Date: Saturday, May 30, 2020
Session Time: 3:15pm-4:00pm
Presentation Time: 3:30pm-4:00pm
*Purpose: Recently, acute kidney injury is a important cause of chronic kidney injury, characterized by glomerular sclerosis and tubular fibrosis. Hypothermia attenuates the acute kidney injury induced by ischemia-reperfusion(IR). We previously reported that phosphorylation of ERK and HIF1 activations are important role in hypothermic protections. Although there has been reported that hypothermia protects acute kidney injury, there is little known that hypothermia reduce renal fibrosis after renal IR injury. We evaluated whether hypothermia protect against renal fibrosis and whether there is mechanism involved in renal IR injury.
*Methods: C57Bl/6 mice were divided into the following groups: sham-operated (32C vs 37C); IR mice (32C vs 37C). Ischemia reperfusion were performed by clamping the both renal peduncles for 27 min. Hypothermia(32C) was maintained from 10 min before ischemic surgery until reperfusion was performed (37min). Temperature was maintained by Animal Temperature Control System (BASi, USA). Blood and kidneys were collected at 0 time, 27 min after ischemia, and 4hr, D1, D3, D7 after reperfusion. Functional and molecular markers of kidney injury were evaluated.
*Results: In sham operated groups, hypothermia decreased TGF beta expression, compared to normal temperature. SOX9, known to play a role in regeneration and differentiation, was significantly reduced in the hypothermic sham group, compared to normal temperature sham. We evaluated the change in proteins of IR kidney, over time. TGF beta is decreased in hypothermic IR kidney at all time zone. Alpha SMA were significantly decreased in hypothermic kidney at 3Day and 7Day. SOX9 is decreased in hypothermic IR kidney at ischemia and 4hr and 3day. However, at 24hr and 7day, SOX 9 were not decreased. The nuclear translocation of NFkB were increased at 3day and 7day. Hypothermic culture of HK2 cell increased the NkFB in TGF beta treatment. In addition, in hypothermic condition TGF beta treatment increased the smad7 and decreased the phosphorylation of smad2/3 compared to normal temperature.
*Conclusions: Hypothermic protection activates NF-kB in kidney, which seems to have a protective effect by inhibiting the TGF beta – smad 2/3 signal.
To cite this abstract in AMA style:Choi D, Kim D, Kim E, Jeong J, Kim J, Ham Y, Chang Y, Na K, Lee K. Hypothermia Attenuates Renal Fibrosis after Renal Ischemia Reperfusion in Mice [abstract]. Am J Transplant. 2020; 20 (suppl 3). https://atcmeetingabstracts.com/abstract/hypothermia-attenuates-renal-fibrosis-after-renal-ischemia-reperfusion-in-mice/. Accessed May 7, 2021.
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