immunostaining. Also, TM was identified at cytoplasm of PTC by immunoelectron microscopy 7 days after operation, not identified in sham rats. In UUO, TM significantly expressed at low oxygen area, tended to co-express with Ki67. We confirmed the increased expression of TM in the whole kidney. In HUVEC, 12 hours hypoxia condition induced the expression of TM in immunofluorescent staining.
Conclusion
TM is a protein related to angiogenesis and increased the expression on PTC at the early stage of TI. This fact suggested TM might be a marker of endothelial damage on PTC to play a work for the protection against hypoxia damage.