BACKGROUND: The development of genetically engineered mice has led to increased use of mouse models to study renal ischemic reperfusion injury (IRI). We hypothesized that susceptibility to IRI could result from strain differences due to genetic factors. METHODS: Our study compared recovery subsequent to renal IRI in NIH Swiss, C57BL/6, and BALB/c mice. Serum creatinine (SCr) and blood urea nitrogen (BUN) levels were evaluated postischemia. We also conducted reverse transcriptase-polymerase chain reaction (RT-PCR) analyses of renal cytokines and adhesion molecules postischemia. RESULTS: At 48 hr postischemia, renal dysfunction in NIH Swiss mice was significantly reduced, compared with other groups (P<0.01). BUN measurements confirmed renal protection at 48 hr in the NIH Swiss group. RT-PCR analysis of mRNA postischemia demonstrated that, between strains, there was little difference in mRNA expression for renal cytokines and adhesion molecules. CONCLUSIONS: NIH Swiss mice appear to be resistant in susceptibility to renal IRI. Early expression of pro-inflammatory genes was not associated with resistance to IRI, thus genetic factors could be important in outcome after renal IRI.
BACKGROUND: The development of genetically engineered mice has led to increased use of mouse models to study renal ischemic reperfusion injury (IRI). We hypothesized that susceptibility to IRI could result from strain differences due to genetic factors. METHODS: Our study compared recovery subsequent to renal IRI in NIH Swiss, C57BL/6, and BALB/c mice. Serum creatinine (SCr) and blood ureanitrogen (BUN) levels were evaluated postischemia. We also conducted reverse transcriptase-polymerase chain reaction (RT-PCR) analyses of renal cytokines and adhesion molecules postischemia. RESULTS: At 48 hr postischemia, renal dysfunction in NIH Swiss mice was significantly reduced, compared with other groups (P<0.01). BUN measurements confirmed renal protection at 48 hr in the NIH Swiss group. RT-PCR analysis of mRNA postischemia demonstrated that, between strains, there was little difference in mRNA expression for renal cytokines and adhesion molecules. CONCLUSIONS: NIH Swiss mice appear to be resistant in susceptibility to renal IRI. Early expression of pro-inflammatory genes was not associated with resistance to IRI, thus genetic factors could be important in outcome after renal IRI.
Authors: Jianlin Chen; John R Hartono; Reji John; Michael Bennett; Xin Jin Zhou; Yanxia Wang; Qingqing Wu; Pamela D Winterberg; Glenn T Nagami; Christopher Y Lu Journal: Kidney Int Date: 2011-06-01 Impact factor: 10.612
Authors: You-Hai Xu; Li Jia; Brian Quinn; Matthew Zamzow; Keith Stringer; Bruce Aronow; Ying Sun; Wujuan Zhang; Kenneth D R Setchell; Gregory A Grabowski Journal: BMC Genomics Date: 2011-01-11 Impact factor: 3.969
Authors: Longhui Qiu; Xingqiang Lai; Jiao-Jing Wang; Xin Yi Yeap; Shulin Han; Feibo Zheng; Charlie Lin; Zhuoli Zhang; Daniele Procissi; Deyu Fang; Lin Li; Edward B Thorp; Michael M Abecassis; Yashpal S Kanwar; Zheng J Zhang Journal: Kidney Int Date: 2020-08-18 Impact factor: 10.612