Acute kidney injury (AKI) is a common complication of critically ill patients and is associated with increased morbidity and mortality. Ischemia/reperfusion (I/R) and nephrotoxic injuries are the major causes of AKI in native and transplanted kidneys. The traditional kidney function test-serum creatinine will not elevate in the early phase of AKI insults. However, studies in animals suggested early treatment of AKI, even before the elevation of serum creatinine. That is the reason why there are many studies engaged in the search of possible biomarker for early detection of AKI, such as ystatin C，neutrophil gelatinaseassociated lipocalin (NGAL)，and microRNAs (miRs）. MiRs are small 22–25-nt-long noncoding RNA molecules that negatively regulate translation of target mRNAs. According to our previous data, we found that urinary miR-16 is up-regulated in patients with AKI by miR microarray computer analysis. In addition, real time PCR analysis also showed that urinary miR-16 excretion was 60-fold higher in AKI patients than who without AKI or normal controls, and the increasing levels of urinary miR-16 in AKI patients are consistent with the comparable AKI biomarker NGAL. However, whether miR-16 can actually act as a biomarker for AKI or the molecular pathophysiological pathways involved in must to be more advanced evaluate. Therefore, this proposal will collect the urine and blood of AKI patients for miR array to find the AKI related miRs. The pathophysiological pathways of miRs in AKI and their regulatory genes will also demonstrate. Our project will elucidate below questions: 1). The pathophysiological roles of miR during AKI. 2) The genes be regulated by target miRs and their signal transduction pathway after AKI. 3) Identify miRs that have the potential to be as a biomarker of AKI. Our result may provide a new therapeutic and diagnostic approaches for intervention in kidney pathophysiology.
|Effective start/end date||8/1/14 → 7/31/15|