Genetic Susceptibility to Renal Ischemia Reperfusion Injury Revealed in a Murine Model

Burne, Melissa J.; Haq, Mahmudul; Matsuse, Hiroto; Mohapatra, Shyam S.; Rabb, Hamid

doi:10.1097/00007890-200003150-00065

Cited by 58 publications

(38 citation statements)

References 9 publications

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“…But, da Silva et al (2007) and Kale et al (2003) reported no mice survived more than 24 hr when submitted to 35-45 min of bilateral renal ischemia with male C57BL/6 mice and Rosa26 mice, respectively. The discrepancy with our results is probably due to mouse strain differences (Burne et al 2000).…”

Section: Discussioncontrasting

confidence: 99%

Gender Differences in the Susceptibility to Renal Ischemia-Reperfusion Injury in BALB/c Mice

Wang

Batteux

et al. 2009

Tohoku J. Exp. Med.

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Section: Discussioncontrasting

confidence: 99%

Gender Differences in the Susceptibility to Renal Ischemia-Reperfusion Injury in BALB/c Mice

Wang

Batteux

et al. 2009

Tohoku J. Exp. Med.

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“…There are several possible mechanisms that may help explain the difference in results compared with previous reports (33,34). Different genetic backgrounds may contribute to this difference in observed injury (53). This might result from pleiotropic functions of OPN as aforementioned.…”

Section: Discussionmentioning

confidence: 76%

“…In contrast, OPN-null mice have reported to have more pronounced IRI (higher creatinine level and kidney histological abnormality) than wildtype mice, which would support a renoprotective function of OPN on TECs (34). The reason(s) for this discrepancy is unknown but may be due to the variable resistance and susceptibility of different mouse strains to IRI (53). In our model, OPN-null mice clearly had less severe kidney injury with reduced creatinine levels, less tissue damage, and fewer infiltrating NK cells.…”

Section: Discussionmentioning

confidence: 98%

Osteopontin Expressed in Tubular Epithelial Cells Regulates NK Cell-Mediated Kidney Ischemia Reperfusion Injury

Zhang

Shek

Wang

et al. 2010

The Journal of Immunology

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Renal ischemia reperfusion injury (IRI) occurs after reduced renal blood flow and is a major cause of acute injury in both native and transplanted kidneys. Studies have shown diverse cell types in both the innate and the adaptive immune systems participate in kidney IRI as dendritic cells, macrophages, neutrophils, B cells, CD4+ NK+ cells, and CD4+ T cells all contribute to this form of injury. Recently, we have found that NK cells induce apoptosis in tubular epithelial cells (TECs) and also contribute to renal IRI. However, the mechanism of NK cell migration and activation during kidney IRI remains unknown. In this study, we have identified that kidney TECs express a high level of osteopontin (OPN) in vitro and in vivo. C57BL/6 OPN-deficient mice have reduced NK cell infiltration with less tissue damage compared with wild-type C57BL/6 mice after ischemia. OPN can directly activate NK cells to mediate TEC apoptotic death and can also regulate chemotaxis of NK cells to TECs. Taken together, our study’s results indicate that OPN expression by TECs is an important factor in initial inflammatory responses that involves NK cells activity in kidney IRI. Inhibiting OPN expression at an early stage of IRI may be protective and preserve kidney function after transplantation.

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“…Variables previously shown to affect performance in response to hepatic IRI are animal sex (Harada et al 2004) strain (Burne et al 2000, Shireman & Quinones 2005, Dodd et al 2006) and intraoperative temperature regulation (Biberthaler et al 2001, Kato et al 2002, Khandoga et al 2003. These factors have been tested in heterogeous models of hepatic IRI, and as a result, experiments cannot be directly compared; their results are difficult to apply directly to the development of new experimental models.…”

Section: Discussionmentioning

confidence: 99%

Effect of temperature control upon a mouse model of partial hepatic ischaemia/reperfusion injury

2008

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SummaryIn vivo models of hepatic ischaemia/reperfusion injury (IRI) are widely used to study both the mechanisms of hepatic ischaemic injury and to seek means of hepatic protection. Achieving high-quality reproducible data are essential if the results of multiple studies are to be compared and reconciled. This paper presents our findings concerning the effect of intraoperative thermoregulation upon signal to noise ratios of hepatic IRI experiments in mice. Four experiments were conducted, using three different strategies for core temperature maintenance. Animals underwent hepatic IRI and euthanized 24 h postoperatively for measurement of plasma alanine aminotransferase (ALT). Duration of ischaemia was used to adjust the severity of injury. Experiment 1 utilized a constant output heating system and resulted in rising postoperative ALTs following increasing durations of hepatic ischaemia. Experiment 2, using the same constant output heating system confirmed a difference between ischaemic and sham-operated animals. Experiment 3 used a thermostatically controlled heating system and resulted in highly variable results with a small, but statistically significant correlation between ALT levels and rectal temperature readings. Experiment 4 used a homeothermic warming system and demonstrated highly reproducible data from increasing durations of ischaemia. High-quality data from hepatic ischaemia/ reperfusion models are dependent upon careful control of intraoperative temperature. The use of homeothermic warming systems is recommended and conversely, the use of thermostatically controlled warming mats is to be avoided in these models.Keywords Liver transplantation; liver resection; ischaemia/reperfusion injury; thermoregulation Human liver transplantation surgery necessitates the interruption of hepatic blood supply while the organ is retrieved from the donor, transported to the transplant centre and implanted in the recipient. Similarly, liver resection surgery often involves occlusion of the hepatic blood supply in order to limit blood loss from the cut surface of the liver. In both cases, the resulting ischaemia/ reperfusion insult leads to impaired hepatic function postoperatively. Ischaemia/reperfusion injury (IRI) most severely affects the livers from older donors and those with fatty infiltration (steatosis) arising from obesity or excessive alcohol intake. In the transplant setting, where the risk of IRI is judged excessive, such marginal livers may be discarded, placing further demands on an already overstretched donor pool. Conversely, overcoming hepatic IRI might alleviate postoperative liver dysfunction and expand the donor pool by recruiting back currently unusable organs (Patel et al. 2004, Devey et al. 2007).

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Genetic Susceptibility to Renal Ischemia Reperfusion Injury Revealed in a Murine Model

Abstract: 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.

Cited by 58 publications

References 9 publications

Gender Differences in the Susceptibility to Renal Ischemia-Reperfusion Injury in BALB/c Mice

Gender Differences in the Susceptibility to Renal Ischemia-Reperfusion Injury in BALB/c Mice

Osteopontin Expressed in Tubular Epithelial Cells Regulates NK Cell-Mediated Kidney Ischemia Reperfusion Injury

Effect of temperature control upon a mouse model of partial hepatic ischaemia/reperfusion injury

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