Kidney Week

Abstract: FR-PO168

Collecting Duct Cell Specific Mitochondrial Dysfunction Influence to Inflammation and Fibrosis in UUO Mice

Session Information

• Mitochondriacs and More
  November 03, 2017 | Location: Hall H, Morial Convention Center
  Abstract Time: 10:00 AM - 10:00 AM

Category: Acute Kidney Injury

• 001 AKI: Basic

Authors

• Jeong, Jin young, Chungnam National University, Daejeon, Korea (the Republic of)

Jin young Jeong,

• Song, Chang hun, Chungnam National University, Daejeon, Korea (the Republic of)

Chang hun Song,

• Bae, Hong jin, Chungnam National University, Daejeon, Korea (the Republic of)

Hong jin Bae,

• Lee, Jiwon M., Chungnam National University, Deajeon, Korea (the Republic of)

Jiwon M. Lee,

• Ham, Youngrok, Chungnam National University, Daejeon, Korea (the Republic of)

Youngrok Ham,

• Na, Kiryang, Chungnam National University, Daejeon, Korea (the Republic of)

Kiryang Na,

• Lee, Kang Wook, Chungnam National University, Daejeon, Korea (the Republic of)

Kang Wook Lee,

• Choi, Dae Eun, Chungnam National University, Daejeon, Korea (the Republic of)

Dae Eun Choi,

Background

Unilateral ureteral obstruction (UUO) induced mitochondrial dysfunction resulting in increase of oxidative stress and infammation in obstructed kidney. Although mitochondria play a role in UUO injury including tubulo-interstitial apoptosis, infammation and fbrosis, the role of collecting duct cells was not evaluated. We evaluated whether collecting duct specifc mitochondrial dysfunction affect the renal injury induced by UUO.

Methods

For generation collecting duct specifc mitochondrial injury mice, CRIF flox/flox mice were bred with Hoxb7-Cre mice. For evaluation of the phenotype of mice, we observed mitochondria using electron microscopy in mice. For evaluation of influence of CRIF1 deletion on mitochondrial function, we measured O2 consumption and membrane potential in control and silencing RNA treated mIMCD cells. For evaluation of effect on UUO induced renal injury, we divided mice into the following 4 groups: CRIF1flox/flox(WT) group; CRIF1 flox/flox-Hob7 Cre (CRIF1-KO) group; WT UUO group; and CRIF1-KO UUO group. I evaluated oxidative stress, inflammatory, and fibrosis marker in urine and kidney tissue.

Results

There are no significant difrenence in phenotype between CRIF1-KO and WT mice. Renal expression of MCP-1, osteopontin (OPN), Numbers of F4/80 positive cells, TGF-b, a-SMA, and Masson Trichrome stained area were significantly increased in CRIF1-KO-UUO kidneys compared with WT UUO kidneys., Urinary 8-OHDG was increased in CRIF1-KO-mice compared with WT mice. Also, Crif1-KO mice had signi��cantly increase of 8-OHDG-positive cell recruitment compared to WT mice. CRIF1-KO-UUO-kidneys were shown more increase recruitment of 8-OHDG-positive cells compared to WT-UUO-kindneys

Conclusion

Collecting duct specific mitochondrial injury induced increase of oxidative stress, renal inflammation, and renal fibrosis in UUO mice