Cell Biochemistry and Biophysics

, Volume 71, Issue 3, pp 1685–1693 | Cite as

Increased Expression of p-Akt correlates with Chronic Allograft Nephropathy in a Rat Kidney Model

  • Li-Na Zhou
  • Ning Wang
  • Yang Dong
  • Yiqin Zhang
  • Hequn Zou
  • Qingqin Li
  • Yangling Shi
  • Ling Chen
  • Wenying Zhou
  • Conghui HanEmail author
  • Yuxin WangEmail author
Original Paper


Chronic allograft nephropathy (CAN) is the most common cause of chronic graft dysfunction leading to graft failure, our study investigates the expression and significance of p-Akt in the pathogenesis of CAN in rats. Kidneys of Fisher (F344) rats were orthotopically transplanted into Lewis (LEW) rats. The animals were evaluated at 4, 8, 12, 16, and 24 weeks post-transplantation for renal function and histopathology. Phosphorate Akt (p-Akt) protein expression was determined by Western blot and immunohistological assays. Our data show that 24-h urinary protein excretion in CAN rats increased significantly at week 16 as compared with F344/LEW controls. Allografts got severe interstitial infiltration of mononuclear cells at week 4 and week 8, but it was degraded as the time went on after week 16. Allografts markedly presented with severe interstitial fibrosis (IF) and tubular atrophy at 16 and 24 weeks. p-Akt expression was upregulated in rat kidneys with CAN, and the increase became more significant over time after transplantation. p-Akt expression correlated significantly with 24-h urinary protein excretion, serum creatinine levels, tubulointerstitial mononuclear cells infiltration, smooth muscle cells (SMCs) migration in vascular wall, and IF. It was concluded that p-Akt overexpression might be the key event that involved mononuclear cells infiltration and vascular SMCs migration at early stage, and IF and allograft nephroangiosclerosis at the late stage of CAN pathogenesis in rats.


Kidney transplantation Kidney diseases p-Akt Chronic allograft nephropathy 



The authors thank Xiongfei Gu for excellent technical support. This study was funded by Xiamen Research Grant. This work was supported by American CMB-SUMS Scholars Program (China Medical Board of New York, Grant Number: #98-677) and National Natural Science Foundation of China (Grant Number: 997034), Xiamen Technology Fund, and Guangdong Provincial Natural Science Foundation (Grant Number: 990106).


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Copyright information

© Springer Science+Business Media New York 2014

Authors and Affiliations

  • Li-Na Zhou
    • 1
  • Ning Wang
    • 2
  • Yang Dong
    • 3
  • Yiqin Zhang
    • 1
  • Hequn Zou
    • 4
  • Qingqin Li
    • 1
  • Yangling Shi
    • 5
  • Ling Chen
    • 6
  • Wenying Zhou
    • 6
  • Conghui Han
    • 3
    Email author
  • Yuxin Wang
    • 1
    Email author
  1. 1.Department of NephrologyThe No. 2 Hospital of XiamenXiamenChina
  2. 2.Medical College Xiamen UniversityXiamenChina
  3. 3.Department of UrologyThe Affiliated School of Clinical Medicine, Xuzhou Medical CollegeXuzhouChina
  4. 4.Department of NephrologyThe No. 3 Affiliated Hospital of Southern Medical UniversityGuanghzouChina
  5. 5.Department of NephrologyThe No. 1 Affiliated Hospital of Wenzhou Medical CollegeWenzhouChina
  6. 6.Department of NephrologyThe No. 5 Affiliated Hospital of Sun Yat-sen UniversityGuanghzouChina

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