Resistant To Renal Acute Ischemia-reperfusion Injury In FVB Mice: An Involvement Of CHOP

Objective:The purpose of this project is to explore a mouse strain that isresistant to acute ischemic kidney injury and to take a first step incharacterizing the molecular basis for the resistance.Methods:Acute renal ischemic injury model was established in male FVB andICR mice (8-10W) by removing right kidney followed by clamping leftrenal pedicle for45min.24hours after injury, blood and kidneywere collected to detect concentration of blood urea nitrogen（BUN）,to assess the degree of damage of renal pathology by PASstaining, to detect the expression of chop mRNA and CHOP in renaltissue by PCR and Western-blot. The control group tested the sameindicators as the model group. Additionally, some mice (n=6/strain)were followed for72hours to examine histology of kidney injuryevolution.Results:(1) PAS staining of renal tissue showed that kidneys were largelynormal in FVB mice after45minutes of ischemia while severe renaltubular injury including extensive cell death and the loss of renalstructure were present in ICR mice;(2) BUN levels were significantlyincreased from baseline in ICR but not in FVB mice;(3) Chop, amolecule that is critically involved in renal tubular cell death was elevated in ischemic ICR mice kidneys but remained relative normal inischemic FVB mice kidneys.Conclusions:In the acute renal ischemia-reperfusion injury model,the degreeof renal tubular epithelial cell injury of ICR mice are more seriousthan FVB mice, the expression of endoplasmic reticulum stressrelated protein CHOP also increases. It indicates that CHOP plays animportant role in acute renal ischemia-reperfusion injury，FVB miceare resistant to ischemic renal injury and the mechanism may beinvolve the expression of CHOP protein.