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Kidney Week

Abstract: SA-PO137

The Role of Akt1 in a Murine Model of AKI to CKD Progression

Session Information

Category: Acute Kidney Injury

  • 103 AKI: Mechanisms

Authors

  • Ye, Byung Min, Pusan National University Yangsan Hospital, Yangsan-si, Korea (the Republic of)
  • Kim, Il Young, Pusan National University Yangsan Hospital, Yangsan-si, Korea (the Republic of)
  • Lee, Dong Won, Pusan National University Yangsan Hospital, Yangsan-si, Korea (the Republic of)
  • Lee, Soo Bong, Pusan National University Yangsan Hospital, Yangsan-si, Korea (the Republic of)
  • Han, Miyeun, Pusan National University Hospital, Busan, Korea (the Republic of)
  • Rhee, Harin, Pusan National University Hospital, Busan, Korea (the Republic of)
  • Seong, Eun Young, Pusan National University Hospital, Busan, Korea (the Republic of)
  • Song, Sang Heon, Pusan National University Hospital, Busan, Korea (the Republic of)
Background

Acute kidney injury (AKI) is an underestimated, yet important risk factor for development of chronic kidney disease (CKD). However, underlying mechanism of AKI to CKD progression are poorly understood. Akt has been reported to be involved in renal ischemic reperfusion injury (IRI). In this study, we investigated the role of Akt1, one of the three Akt isoforms, in murine model of IRI-induced AKI to CKD progression

Methods

We subjected the wild type and Akt1−/− mice to renal IRI. Renal IRI was induced by clamping the left renal artery for 30 min followed by reperfusion. After 6 weeks of IRI, the renal fibrosis was assessed by histologic grading and Masson’s-trichrome staining. Fibrosis/apoptosis markers and MAPKs were also assessed by western blot.

Results

After 6 weeks after IRI, IRI kidneys in wild type mice showed the typical features of progressive CKD: widespread interstitial fibrosis/tubular atrophy, as indicated by collagen deposition assessed by Masson’s-trichrome staining. These fibrotic changes were significantly alleviated in Akt1−/− mice compared with the wild type mice. In addition, western blot analysis showed that Akt1−/− had attenuated expressions of fibrosis marker (vimentin and α-SMA) and phosphorylated-p44/42 MAPK (Erk1/2) compared with the wild type mice. Western blot analysis and TUNEL assay showed that the apoptosis was attenuated in Akt1−/− mice compared with wild type mice.

Conclusion

Our findings demonstrate that Akt1 contributes to IRI-induced AKI to CKD progression, suggesting that inhibition of this signaling pathway may provide a therapeutic approach of preventing IRI-induced AKI to CKD progression.